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Departments of 1 Physiology, 2 Pharmacology and Toxicology, and 3 Internal Medicine (Cardiology), Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We studied the effects of osmotic swelling on the components of excitation-contraction coupling in ventricular myocytes. Myocyte volume rapidly increased 30% in hyposmotic (0.6T) solution and was constant thereafter. Cell shortening transiently increased 31% after 4 min in 0.6T but then decreased to 68% of control after 20 min. In parallel, the L-type Ca2+ current (ICa-L) transiently increased 10% and then declined to 70% of control. Similar biphasic effects on shortening were observed under current clamp. In contrast, action potential duration was unchanged at 4 min but decreased to 72% of control after 20 min. Ca2+ transients were measured with fura 2-AM. The emission ratio with excitation at 340 and 380 nm (f340/f380) decreased by 12% after 3 min in 0.6T, whereas shortening and ICa-L increased at the same time. After 8 min, shortening, ICa-L, and the f340/f380 ratio decreased 28, 25, and 59%, respectively. The results suggest that osmotic swelling causes biphasic changes in ICa-L that contribute to its biphasic effects on contraction. In addition, swelling initially appears to reduce the Ca2+ transient initiated by a given ICa-L, and later, both ICa-L and the Ca2+ transient are inhibited.
osmolarity; action potential duration; calcium current; calcium transient; cell shortening
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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SWELLING OF CARDIAC MYOCYTES is a prominent aspect of the response to ischemia-reperfusion and elective cardioplegia and also may arise in renal insufficiency and syndromes with inappropriate secretion of antidiuretic hormone. Altered myocyte hydration has important functional consequences. Osmotic perturbations modulate both electrical activity (for reviews, see 34, 38, 42) and the ability of cardiac muscle to contract (5, 16, 17).
Although facets of the contractile response to osmotic swelling are known from studies on multicellular preparations, little mechanistic information is available at the single cell level to explain the implications of myocyte swelling for excitation-contraction (E-C) coupling. Moreover, the effect of swelling on L-type Ca2+ current (ICa-L), a critical aspect of E-C coupling, remains controversial. Under ruptured patch voltage-clamp conditions, for example, swelling is reported to enhance ICa-L in rabbit atrial and sinoatrial node cells (22), depress ICa-L in rat ventricular cells (4), and to have no significant effect in guinea pig (13, 31) and canine (44) ventricular cells. A swelling-induced enhancement of ICa-L also has been claimed based on fura 2 measurements of diltiazem-sensitive Ca2+ influx (36). It is unclear whether these differences in the response of ICa-L to myocyte swelling arise from species differences or from methodological issues, such as the composition of the patch pipette solution, the effectiveness of cell dialysis, or the variable extent of myocyte swelling under ruptured-patch conditions (6, 33). Several other species differences in E-C coupling, including the sensitivity of contraction to inhibition of the sarcoplasmic reticulum (SR), are well known (2).
The present study was designed to determine how osmotic swelling affects cardiac E-C coupling in rabbit ventricular myocytes cells by assessing several components of the E-C coupling pathway simultaneously. Electrophysiological parameters were measured with perforated patch voltage and current clamp, cell shortening and relative cell volume were followed by imaging techniques, and the Ca2+ transient was detected with fura 2. Osmotic swelling caused an initial increase and then a decrease in cell shortening elicited by both stimulated action potentials and voltage-clamp depolarizations of constant duration. ICa-L underwent biphasic changes that paralleled the enhancement and depression of cell shortening. In contrast, the Ca2+ transient and action potential duration (APD) decreased monotonically over time. A preliminary report of some of these results has appeared (19). Since this study was begun, Brette et al. (4) reported on the effects of myocyte swelling on E-C coupling. Several aspects of their results on rat ventricular myocytes differ from those of the present study.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Myocyte preparation and solutions. Hearts were excised from anesthetized rabbits (New Zealand White, 2-3 kg body wt, either sex), and ventricular myocytes were dissociated as previously described (7, 20). The heart was mounted on a Langendorff column and initially perfused with 37°C oxygenated Tyrode solution containing (in mmol/l) 140 NaCl, 5.4 KCl, 1 MgCl2, 1.8 CaCl2, 0.33 NaH2PO4, 10 glucose, and 10 HEPES (adjusted to pH 7.4 with NaOH). After perfusion with Ca2+-free Tyrode solution for ~5 min, the heart was then digested with a solution containing 0.5 mg/ml collagenase (Type II, Worthington; Freehold, NJ) and 1 mg/ml bovine serum albumin (Sigma; St. Louis, MO). Myocytes were stored in a high-K+ media containing (in mmol/l) 10 KCl, 10 KH2PO4, 120 K-glutamate, 10 taurine, 1.0 MgSO4, 10 HEPES, 20 glucose, and 0.5 EGTA (adjusted to pH 7.2 with KOH) and used within 5 h.
Myocytes were placed in a chamber (~0.3 ml) on an inverted microscope and suprafused at room temperature (21-22°C) with either 0.6T solution (~180 mosmol/l) containing (in mmol/l) 80 NaCl, 5.4 KCl, 1 MgCl2, 5 HEPES, 0.33 NaH2PO4, 10 glucose, and 1.8 CaCl2 (adjusted to pH 7.4 with NaOH) or with 1T solution (~300 mosmol/l), which was made by adding 125 mmol/l mannitol to 0.6T. Only quiescent rod-shaped cells showing clear striations were used.Electrophysiology.
Patch pipettes were drawn from thin-walled Corning 7740 glass (1.12 mm
ID, 1.5 mm OD) to a tip diameter of 3-4 µm. The electrode resistance was 0.8-1.2 M
when the pipettes were filled with
solution containing (in mmol/l) 120 potassium aspartate, 20 KCl, 5 NaCl, 1 MgCl2, and 10 HEPES (adjusted to pH 7.2 with KOH).
The perforated-patch method was used for all studies to avoid
unpredictable cell swelling and changes in membrane currents that often
slowly occur with the ruptured patch technique (6, 33).
Amphotericin-B (Sigma) was freshly dissolved in dimethyl sulfoxide
(Sigma) and then diluted in pipette-filling solution to give final
amphotericin concentration of 160 µg/ml. The tip of the pipette was
dipped into amphotericin-free solution for 2-3 s, the pipette was
then backfilled with the ionophore, and gigaseals were formed as
rapidly as possible. Access resistance decreased to 7-10 M
within 15 min of seal formation, and the experimental protocols were
then begun. A 3 M KCl-agar bridge was used to ground the bath.
Contractility.
Cell shortening in response to field stimulation, intracellular current
injection, or depolarizing voltage steps was recorded with a video
edge-tracking detector (VED-104, Crescent Electronics; Sandy, UT).
Field stimulation was utilized for intact cells not undergoing
perforated patch clamp, and 4- to 5-V pulses, 5 ms in duration, were
applied at 0.2 Hz with a pair of Ag electrodes. When electrical
activity and contraction were measured simultaneously under perforated
patch conditions, either 70-95 pA, 2-ms depolarizing pulses were
applied via the patch pipette to record action potentials or 300-ms
depolarizations from 
50 to 0 mV at 0.1 Hz were employed to record
membrane currents. APD was measured at 90% repolarization (APD90). To isolate ICa-L,
the Na+ current was inactivated by holding at 50 mV, and
5 mmol/l 4-aminopyridine, 0.5 mmol/l BaCl2, and 2 µmol/l
dofetilide were added to block the transient outward K+
current (Ito), the inwardly rectifying
K+ current (IK1), and the rapidly
activating component of the delayed rectifier K+ current
(IKr), respectively.
ICa-L was measured as the peak inward current
relative to the current at the end of the 300-ms depolarization.
Cell volume. Methods for determining relative cell volume have been described previously (7). An inverted microscope (Diaphot, Nikon; Garden City, NY) equipped with Hoffman modulation optics (×40, 0.55 numerical aperature) and a high-resolution TV camera (CCD72, Dage-MTI; Michigan City, IN) coupled to a video framegrabber (PIXCI-SV4, Epix; Buffalo Grove, IL) was used to image myocytes. Images were captured on-line at selected time points during the period of the experiment. A combination of commercial (SigmaScan Pro, SPSS; Chicago, IL) and custom programs were used to determine cell width, length, and the planar area of the image. Changes in cell width and thickness are proportional (9). Taking each cell as its own control, relative cell volume was calculated as volt/volc = (areat × widtht)/(areac × widthc), where t and c refer to test (e.g., 0.6T) and control (1T) solutions, respectively. The calculated values are independent of assumptions regarding the geometric shape of the cross section of the myocyte as long as the shape does not change. These methods provide estimates of relative cell volume that are reproducible to <1% (7, 9).
Statistical analysis. Group data are expressed as means ± SE. Repeated-measures analysis of variance and Dunnett's test were used for comparisons of multiple time points to control values, and paired Student's t-tests were used to evaluate differences between two group means. All statistical analysis was done in SigmaStat (SPSS), and P < 0.05 was considered to indicate significance.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Effect of brief osmotic swelling on cell shortening.
Figure 1 illustrates the effects of
switching from an isosmotic 1T solution to a hyposmotic 0.6T solution
for 6 min and then back to the 1T solution in an intact myocyte. Upon
exposure to 0.6T, cell shortening (Fig. 1A) elicited by
field stimulation rapidly increased from 6.1 to 9.5 µm, about a 55%
enhancement of contractile performance that was maintained throughout
the brief exposure to hyposmotic solution. The calculated relative cell
volume (Fig. 1B), which was obtained at 1-min intervals, increased by 29% in 0.6T solution without evidence of compensatory volume regulation. The increase in cell volume resulted from a distinct
increase in the width of the cell in 0.6T solution with little or no
change in cell length, as previously reported (9). Augmentation of cell shortening already was obvious within the first
minute of the osmotic challenge at a time when cell volume had
increased by <12%. When switched back to 1T solution, cell volume and
the extent of cell shortening returned to their initial values rapidly.
Similar results were obtained in five cells. On average, relative cell
volume increased by 29 ± 3% (P < 0.01) and cell
shortening increased by 34 ± 5% after 4 min in 0.6T solution (P < 0.01), and both parameters were indistinguishable
from control after 4 min of recovery in 1T solution. A rapid
enhancement of cell shortening upon osmotic swelling also was reported
recently in rat ventricular myocytes (4).
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APD and cell shortening.
To study the effects of brief swelling on cardiac E-C coupling,
the action potential and cell shortening were recorded simultaneously under current clamp conditions. Figure 2
shows representative recordings under isosmotic control conditions
(1T), after 3 min in hyposmotic solution (0.6T), and after recovery for
5 min in 1T solution (1T, recovery). Cell swelling decreased APD and
slightly depolarized the resting membrane potential
(Em), and both effects were fully reversible
(Fig. 2A). Simultaneously, cell shortening increased in 0.6T
(Fig. 2B), as previously was shown when the myocyte was not
undergoing dialysis through the patch pipette (Fig. 1B), and
the time to the peak of shortening decreased (Fig. 2B).
After 3 min of exposure to 0.6T, APD90 decreased from
418.6 ± 16.1 to 370.3 ± 14.2 ms (P < 0.01), resting Em depolarized from 80.9 ± 1.3 to 79.2 ± 1.2 mV (P < 0.05), cell
shortening increased by 28.4 ± 3.1% (P < 0.01)
from 3.2 ± 0.6 to 4.1 ± 0.7 µm, and time to peak of cell
shortening decreased from 386 ± 31 to 322 ± 27 ms
(P < 0.01) (n = 6 for each paired
measurement). The results indicated that osmotic swelling enhanced
cardiac contractile performance at the time when the duration of the
action potential was reduced.
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79.1 ± 0.7 to 76.1 ± 0.6 mV at 20 min
(P < 0.01), was associated with cell swelling in 0.6T,
but comparison of the time course of cell swelling and membrane
depolarization shows that the fall in resting Em
was completed ~2 min after cell swelling was complete. Both cell
volume and resting Em promptly returned to their
control values when switched back to 1T solution.
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Effects of osmotic swelling on ICa-L and the
Ca2+ transient.
One possibility is that the biphasic response of cell shortening to
osmotic swelling results, at least in part, from a biphasic modulation
of ICa-L. Such biphasic changes in
ICa-L also might help explain the inconsistency
of previous studies on swelling-induced changes in cardiac
ICa-L under ruptured patch conditions (4, 22, 31, 44). To evaluate the effect of osmotic swelling on
ICa-L, ICa-L was measured
under perforated patch conditions with a 300-ms voltage step from 50
to 0 mV at 0.1 Hz. Figure 5 illustrates
the time dependence of ICa-L upon switching from 1T to 0.6T solution for 10 min and during a 10-min recovery period in
1T solution. Paralleling the biphasic effects of osmotic swelling on
cell shortening (Fig. 4A), ICa-L
initially increased by 12% from 680 to 762 pA, reaching a maximum
after ~2 min in 0.6T, a time when cell swelling was complete. Then,
while the cell volume remained constant, ICa-L
slowly declined to 465 pA, 68% of its control value. This slow decay
of ICa-L in 0.6T was not due to rundown of the
Ca2+ current. On returning to 1T solution,
ICa-L slowly returned to its initial value and
was 678 pA after 10 min of recovery. Similar results were obtained in
five cells. On average, hyposmotic swelling increased
ICa-L by 9.6 ± 1.8% (P < 0.01) from 709.5 ± 37.2 to 772.2 ± 25.8 pA after
2.8 ± 0.3 min in 0.6T. The current then decreased by 28.5 ± 4.1% (P < 0.01) to 508.6 ± 37.3 pA after 10 min in 0.6T, and ICa-L partially recovered to
619.6 ± 26.6 pA, 87.4 ± 3.6% (P < 0.01) of
its initial value in 1T. These data suggest that
swelling-induced changes in ICa-L contribute to
both the transient increase in contractile performance and the
subsequent decline.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Osmotic swelling of ventricular myocytes in 0.6T solution had a biphasic effect on contractile performance both in intact ventricular myocytes not subject to patch clamp and in myocytes under perforated patch conditions. Cell shortening initially was enhanced by 28 to 34% within 3-4 min, but at latter times cell shortening was reduced to about 70% of its control value. Similar results have been obtained for twitch tension in multicellular cardiac preparations (5, 16, 17) and more recently (4) for cell shortening in rat ventricular myocytes. The present data suggest that biphasic changes in ICa-L, as well as decreased APD and Ca2+ transients, contribute to the modulation of cell shortening by osmotic swelling. These same factors are expected to contribute to osmotic swelling-induced changes in force development in multicellular preparations (5, 16, 17), although cell shortening and force development are not identical measures of contractile performance.
Effect of swelling on ICa-L . The basis for the transient increase in twitch tension and cell shortening in response to osmotic swelling has been obscure. Brette et al. (4) recently postulated that the initial increase in cell shortening was due to an unspecified enhanced coupling between Ca2+ entry and Ca2+ release. We found, however, that the magnitude of ICa-L undergoes biphasic changes after osmotic swelling that parallel cell shortening. Initially ICa-L increased by 10% at about 3 min, but latter it decreased to 72% of control. The decline in ICa-L over time in these perforated patch experiments cannot be attributed to current rundown because ICa-L recovered nearly to its control value on returning to isosmotic conditions (Fig. 5B). Thus the observed transient increase in ICa-L is an alternative explanation for the transient increase in contractile performance.
Previous studies of the effect of osmotic swelling on cardiac ICa-L have given conflicting results. Brette et al. (4) reported a monotonic decrease in ICa-L, whereas Taouil et al. (36) and Matsuda et al. (22) found an increase and Groh et al. (13), Sasaki et al. (31), and Zhou et al. (44) detected no change. The reasons for the disparate reports on the effect of osmotic swelling on ICa-L remain uncertain, but the present results emphasize that the time point selected for measuring ICa-L is important. In addition, methodological issues such as perforated versus ruptured patch techniques and species differences may contribute to the inconsistent results in the literature. Although this apparently is the first report of a biphasic effect of osmotic swelling on cardiac ICa-L, a similar transient response was noted in pancreatic
-cells
(10). Furthermore, it recently was reported that the T-type Ca2+ current is enhanced by osmotic swelling in
guinea pig myocytes (27). The T-type Ca2+
current should not significantly contaminate the present measurements of ICa-L because the holding potential was set
at 50 mV, which inactivates T-type Ca2+ channels.
Although the cell membrane is stretched by osmotic swelling, swelling
often has distinct effects from axial mechanical stretch. Osmotic
swelling dilutes the cytoplasm and stretches the membrane by increasing
cell width and thickness, whereas there is little or no effect on
length (9). In contrast to the present results, axial
mechanical stretch does not appear to alter
ICa-L (14, 31).
Other factors regulating cell shortening. Multiple factors regulate contractile function in cardiac muscle and are likely to play a role in the observed effects on cell shortening. Osmotic swelling modulates several membrane currents (34, 38, 42), and cell swelling induced a slowly developing shortening of APD90 from ~450 to 330 ms that may itself modulate contractile performance by affecting transmembrane Ca2+ fluxes. It is important to note, however, that APD was unaffected after 4 min in 0.6T at a time when cell volume changes were long since complete and the transient increase in cell shortening was observed (Fig. 4). The eventual reduction in APD is likely to be due to the slow activation of swelling-activated currents including ICl,swell (8, 11, 33) and the slow delayed rectifying K current (IKs) (29, 44), as well as the depression of ICa-L shown here and by others (4).
Another important issue is the effect of osmotic swelling on SR Ca2+ stores. The reduction in Ca2+ influx via Ca2+ current and the shortening of APD observed here favor the depletion of SR Ca2+ stores over time. Consistent with this idea, caffeine-inducible SR Ca2+ release is depressed after 10 min of osmotic swelling (4). Moreover, osmotic swelling has been shown to cause a persistent reduction of intracellular Na+ and Ca2+ activity in multicellular ventricular and Purkinje fiber preparations (18). Reduction of Na+ by dilution (18) and stimulation of the Na+-K+ pump (3, 40) favors extrusion of Ca2+ by the Na+/Ca2+ exchanger. On the other hand, osmotic swelling directly inhibits Na+/Ca2+ exchange in isolated myocytes when ionic concentrations are maintained in the steady state by ruptured patch (43). Even under patch-clamp conditions, however, osmotic swelling must initially reduce intracellular Na+ in patch-clamped myocytes, because water movement is much more rapid (35) than dialysis of the cytoplasm by the patch pipette (21). Such a transient fall in intracellular Na+ is expected to result in extrusion of Ca2+ and contribute to the depletion of SR Ca2+ stores. A surprising result was that the Ca2+ transient detected with fura 2 was slightly depressed after 3 min in 0.6T, whereas at the same time point ICa-L and cell shortening were enhanced and swelling was complete (Fig. 6). One interpretation is that osmotic swelling reduced the efficiency of the coupling between Ca2+ entry and Ca2+ release, a conclusion opposite to that reached for rat myocytes (4). Alternatively, this observation may simply reflect the larger cytoplasmic volume into which Ca2+ flows in osmotically swollen cells. The effects of swelling on fura 2 (see below), however, preclude rigorously distinguishing between these possibilities. Comparison of the effect of swelling on the Ca2+ transient and on cell shortening also suggest that osmotic swelling increases cell shortening at a given level of Ca2+. Enhanced Ca2+ sensitivity is likely to reflect, at least in part, the reduction in the ionic strength of the cytoplasm as water flows rapidly into the myocyte. An inverse relationship between ionic strength and tension development is well established in skinned cardiac (26) and skeletal muscle (12, 15) and has been attributed to increased affinity of troponin-C for Ca2+ at reduced ionic strength and several other mechanisms (1, 25, 32). A fall in cytoplasmic viscosity due to osmotic swelling also would favor enhanced shortening. On the other hand, if interfilament spacing increased as cell width increased during osmotic swelling, a decrease in myofilament Ca2+ sensitivity would be expected (23, 39). Decreased cytoplasmic ionic strength and viscosity may also confound interpretation of the fura 2 fluorescence ratio. Based on an increase in the f340/f380 ratio, osmotic swelling was claimed to initially increase the Ca2+ transient in the rat ventricle (4). Reduction in ionic strength decreases the dissociation constant for Ca2+ (37, 41), however, and a reduction of viscosity preferentially suppresses fluorescence at longer wavelengths (28, 30). Both of these effects augment the f340/f380 ratio, suggesting an increase in Ca2+ when none has occurred. To the contrary, we initially observed a small decrease in the f340/f380 ratio upon osmotic swelling, a finding that cannot be attributed to swelling-induced alterations in the properties of fura 2. Nevertheless, the effects of ionic strength and viscosity on fura 2 suggest that the initial decrease in the Ca2+ transient is greater than would be calculated from the f340/f380 ratio based on an in situ calibration in isosmotic solutions. Comparisons between the f340/f380 ratio transients recorded at different times after osmotic swelling was complete should not be affected by these calibration issues. Swelling in hyposmotic solution is sometimes taken as a model for the swelling that occurs under pathological conditions, such as ischemia and reflow. An important distinction should be noted, however. Swelling after ischemia and reflow occurs as a result of a hyperosmotic intracellular milieu rather than a hyposmotic extracellular environment. Because several components of contractile function are sensitive to ionic strength (1, 25, 26, 32), it is uncertain whether the present results apply to myocyte swelling in the setting of ischemia. In summary, osmotic swelling caused a transient enhancement and then a depression of ICa-L that paralleled the enhancement and depression of shortening of ventricular myocytes. APD and the Ca2+ transient decreased monotonically over time and also contributed to the depression of contractile function after prolonged myocyte swelling.| |
ACKNOWLEDGEMENTS |
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This study was supported by National Heart, Lung, and Blood Institute Grant HL-46764 and the American Heart Association Grant 51049U.
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FOOTNOTES |
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First published November 23, 2001;10.1152/ajpheart.00946.2001
Present address for G-R Li: Institute of Cardiovascular Science & Medicine, University of Hong Kong, Pok Fu Lam, Hong Kong.
Address for reprint requests and other correspondence: C. M. Baumgarten, Dept. of Physiology, Medical College of Virginia, 1101 E. Marshall St., Richmond, VA 23298-0551 (E-mail: baumgart{at}hsc.vcu.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.
Received 31 October 2001; accepted in final form 20 November 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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P < 0.01 vs. 1T control; n = 7.
