AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 294: H2535-H2539, 2008. First published April 11, 2008; doi:10.1152/ajpheart.01369.2007
0363-6135/08 $8.00
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
294/6/H2535    most recent
01369.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Edwards, D. G.
Right arrow Articles by Prasad, R. Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Edwards, D. G.
Right arrow Articles by Prasad, R. Y.

Wave reflection augments central systolic and pulse pressures during facial cooling

David G. Edwards, Matthew S. Roy, and Raju Y. Prasad

Department of Health, Nutrition, and Exercise Sciences, University of Delaware, Newark, Delaware

Submitted 27 November 2007 ; accepted in final form 10 April 2008


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Cardiovascular events are more common in the winter months, possibly because of hemodynamic alterations in response to cold exposure. The purpose of this study was to determine the effect of acute facial cooling on central aortic pressure, arterial stiffness, and wave reflection. Twelve healthy subjects (age 23 ± 3 yr; 6 men, 6 women) underwent supine measurements of carotid-femoral pulse wave velocity (PWV), brachial artery blood pressure, and central aortic pressure (via the synthesis of a central aortic pressure waveform by radial artery applanation tonometry and generalized transfer function) during a control trial (supine rest) and a facial cooling trial (0°C gel pack). Aortic augmentation index (AI), an index of wave reflection, was calculated from the aortic pressure waveform. Measurements were made at baseline, 2 min, and 7 min during each trial. Facial cooling increased (P < 0.05) peripheral and central diastolic and systolic pressures. Central systolic pressure increased more than peripheral systolic pressure (22 ± 3 vs. 15 ± 2 mmHg; P < 0.05), resulting in decreased pulse pressure amplification ratio. Facial cooling resulted in a robust increase in AI and a modest increase in PWV (AI: –1.4 ± 3.8 vs. 21.2 ± 3.0 and 19.9 ± 3.6%; PWV: 5.6 ± 0.2 vs. 6.5 ± 0.3 and 6.2 ± 0.2 m/s; P < 0.05). Change in mean arterial pressure but not PWV predicted the change in AI, suggesting that facial cooling may increase AI independent of aortic PWV. Facial cooling and the resulting peripheral vasoconstriction are associated with an increase in wave reflection and augmentation of central systolic pressure, potentially explaining ischemia and cardiovascular events in the cold.

arterial stiffness; augmentation index; blood pressure; cold

EPIDEMIOLOGIC STUDIES have demonstrated that there is an increase in cardiovascular events and deaths in the winter months (10, 13, 26, 27, 39). Additionally, exposure to cold has been reported to make symptoms of angina more severe in those with cardiovascular disease (14, 21). Identifying the mechanisms by which cold exposure increases cardiovascular events and myocardial ischemia is important in understanding this phenomenon, potentially leading to countermeasures to minimize risk in those with cardiovascular disease.

It has been suggested that increased sympathetic activation and blood pressure in response to cold exposure may contribute to cardiovascular events in the cold (9, 27). Sympathetic activation could lead to an increase in peripheral arterial stiffness via vasoconstriction (4) and passively increase central elastic arterial stiffness via changes in arterial pressure (29). An increase in arterial stiffness can elevate central systolic pressure due to an inability to absorb pulsations from the heart and an increase in wave reflection from the periphery (30). Central pressure is the pressure that the left ventricle must overcome, thus determining left ventricular workload (31, 44). Additionally, central systolic and pulse pressures are clinically important because they have been shown to be markers of disease (3, 33, 42) and predictors of cardiovascular outcomes (34, 35, 45).

We have demonstrated (11) that full-body cold exposure for 30 min at 4°C increased aortic augmentation index (AI), a measure of wave reflection, leading to augmented central systolic pressure, indicating that cold-induced increases in arterial stiffness and wave reflection may be an important underlying mechanism explaining the high prevalence of cardiovascular events in cold environments. Facial cooling results in sympathetic activation, vasoconstriction, and increased systolic and diastolic peripheral blood pressure (5, 18, 20) similar to whole body cooling in a cold environment. Facial cooling may be a more appropriate model to examine the effects of cold-induced sympathetic activation on vascular function given that individuals are typically properly clothed in cold weather and cold exposure is restricted to smaller body regions such as the face. Thus, studying the effects of facial cooling may be a better model for examining the effects of cold exposure. Additionally, assessment of aortic stiffness should be included in studies of cold exposure since an acute change in aortic stiffness is one mechanism by which cold may increase wave reflection; however, the contribution of acute changes in aortic stiffness to increased wave reflection during cold exposure has yet to be studied. The purpose of this study was to determine the effects of facial cooling on central blood pressure, wave reflection, and aortic stiffness. We hypothesized that facial cooling would result in increased central blood pressure, wave reflection, and aortic stiffness.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Subjects. Twelve apparently healthy men (n = 6) and women (n = 6), as assessed by medical history questionnaire, participated in this study (age 23 ± 3 yr; mass 68 ± 9 kg; height 171 ± 9 cm; body mass index 23 ± 2 kg/m2). Subjects were nonsmokers, were asked to refrain from caffeine, alcohol, and exercise for at least 24 h before testing, and reported to the lab at least 4 h after eating. All procedures were reviewed and approved by the Institutional Review Board, and all subjects gave written informed consent.

Study design. Testing involved two visits to the lab, where subjects underwent two trials under either facial cooling or control conditions. The two trials consisted of measurement of either arterial stiffness (carotid-femoral pulse wave velocity, PWV) or central pressures and wave reflection (pulse wave analysis, PWA). Two trials were performed because our lab only has two tonometers; therefore, assessment of carotid-femoral PWV and radial artery tonometry could not be performed simultaneously. The order of trials (PWV or PWA) and selection of conditions (facial cooling or control) were randomized, with the remaining condition performed during the second visit. Visits were performed within 5 days of each other at the same time of day. All testing in female subjects was completed within 5 days of the onset of their menstrual cycle.

Experimental protocol. Control trials involved supine rest, and facial cooling trials involved applying a cold gel pack (0°C) to the forehead with a damp paper towel forming a barrier between the gel pack and forehead. The gel pack was secured in place with an ACE bandage. Gel packs were kept in a thermostat-controlled standard freezer. Baseline measurements were performed after 15 min of supine rest. Measurements were repeated after 2 min of facial cooling/control and again 5 min later (7 min total), with the same procedures as baseline measurements. Two minutes was chosen for the first measurement because peak sympathetic nervous system activity has been observed at 90 s and peak systolic and diastolic pressure by 2 min of ice on forehead facial cooling (19). The measurement at 7 min was taken to evaluate the effects of prolonged facial cooling. After 4 min of facial cooling, the gel pack was replaced with a new gel pack for the remainder of the protocol to maintain the cold stimulus. Subjects rested for 20 min between trials to allow heart rate and blood pressure to return to baseline values.

Physiological measures. Baseline blood pressure was assessed in triplicate and averaged with oscillometric sphygmomanometry (Dash 2000, GE Medical Systems) and heart rate with three-lead ECG telemetry (Dash 2000, GE Medical Systems) after subjects were lying quietly in a supine position for 15 min. Carotid-femoral PWV was measured with the use of applanation tonometry to record both carotid artery and femoral artery waveforms simultaneously, by clamping high-fidelity strain gauge transducers (Millar Instruments, Houston, TX) in place over the right carotid and femoral arteries. These data were continuously collected during the facial cooling or control protocol (BIOPAC Systems, Goleta, CA). External distances were measured proximally from the carotid measurement site to the sternal notch and distally from the sternal notch to the femoral measurement site via the navel. Aortic distance was calculated by subtracting the carotid to sternal distance from the sternal to femoral distance. Carotid-femoral PWV was calculated by dividing the measured aortic distance by the average measured time delay between the initial upstrokes of 10 consecutive corresponding carotid and femoral waveforms. Carotid-femoral PWV is a regional measurement of aortic stiffness (40).

Applanation tonometry was used to record a radial arterial waveform by clamping a high-fidelity strain gauge transducer in place over the radial artery (Millar Instruments). Applanation tonometry has been shown previously to record a pressure wave that does not differ from waveforms obtained from intra-arterial measurements (23). The radial waveform was calibrated from the brachial sphygmomanometric measurement of systolic and diastolic pressures. A central aortic pressure wave was synthesized from the measured radial artery pressure waveform with the SphygmoCor Px system (AtCor Medical, Sydney, Australia), which uses a transfer function and is FDA approved. The use of a transfer function to approximate the central pressure wave from the radial wave has been validated with both intra-arterially (7, 22, 32) and noninvasively (15) obtained radial pressure waves. Central systolic and pulse pressures derived with this system have also shown good agreement with estimates using carotid recordings (1). We chose to record radial waves instead of carotid because they are easier to obtain. Central pressures, AI, and the time delay of the reflected wave (TR) were obtained from the synthesized wave. AI is defined as the ratio of reflected wave amplitude and pulse pressure, or AI = (Ps – Pi)/(Ps – Pd), where Ps is peak systolic pressure, Pd is end-diastolic pressure, and Pi is an inflection point marking the beginning upstroke of the reflected pressure wave. TR is the travel time of the forward wave from the heart to the major reflecting site and back. Additional calculations derived from the synthesized aortic pressure wave were the systolic pressure time index (STI), the diastolic pressure time index (DTI), and the subendocardial viability ratio (SEVR). STI, the area under the systolic portion of the curve, has been shown to be related to systolic load or the work of the heart and oxygen consumption, and DTI, the area under the diastolic portion of the curve, is associated with coronary perfusion (6). SEVR is the ratio of DTI to STI expressed as a percentage and an index of subendocardial perfusion (6).

Pulse pressure amplification ratio was calculated as brachial pulse pressure/central pulse pressure. Mean arterial pressure (MAP) was calculated over the cardiac cycle from the calibrated radial pressure waveform.

Statistical analysis. A 2 x 3 (condition x time) analysis of variance with repeated measures was used to compare differences among trials. Bonferroni adjusted post hoc analyses were performed to determine differences within and between conditions. Pearson correlations were determined between change in AI and change in MAP, PWV, and TR after 2 min of facial cooling. Multiple linear regression was performed to determine the best predictor(s) of change in AI. Statistical analysis was performed with the SPSS statistical program (version 13, SPSS). An {alpha}-level of 0.05 was required for statistical significance.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
All subjects completed each experimental trial. There were no differences in baseline measurements between facial cooling and control conditions. Heart rate and blood pressure data are presented in Table 1. Heart rate remained unchanged during control trials and facial cooling trials. MAP did not change during control trials but was increased (P < 0.05) above baseline at both 2 and 7 min of each facial cooling trial. Peripheral systolic and diastolic blood pressure did not change during control trials and were increased (P < 0.05) at 2 and 7 min of each facial cooling trial. Similarly, central aortic systolic and diastolic blood pressures did not change during control trials but increased (P < 0.05) during facial cooling. Facial cooling induced an average increase of 22 ± 3 mmHg in central aortic systolic pressure from baseline to 2 min, compared with only a 15 ± 2 mmHg increase in brachial systolic pressure (P < 0.05; Fig. 1). Brachial pulse pressure remained unchanged throughout both control and facial cooling trials, whereas central aortic pulse pressure did not change during control trials but increased (P < 0.05) above baseline at both 2 and 7 min of each facial cooling trial. Pulse pressure amplification ratio (brachial pulse pressure/central pulse pressure) was decreased (P < 0.05) below baseline at both 2 and 7 min of facial cooling but remained unchanged during control trials.


View this table:
[in this window]
[in a new window]

  		Table 1. Hemodynamic variables

 

Figure 1
View larger version (8K):
[in this window]
[in a new window]

  		Fig. 1. Change in systolic pressure induced by 2 min of facial cooling. Values are means ± SE. *P < 0.05 vs. brachial.

 
AI was increased at 2 and 7 min of facial cooling (P < 0.05; Table 1). There was an increase in carotid-femoral PWV and a decrease in TR at 2 and 7 min of facial cooling (P < 0.05; Table 1). STI and DTI both increased at 2 and 7 min of facial cooling (P < 0.05; Fig. 2, A and B). Facial cooling did not elicit any changes in SEVR compared with baseline (Fig. 2C). There were no changes in AI, carotid-femoral PWV, STI, DTI, or SEVR during control trials.


Figure 2
View larger version (9K):
[in this window]
[in a new window]

  		Fig. 2. Systolic time index (A), diastolic time index (B), and subendocardial viability ratio (C) at baseline (BSLN), 2 min, and 7 min during facial cooling and control trials. Values are means ± SE. *P < 0.05, 2 and 7 min vs. baseline; {dagger}P < 0.05, 2 and 7 min vs. control.

 
Pearson correlations between change in AI and change in MAP, PWV, and TR after 2 min of facial cooling revealed that only change in MAP was significantly correlated with change in AI (r = 0.796, r2 = 0.63, P = 0.002). Furthermore, multiple linear regression revealed that only change in MAP was a significant predictor of change in AI.


   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The purpose of this study was to examine the effect of acute facial cooling on arterial stiffness, wave reflection, and central blood pressure. The primary findings of this study were that 1) carotid-femoral PWV, a measure of aortic arterial stiffness, was increased during facial cooling; 2) wave reflection, as assessed by AI, increased during facial cooling; and 3) brachial and central systolic pressures both increased during facial cooling, but the magnitude of facial cooling-induced change in central systolic pressure was greater than the change in brachial systolic pressure. Furthermore, brachial pulse pressure did not change whereas central pulse pressure increased during facial cooling.

Our finding of increased systolic, diastolic, and mean arterial pressure during facial cooling is consistent with previous facial cooling studies (2, 19, 20). Allen et al. (2) compared full-face cooling to forehead-only cooling, using bags of ice water placed on the face for 90 s, and found similar increases in systolic pressure with both techniques, suggesting that forehead cooling alone as used in the present study elicits an pressure response equivalent to full facial cooling. Facial cooling for 150 s resulted in an increase in systolic pressure that peaked at 2 min of facial cooling (19). The present study found that the rise in systolic pressure was maintained 7 min after the application of cold.

To our knowledge, the present study is the first to examine the effects of an acute cold stimulus on carotid-femoral PWV, a regional measure of aortic stiffness. Facial cooling modestly increased carotid-femoral PWV in our subjects, indicating stiffening of the central elastic arteries. Wave reflection, as assessed by AI, was substantially increased during facial cooling. AI was previously reported to increase after cold exposure utilizing a cold pressor test (CPT; hand in ice water) (17) or whole body cooling (11). We also observed a decrease in pulse pressure amplification ratio during facial cooling. Previous pharmacological experiments demonstrated that reflected waves affect peak central systolic pressure but not peripheral pressure (41). This occurs because the reflected wave arising from the lower body may arrive before peak systolic pressure centrally and typically arrives after peak systolic pressure peripherally (29). Thus our observed increase in wave reflection likely augmented central systolic and pulse pressure, whereas peripheral pulse pressure was unaffected, explaining the drop in pulse pressure amplification ratio.

The cold stimulus during facial cooling results in an increase in muscle sympathetic nerve activity (19, 20), which likely increases wave reflection by altering the amplitude and timing of the reflected wave (29). An increase in wave reflection can result from alterations in the arterial system via changes in PWV (29). Interestingly, only the change in MAP was correlated with the change in AI following 2 min of facial cooling. This suggests that facial cooling may increase AI independent of aortic PWV and that increased smooth muscle tone in resistance vessels is potentially the primary determinant of increased wave reflection during facial cooling-induced sympathetic activation. In support of this, Kelly et al. (24) demonstrated that AI can change independently from aortic PWV during administration of nitroglycerin or angiotensin II, which have primarily peripheral effects. These authors observed relatively small changes in aortic PWV (<1 m/s) in the presence of large changes in AI during both angiotensin II and nitroglycerin administration (24). These findings are similar to the small change in PWV and the large change in AI observed in the present study. Acute increases in stiffness of elastic arteries, such as the aorta as observed in the present study, are thought to be passive (29). As MAP increases higher levels of wall stress are supported by stiffer collagen fibers, causing a stiffer arterial wall, as opposed to a more compliant arterial wall at lower pressures when elastin fibers predominate (9). Indeed, aortic stiffness is unaltered during sympathetic activation induced by lower body negative pressure when MAP does not change (37).

In addition to PWV, AI may depend on alterations in tone of small arteries and arterioles determining the amplitude and site of wave reflections (24). We could not calculate vascular resistance since we did not measure cardiac output; however, we did not observe any change in heart rate, and it was previously reported that facial cooling does not alter cardiac output (25, 36). Therefore, the rise in MAP would indicate that smooth muscle tone increased in resistance vessels as a result of facial cooling. Given the statistical relationship between MAP and AI in the present study, we speculate that the primary mechanism of increased wave reflection during facial cooling is alteration in the amplitude and site of wave reflections as a result of sympathetic activation. Previous observations of increased wave reflection during handgrip exercise (12) or CPT (17) may be due to the same mechanism.

We also examined systolic and diastolic time indexes (STI and DTI) as well as SEVR. STI and DTI were both increased during facial cooling, resulting in no change in SEVR. In the present study, normal coronary perfusion would be expected even during increased demand on the heart (STI), because of a parallel increase in perfusion pressure (DTI). It has been demonstrated that normal coronary arteries dilate in response to cold stimulus with CPT (28), aiding coronary blood supply in young healthy individuals. Atherosclerotic coronary arteries have been shown to constrict in response to cold-induced sympathetic outflow with CPT (28), potentially altering the balance between myocardial oxygen supply and demand. Constriction of the coronary arteries may reduce myocardial oxygen supply even under conditions of increased diastolic perfusion pressure, as observed in the present study, increasing the likelihood of myocardial ischemia.

It should be noted that our study involved direct application of cold to the forehead and therefore may not be the best representation of environmental exposure to cold. Others have investigated the effect of blowing cold air on the face and found that peripheral systolic and diastolic pressures increased to varying degrees depending on the temperature and wind speed used (8, 16, 38, 43); however, the pressure increases observed in the present study are within the range of observed values found in those studies. Future work could examine the effects of facial exposure to cold air and wind on arterial stiffness and wave reflection.

In summary, facial cooling resulted in a greater increase in central systolic pressure compared with peripheral systolic pressure. The greater change in central systolic pressure can be attributed to the observed increase in wave reflection. Thus facial cooling and the resulting augmentation in central systolic pressure might play a role in the occurrence of ischemia and cardiovascular events in the cold. Future investigations should examine the effect of cold exposure on arterial stiffness, wave reflection, and myocardial oxygen demand in older or cardiovascular disease populations.


   FOOTNOTES
 

Address for reprint requests and other correspondence: D. G. Edwards, Dept. of Health, Nutrition, and Exercise Sciences, 541 South College Ave., 142 HPL, Newark, DE 19716 (e-mail: dge{at}udel.edu)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Adji A, O'Rourke MF. Determination of central aortic systolic and pulse pressure from the radial artery pressure waveform. Blood Press Monit 9: 115–121, 2004.[CrossRef][Web of Science][Medline]
  2. Allen MT, Shelley KS, Boquet AJ Jr. A comparison of cardiovascular and autonomic adjustments to three types of cold stimulation tasks. Int J Psychophysiol 13: 59–69, 1992.[CrossRef][Web of Science][Medline]
  3. Boutouyrie P, Bussy C, Lacolley P, Girerd X, Laloux B, Laurent S. Association between local pulse pressure, mean blood pressure, and large-artery remodeling. Circulation 100: 1387–1393, 1999.[Abstract/Free Full Text]
  4. Boutouyrie P, Lacolley P, Girerd X, Beck L, Safar M, Laurent S. Sympathetic activation decreases medium-sized arterial compliance in humans. Am J Physiol Heart Circ Physiol 267: H1368–H1376, 1994.[Abstract/Free Full Text]
  5. Brown CM, Sanya EO, Hilz MJ. Effect of cold face stimulation on cerebral blood flow in humans. Brain Res Bull 61: 81–86, 2003.[CrossRef][Web of Science][Medline]
  6. Buckberg GD, Fixler DE, Archie JP, Hoffman JI. Experimental subendocardial ischemia in dogs with normal coronary arteries. Circ Res 30: 67–81, 1972.[Abstract/Free Full Text]
  7. Chen CH, Nevo E, Fetics B, Pak PH, Yin FC, Maughan WL, Kass DA. Estimation of central aortic pressure waveform by mathematical transformation of radial tonometry pressure. Validation of generalized transfer function. Circulation 95: 1827–1836, 1997.[Abstract/Free Full Text]
  8. Collins KJ, Abdel-Rahman TA, Easton JC, Sacco P, Ison J, Dore CJ. Effects of facial cooling on elderly and young subjects: interactions with breath-holding and lower body negative pressure. Clin Sci (Lond) 90: 485–492, 1996.[Medline]
  9. Culic V. Acute risk factors for myocardial infarction. Int J Cardiol 117: 260–269, 2007.[CrossRef][Web of Science][Medline]
  10. Danet S, Richard F, Montaye M, Beauchant S, Lemaire B, Graux C, Cottel D, Marecaux N, Amouyel P. Unhealthy effects of atmospheric temperature and pressure on the occurrence of myocardial infarction and coronary deaths. A 10-year survey: the Lille-World Health Organization MONICA project (Monitoring Trends and Determinants in Cardiovascular Disease). Circulation 100: E1–E7, 1999.[Medline]
  11. Edwards DG, Gauthier AL, Hayman MA, Lang JT, Kenefick RW. Acute effects of cold exposure on central aortic wave reflection. J Appl Physiol 100: 1210–1214, 2006.[Abstract/Free Full Text]
  12. Edwards DG, Mastin CR, Kenefick RW. Wave reflection and central aortic pressure are increased in response to static and dynamic muscle contraction at comparable workloads. J Appl Physiol 104: 439–445, 2008.[Abstract/Free Full Text]
  13. Enquselassie F, Dobson AJ, Alexander HM, Steele PL. Seasons, temperature and coronary disease. Int J Epidemiol 22: 632–636, 1993.[Abstract/Free Full Text]
  14. Frank SM, Higgins MS, Fleisher LA, Sitzmann JV, Raff H, Breslow MJ. Adrenergic, respiratory, and cardiovascular effects of core cooling in humans. Am J Physiol Regul Integr Comp Physiol 272: R557–R562, 1997.[Abstract/Free Full Text]
  15. Gallagher D, Adji A, O'Rourke MF. Validation of the transfer function technique for generating central from peripheral upper limb pressure waveform. Am J Hypertens 17: 1059–1067, 2004.[CrossRef][Web of Science][Medline]
  16. Gavhed D, Makinen T, Holmer I, Rintamaki H. Face temperature and cardiorespiratory responses to wind in thermoneutral and cool subjects exposed to –10 degrees C. Eur J Appl Physiol 83: 449–456, 2000.[CrossRef][Web of Science][Medline]
  17. Geleris P, Stavrati A, Boudoulas H. Effect of cold, isometric exercise, and combination of both on aortic pulse in healthy subjects. Am J Cardiol 93: 265–267, 2004.[CrossRef][Web of Science][Medline]
  18. Heath ME, Downey JA. The cold face test (diving reflex) in clinical autonomic assessment: methodological considerations and repeatability of responses. Clin Sci (Lond) 78: 139–147, 1990.[Medline]
  19. Heindl S, Struck J, Wellhoner P, Sayk F, Dodt C. Effect of facial cooling and cold air inhalation on sympathetic nerve activity in men. Respir Physiol Neurobiol 142: 69–80, 2004.[CrossRef][Web of Science][Medline]
  20. Heistad DD, Abbound FM, Eckstein JW. Vasoconstrictor response to simulated diving in man. J Appl Physiol 25: 542–549, 1968.[Free Full Text]
  21. Juneau M, Johnstone M, Dempsey E, Waters DD. Exercise-induced myocardial ischemia in a cold environment. Effect of antianginal medications. Circulation 79: 1015–1020, 1989.[Abstract/Free Full Text]
  22. Karamanoglu M, O'Rourke MF, Avolio AP, Kelly RP. An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man. Eur Heart J 14: 160–167, 1993.[Abstract/Free Full Text]
  23. Kelly R, Hayward C, Avolio A, O'Rourke M. Noninvasive determination of age-related changes in the human arterial pulse. Circulation 80: 1652–1659, 1989.[Abstract/Free Full Text]
  24. Kelly RP, Millasseau SC, Ritter JM, Chowienczyk PJ. Vasoactive drugs influence aortic augmentation index independently of pulse-wave velocity in healthy men. Hypertension 37: 1429–1433, 2001.[Abstract/Free Full Text]
  25. Kelsey RM, Patterson SM, Barnard M, Alpert BS. Consistency of hemodynamic responses to cold stress in adolescents. Hypertension 36: 1013–1017, 2000.[Abstract/Free Full Text]
  26. Mannino JA, Washburn RA. Environmental temperature and mortality from acute myocardial infarction. Int J Biometeorol 33: 32–35, 1989.[CrossRef][Web of Science][Medline]
  27. Marchant B, Ranjadayalan K, Stevenson R, Wilkinson P, Timmis AD. Circadian and seasonal factors in the pathogenesis of acute myocardial infarction: the influence of environmental temperature. Br Heart J 69: 385–387, 1993.[Abstract/Free Full Text]
  28. Nabel EG, Ganz P, Gordon JB, Alexander RW, Selwyn AP. Dilation of normal and constriction of atherosclerotic coronary arteries caused by the cold pressor test. Circulation 77: 43–52, 1988.[Abstract/Free Full Text]
  29. Nichols WW. Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms. Am J Hypertens 18: 3S–10S, 2005.[Web of Science][Medline]
  30. Nichols WW, Edwards DG. Arterial elastance and wave reflection augmentation of systolic blood pressure: deleterious effects and implications for therapy. J Cardiovasc Pharmacol Ther 6: 5–21, 2001.[Abstract/Free Full Text]
  31. Nichols WW, O'Rourke MF. McDonald's Blood Flow in Arteries. New York: Oxford Univ. Press, 2005.
  32. Pauca AL, O'Rourke MF, Kon ND. Prospective evaluation of a method for estimating ascending aortic pressure from the radial artery pressure waveform. Hypertension 38: 932–937, 2001.[Abstract/Free Full Text]
  33. Philippe F, Chemaly E, Blacher J, Mourad JJ, Dibie A, Larrazet F, Laborde F, Safar ME. Aortic pulse pressure and extent of coronary artery disease in percutaneous transluminal coronary angioplasty candidates. Am J Hypertens 15: 672–677, 2002.[CrossRef][Web of Science][Medline]
  34. Roman MJ, Devereux RB, Kizer JR, Lee ET, Galloway JM, Ali T, Umans JG, Howard BV. Central pressure more strongly relates to vascular disease and outcome than does brachial pressure: the Strong Heart Study. Hypertension 50: 197–203, 2007.[Abstract/Free Full Text]
  35. Safar ME, Blacher J, Pannier B, Guerin AP, Marchais SJ, Guyonvarc'h PM, London GM. Central pulse pressure and mortality in end-stage renal disease. Hypertension 39: 735–738, 2002.[Abstract/Free Full Text]
  36. Sherwood A, May CW, Siegel WC, Blumenthal JA. Ethnic differences in hemodynamic responses to stress in hypertensive men and women. Am J Hypertens 8: 552–557, 1995.[CrossRef][Web of Science][Medline]
  37. Sonesson B, Vernersson E, Hansen F, Lanne T. Influence of sympathetic stimulation on the mechanical properties of the aorta in humans. Acta Physiol Scand 159: 139–145, 1997.[CrossRef][Web of Science][Medline]
  38. Stroud MA. Effects on energy expenditure of facial cooling during exercise. Eur J Appl Physiol Occup Physiol 63: 376–380, 1991.[CrossRef][Web of Science][Medline]
  39. Thakur CP, Anand MP, Shahi MP. Cold weather and myocardial infarction. Int J Cardiol 16: 19–25, 1987.[CrossRef][Web of Science][Medline]
  40. Van Bortel LM, Duprez D, Starmans-Kool MJ, Safar ME, Giannattasio C, Cockcroft J, Kaiser DR, Thuillez C. Clinical applications of arterial stiffness, Task Force III: recommendations for user procedures. Am J Hypertens 15: 445–452, 2002.[CrossRef][Web of Science][Medline]
  41. Vlachopoulos C, Hirata K, O'Rourke MF. Pressure-altering agents affect central aortic pressures more than is apparent from upper limb measurements in hypertensive patients: the role of arterial wave reflections. Hypertension 38: 1456–1460, 2001.[Abstract/Free Full Text]
  42. Waddell TK, Dart AM, Medley TL, Cameron JD, Kingwell BA. Carotid pressure is a better predictor of coronary artery disease severity than brachial pressure. Hypertension 38: 927–931, 2001.[Abstract/Free Full Text]
  43. Walsh JT, Andrews R, Batin PD, Cowley AJ. Haemodynamic and hormonal response to a stream of cooled air. Eur J Appl Physiol Occup Physiol 72: 76–80, 1995.[CrossRef][Web of Science][Medline]
  44. Westerhof N, O'Rourke MF. Haemodynamic basis for the development of left ventricular failure in systolic hypertension and for its logical therapy. J Hypertens 13: 943–952, 1995.[Web of Science][Medline]
  45. Williams B, Lacy PS, Thom SM, Cruickshank K, Stanton A, Collier D, Hughes AD, Thurston H, O'Rourke M. Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) study. Circulation 113: 1213–1225, 2006.[Abstract/Free Full Text]




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
294/6/H2535    most recent
01369.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Edwards, D. G.
Right arrow Articles by Prasad, R. Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Edwards, D. G.
Right arrow Articles by Prasad, R. Y.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.