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Department of Biology, The University of Scranton, Scranton, Pennsylvania
Submitted 18 September 2006 ; accepted in final form 9 August 2007
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ABSTRACT |
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hamster; vascular architecture; vascular control; menstrual cycle; reproduction
The ovary experiences up to threefold changes in blood flow amplitude throughout the estrous cycle (11, 35), with still greater increases during pregnancy and pseudopregnancy (2, 22). Total ovarian blood flow peaks during the preovulatory phase, when follicular growth is rapid and estrogen levels are high (11, 35). With ovulation and the commencement of luteal function, total ovarian flow begins to fall and initially is delivered predominantly to the corpora lutea before shifting to the next cohort of growing follicles following luteal regression (11, 35).
Several vascular components appear to be critical to vascular regulation of the ovary. The ovarian resistance arteries, which in many species anastomose with major vessels of the uterus, may help regulate ovarian flow magnitude and ovarian capillary pressure. Together with paired veins and lymphatics, they also may constitute an important countercurrent pathway for cross-regulation of the ovary and uterus (3, 14, 19). Ovarian arterioles that reside in stromal tissue may modulate flow distribution to the follicles and corpora lutea. Follicular and luteal capillaries, which undergo a dramatic change in number and distribution throughout the estrous cycle (9), clearly affect the capacity for exchange in these ovarian compartments.
Although the coarse outline of these hemodynamic changes is known, it is not clear how modulation of ovarian flow and its changing distribution are brought about, nor which segments of the vascular pathway most contribute to flow control. Our previous observations indicate that the terminal arterioles feeding follicular and luteal capillaries have little tone (30). Larger upstream arterioles reside deep in the ovary, hidden from observation. Capillary angiogenesis, so predominant in the ovary (9), may strongly affect intraovarian blood flow distribution, but capillary beds typically account for only a small percentage of total vascular resistance (13, 24). Recent evidence also has shown that uterine artery endothelium is responsive to estrogen, leading to upregulation of endothelial nitric oxide synthase (eNOS) (34) and the potential for increased nitric oxide (NO) production (37), suggesting a mechanism for resistance artery control of ovarian blood flow. Moreover, there is evidence that in some pathological conditions, such as diabetes, ovulatory dysfunction may be related to defects in vascular control such as decreased bioavailability of NO (26). In the testicular circulation, an embryologically related vascular bed serving a parenchyma with many of the same transport demands as the ovary, a large proportion of the total vascular resistance resides in the resistance arteries (32). Thus we hypothesized that a large proportion of the total vascular resistance establishing ovarian blood flow amplitude resides in the utero-ovarian resistance arteries and that these vessels have the capacity to manipulate their tone, and thus manipulate total ovarian resistance, in relation to the stage of the estrous cycle.
The Golden hamster has been an important experimental model for the study of reproduction for nearly 70 years (6) because of a number of advantages it conveys. Its strong light-cycle dependency underlies the highly reproducible 4-day estrous cycle under laboratory conditions (9, 20). Furthermore, determination of the estrous-cycle phase is simple and unambiguous, with the day of estrous marked by a vaginal discharge that is so prominent and distinct (6) that it is the routine method for determining cycle phase (9, 35). Coupling these advantages with the deep body of knowledge in hamster reproductive physiology as well as the extensive use of the hamster for in vivo microcirculatory studies (7, 16, 25, 30, 32) establishes the hamster as an excellent model for the study of vascular control of reproductive function.
We have employed our in vivo preparation of the hamster utero-ovarian vascular network (30) to pursue the three following experimental objectives: 1) to characterize the architectural arrangement of the network of arteries that supply and interconnect the ovary and the uterus, 2) to quantify the intravascular pressure profile across this arterial network to estimate the resistance artery contribution to total ovarian vascular resistance, and 3) to determine whether the utero-ovarian resistance arteries modulate their diameters in an estrous cycle-specific manner.
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METHODS |
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Microvascular preparation. The utero-ovarian resistance artery network was investigated by using an in vivo preparation of the Golden hamster ovary that we previously described (30). Briefly, each animal was anesthetized with pentobarbital sodium (70 mg/kg ip), the trachea was intubated, and the left femoral artery and vein were cannulated. The jugular vein was cannulated for the injection of fluorescent label (see Microscopy). Systemic arterial pressure was recorded with a Spectramed (model TNF-R) pressure transducer via the arterial catheter. Saline containing 7.27 mg/ml pentobarbital sodium was infused (0.56 ml/h) via the femoral venous catheter to maintain anesthesia and to compensate for renal and respiratory fluid losses. The surgical protocol involved exteriorization of the right ovary and the cranial aspect of the uterine horn into a 5-ml well, stabilization of the tissue within the well, and continuous flow (5 ml/min) of a buffered, gassed (95% N2-5% CO2) Ringer solution through the well to maintain tissue temperature at 38°C and pH at 7.38 and to minimize oxygen delivery from the well solution. All microvascular data were collected during mid to late afternoon.
Separate pilot experiments were performed to assess resistance artery tone in our preparation because vasodilators dramatically elevate ovarian microvascular permeability beyond its already extreme control values, causing rapid dye leakage. After control diameter measurements were obtained in these experiments, the vascular bed was maximally vasodilated via the addition of 10–4 M adenosine to the superfusate, and diameter measurements were repeated. Resistance arteries from all the locations observed in our study were found to have tone, which, expressed as percent constriction from maximum diameter, averaged 20.3 ± 1.9 (±SE) percent. No vessels were observed to be maximally dilated in the control state.
Microscopy. Ovarian vessels were observed with a fixed-stage microscope by using water-immersion objectives (Olympus). The vasculature was visualized by epi-illumination after intravenous injection of 2 x 106 mol wt TRITC dextran (18 mg; Research Organics). The image was captured with a low-light video system (Dage-MTI), displayed on a high-resolution monitor (Panasonic), and recorded with a Super VHS video recorder (Panasonic).
Vascular network analysis and diameter measurement. Video images were digitized from the analog recordings by using iMovie software (Apple) on Macintosh computers (Apple). Resistance artery networks were reconstructed for each animal by using Adobe Photoshop. Network and vessel dimensional measurements were made from the digitized networks by using NIH Image software. All dimensional measurements were calibrated against digitized recordings of a stage micrometer.
Microvascular network pressure profile. To establish whether utero-ovarian resistance arteries comprised a significant proportion of the total utero-ovarian vascular resistance, we determined the network pressure profile by measuring resistance artery intravascular pressure in 11 animals at discrete locations along the utero-ovarian circuit, corresponding to distinct elements of the vascular architecture. To ensure that all measurements were made within a reasonable time after the induction of anesthesia, pressure was not measured at every measurement site in each animal; rather, the pressure profile was compiled from all measurements made. All measurements were made with the animals at the same depth of anesthesia and within 4–5 h of the induction of anesthesia (typically during the final 2 h of anesthesia). Twenty-five resistance artery and two uterine vein pressure measurements were made. Estrous cycle was tracked for each animal observed, and animals from each cycle day were used, but data were pooled across all cycle days because preliminary data indicated that cycle day-specific differences in pressure within the resistance artery network would not be resolvable. An IPM model 4A servo-micropressure system was used with triple-beveled glass micropipettes. Pipettes were polished to 1–2 µm outer diameter on a WPI beveler coated with 0.3 µm alumina abrasive film. To visualize the pipettes under epifluorescence illumination, Acridine red (125 µg/ml; Polysciences) was added to the 2 M NaCl solution used to fill the pipettes. Pipettes were calibrated before and after each measurement. Pressure data were acquired and analyzed by using a MacLab data-collection system (ADInstruments) and a Macintosh computer (Apple). Systemic pressure measurements were collected simultaneously with each servo-null pressure measurement and in each case showed the same periodicity generated by the cardiac cycle. Servo-null pressure measurements are presented normalized against their simultaneously determined systemic arterial pressure measurement. To the extent that diameter measurements are reported from vessel segments on which servo-null pressure measurements were performed, the diameters reported reflect the diameters observed during the pressure recording.
Resistance artery diameter measurements sites. Resistance artery diameter was measured and compiled for each day of the hamster estrous cycle. Our determination of the utero-ovarian resistance artery network architecture enabled routinely identifiable segments of the ovarian and uterine arteries to be chosen for diameter measurement. Three segments were chosen along the ovarian artery and were designated the upper coils, middle, coils and lower coils (Fig. 1C). Two uterine artery segments were chosen, one located just distal to the separation of the uterine artery and vein (Fig. 1C) and one located just distal to the "symmetrical bifurcation" (Fig. 1C). (Additionally, diameter was recorded to accompany pressure measurements made at the ovarian insertion point, where the ovarian and uterine arteries join; these data were not separated by cycle day.) To allow cataloguing and spatial comparison of measurements made in each animal, the vascular pathway was traced in each digitally reconstructed network and numbered hash marks were made each 1,000 µm, as shown in Fig. 1A.
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RESULTS |
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9,000 µm from the ovary (separation point, Fig. 1C). It then followed a smaller venous branch, coiled or curved to varying degrees, eventually bifurcated symmetrically (Fig. 2; Fig. 1C) after giving rise to a number of smaller side branches, and experienced an abrupt decrease in diameter before joining the ovarian artery and entering the ovary (IP, Fig. 2). The ovarian artery arose from the abdominal aorta and followed a straight-line path with the ovarian vein until 10,000 µm from the ovary. At this point, it underwent dramatic coiling (OA, Fig. 2) as well as abrupt diameter changes at (typically) symmetrical bifurcations that created three distinct segments: the upper, middle, and lower coils identified in Fig. 1C. Distal to the lower coils, the ovarian artery anastomosed with the uterine artery and, directly beyond this junction, entered the ovary (IP, Fig. 2). The ovarian and uterine arteries anastomosed with each other at least twice in every animal observed. One anastomosis occurred at the ovary, as described above. The second regularly occurring anastomosis is prominent in Fig. 1A (labeled "A") and is also partly evident in Fig. 1C, where it is similarly labeled. This anastomosis joined the ovarian artery typically at the middle coils, although variations did occur. In most animals, this anastomosis was of smaller diameter than that shown in Fig. 1A; nevertheless, it was always present. Because the uterine and ovarian arteries anastomosed in multiple locations, flow within portions of the vessels could (and was observed to) vary in direction from animal to animal. Our experimental approach did not allow us to statistically correlate flow direction with estrous-cycle phase.
Resistance artery pressure profile. To ascertain the potential of the utero-ovarian resistance arteries to influence ovarian blood flow, we determined the arterial network intravascular pressure profile in 25 measurements from 11 animals and confirmed that a significant proportion of the total vascular resistance resided in these resistance arteries. Systemic arterial pressure during the resistance artery pressure measurements averaged 87.5 ± 1.8 mmHg. Pressure in the uterine vein (diameter = 616 ± 59 µm) measured 9,000 µm from the ovary averaged 7.0 ± 1.3% of systemic pressure.
Servo-null pressure measurements showed that a large proportion of the total pressure drop across the utero-ovarian vascular network occurred in the resistance arteries before their insertion into the ovary. Figure 3 illustrates the intravascular pressure profile of the utero-ovarian resistance artery network, as determined by pressure measurements made at prominent locations along the network. Arterial pressure dropped to 58.2 ± 0.4% of systemic arterial pressure before the feed artery entered the ovary. Along the ovarian artery, the bulk of the pressure drop occurred within 3,000 µm of the ovary and coincided with a two- to fourfold decrease in arterial diameter at and beyond the lower coils. The major pressure drop occurred more distally along the uterine artery. Pressure changed little with distance across the proximal uterine artery segments, where diameter was quite constant along the length of the segment (Fig. 1C; artery/vein separation). On average, pressure changed here by <1 mmHg across a distance of 2,500 µm (data not shown). It was in the most distal 1,000 µm of the uterine artery, from the point of the symmetrical bifurcation identified in Fig. 2 to the insertion point into the ovary (IP, Fig. 2), that diameter and intravascular pressure both dropped sharply.
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Changes in resistance artery diameter correlated with the 4-day hamster estrous cycle in segments of both the uterine and ovarian arteries, with the smallest diameters occurring on cycle day 1, following ovulation, which occurs during the early-morning hours of cycle day 1 (35). Cycle day-specific arterial diameters at prominent network locations are shown in Fig. 3. Along the uterine artery, vessel diameter at the point of separation of the artery and vein (Fig. 1C) changed significantly with estrous cycle day. Day 1 and day 2 diameters, 209 ± 9 µm and 217 ± 8 µm, respectively, were significantly less than the day 3 diameter, 260 ± 9 µm. At the point just distal to the symmetrical bifurcation of the uterine artery identified in Fig. 1C, there were no day-specific differences in arterial diameter (Fig. 3); diameter here averaged 143 ± 5 µm across the four cycle days. Arterial diameter dropped further from this point to the point of insertion into the ovary, where it averaged 62 ± 2 µm.
Ovarian artery diameter at the lower coils (Fig. 1C) also changed significantly with estrous cycle day. As with the uterine artery, vessel diameter was smallest on cycle day 1. Lower-coil mean diameter on day 1 (48 ± 4 µm) was significantly less than the mean diameters on day 2 (99 ± 9 µm) and day 3 (87 ± 5 µm). The day 4 lower-coil mean diameter (71 ± 11 µm) was not significantly different from the diameter on any other cycle day. In the upper and middle coils of the ovarian artery, there were no significant changes in diameter with cycle day. Across the 4 days of the cycle, upper coil diameter averaged 231 ± 6 µm and middle coil diameter averaged 125 ± 6 µm. It is interesting to note that for the two vessel segments that showed significant cycle-dependent diameter changes, the temporal pattern of diameter change was not identical (Fig. 3). Although both the uterine artery and ovarian artery segments were smallest in diameter on day 1, in the uterine artery, the day 2 diameter was the most similar to the day 1 diameter, yet in the ovarian artery, the day 2 diameter was the most different from the day 1 diameter.
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DISCUSSION |
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Vascular architecture. The hamster utero-ovarian arterial and venous network is characterized by a high degree of arterial coiling, especially along the ovarian artery, and close apposition between the arteries and veins. It also is a multiply anastomotic network that establishes shared supply and drainage between the ovary and uterus. The resistance arteries assume extremely small diameters (<100 µm) along portions of both the ovarian and uterine supply routes to the ovary, and venous diameters are large.
Comparative studies have shown that the utero-ovarian vascular architecture observed in the hamster is shared with other species, including rats, guinea pigs, cattle, sheep, and swine (for review, see Ref. 12). With variation, it is also present in rabbits and horses (12) and also has been described in women (1).
The most commonly described functional consequence of this architecture is its capacity to operate as a countercurrent exchanger for both ovarian and uterine products. The countercurrent exchanger, which also involves the lymphatics (3, 14, 19), has been cited for its role in delivering uterine-derived prostaglandin F2
(PGF2), the luteolytic agent in many species (12, 18, 23), and for its potential to provide a concentrating mechanism for ovarian steroids (1, 21, 29).
The similarities of the utero-ovarian network to the countercurrent exchanger present between the testicular arterial and venous circulation are striking. The testicular network, which has the same embryological origins as the utero-ovarian network, serves to preserve high testicular testosterone concentrations (10). The coiled nature and small resistance artery diameter in the testicular vasculature also were associated with a large pressure drop across the resistance arteries (32), as is reported in this study for the ovarian artery.
Resistance artery pressure profile. Resistance artery pressure dropped steeply proximal to the arterial entry point into the ovary. The pressure drop occurred along both ovarian and uterine artery supply routes, but the profile of the pressure drop differed in the two arteries. Pressure dropped in multiple steps along the ovarian artery, whereas along the uterine artery it dropped mostly in a single large step near the artery's termination at the ovary. Abrupt reductions in pressure along both arteries coincided with sharp reductions in arterial diameter at bifurcations that typically yielded equal-diameter daughter vessels.
The reduction of resistance artery pressure to 58% of the systemic value before the ovarian entry point establishes that a large proportion of the total resistance of this vascular bed resides in the resistance arteries. Our pressure measurements using the servo-null technique represent the most direct and least invasive in vivo pressure measurements made in this network.
An estimate of the resistance arteries' contribution to total ovarian vascular resistance was made on the basis of the simple series resistance model first proposed by Pappenheimer and Soto-Rivera (24) and subsequently used by Gore (13) and others (5, 32). Beginning with a formula analogous to that of Gore's (13) for determining the pre- to postcapillary resistance ratio, one can estimate the ratio of resistance before and beyond the insertion point of the resistance arteries into the ovary as
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The accuracy of this estimate is subject to the assumptions delineated by Pappenheimer and Soto-Rivera (24), the most relevant of which is that the utero-ovarian vascular network is not accurately described as consecutive resistive elements arranged in series, but rather as groups of parallel resistive elements arranged in series. Nevertheless, the model provides an informative first estimate of the contribution of the resistance arteries to total ovarian vascular resistance. We applied this model by using the pressure data reported here, including the uterine vein pressure of 7% of systemic pressure, which agrees well with similar venous pressure measurements we made previously in the most distal testicular veins (31, 32).
On the basis of this model, we calculate the proportion of the total utero-ovarian vascular resistance that the resistance arteries contribute to be 45%. This falls between two previous estimates: that of Reynolds (27) (50–70% of total resistance, based on hemodynamic and anatomical arguments) and that of Massa and Bruce (17) (19% of total vascular resistance, based on measurements with a 70-µm-diameter glass cannula in a ligated, venous outflow rat preparation).
The degree of pressure drop in the utero-ovarian resistance arteries was similar to that which we previously measured along the embryologically related testicular artery network (32). Both networks are characterized by coiled, small-diameter resistance arteries (36) and large-diameter veins. In the ovary, as in the testis (32), the characteristic of large venous diameters begins at the immediate postcapillary level (21). The network architecture and our pressure measurements thus suggest a high pre- to postcapillary resistance ratio in the utero-ovarian vascular network, typically leading to low capillary pressure, as we found previously in the testis (32). As in the testis, low ovarian capillary pressure would serve to hold fluid filtration in check in an exchange bed known for its incredibly high protein permeability, which becomes still higher as ovulation is approached (3, 19, 30). Although a resistance distribution such as this buffers capillary pressure from changes brought about by changes in arterial pressure, it makes capillary pressure highly sensitive to increases in venous pressure (31). Even modest increases in venous pressure have been shown to cause dramatic increases in filtration and lymph formation in the ovary (3, 19).
We did not systematically assess cycle day-specific changes in resistance artery pressure. As flow amplitude changes, pressure at a given site is as likely to rise as it is to fall, dependent as pressure values are on the flow rate and the distribution of the changing resistance. In fact, one might expect that changes in pressure at a given site may be quite minimal as flow changes, as a consequence of potential autoregulatory mechanisms such as the myogenic and flow-dependent responses. Preliminary data of ours on isolated, cannulated utero-ovarian resistance arteries that show that both these mechanisms operate in this network (unpublished observations). The pressure data of the current study, preliminary as they might be in determining cycle-related changes in pressure, support the insensitivity of pressure at a given site to cycle phase. Given the fourth-power relationship between vessel diameter and vascular resistance, vessel diameter measurements are much more sensitive indicators of site-specific modulation of vascular resistance than is intravascular pressure.
Implications for mechanisms of control of ovarian blood flow. Ovarian blood flow has been reported to vary up to nearly threefold throughout the estrous cycle, with peak flow occurring during the preovulatory phase and flow decreasing during the luteal phase (11, 35). Larger increases in ovarian flow occur with pregnancy or pseudopregnancy (2, 22). Intraovarian vascular changes, including cyclical angiogenesis, certainly contribute to the change in ovarian blood flow (9). Nevertheless, because such a large proportion of the total vascular resistance resides in the utero-ovarian resistance arteries, we investigated the role of resistance artery diameter changes in the cyclical change in ovarian vascular resistance.
Our data showed that the resistance arteries feeding the ovary changed diameter in sync with the estrous cycle, with minimum diameters occurring in the postovulatory period. The diameter of the most proximal uterine artery segment we measured was reduced by 17–20% on cycle days 1 and 2, compared with the peak diameter on day 3. All segments of the uterine artery that we measured were distal to the portion of the uterine artery that feeds that uterus and as such represent the ovarian feed vessel emanating from this supply. Along the other supply route, the lower coils of the ovarian artery showed a more striking change, where the day 1 diameter was 45–52% smaller than the peak diameters on days 2 and 3. The cyclical progression of changes in uterine and ovarian artery diameter were not completely in sync; uterine artery diameter peaked on day 3, whereas ovarian artery diameter peaked on day 2.
It is difficult to quantitatively estimate how the observed changes in resistance artery tone alter ovarian blood flow because blood flow was not measured in this study. Nevertheless, hemodynamics dictate that the lower coils of the ovarian artery should contribute the greatest proportion of vascular resistance along this supply route, because their length is similar to larger-diameter upstream segments, yet their diameter is smallest. They also were the ovarian artery segments that showed the greatest cyclical changes in diameter. The increase in tone of the lower ovarian coils late in cycle day 1, which most likely alters flow amplitude, may have the additional effect of altering the ovarian hormonal milieu by shifting the source of ovarian blood flow to the uterine feed. The overall effect on the source of ovarian flow is uncertain, however, because the proximal segment of the uterine artery that we observed also had its smallest diameter on day 1. At this time in the cycle, the uterus is releasing the putative luteolytic agent PGF2, which is delivered to the ovary via a countercurrent-exchange mechanism involving uterine venous and lymphatic vessels and the uterine artery (12, 18, 23). Chaichareon and colleages (4) documented variability in the relative contributions of the uterine and ovarian arteries to ovarian blood flow in the guinea pig and suggested that it reflected competing effects of the local mediators of blood flow. Along the uterine artery supply route, it is likely that the long segment proximal to the symmetrical bifurcation is most influential in cyclically altering the ovarian blood supply from this source. Although this segment is larger in diameter than the segment beyond the symmetrical bifurcation, it is many times longer, increasing its influence on flow amplitude as it cyclically changes its tone. The segment distal to the symmetrical bifurcation, which did not show cyclical changes in tone, may be more critical to dropping pressure than controlling flow, because it was across this segment of the uterine artery pathway that pressure dropped most precipitously.
Reconciling the cyclical changes in tone that we observed with ovarian blood flow measurements made previously by other investigators (11, 35) is made difficult by a number of factors. Among these are the complexity of the vascular network, the duality of blood flow sources, and the exclusion of inflow or outflow pathways in prior assessments of ovarian blood flow (11, 35). The most consistent temporal relationships are the large diameters and peak flows in the immediate preovulatory period and, in the case of Varga and Greenwald's data (35), the sharp falloff in flow on day 1 that parallels the vasoconstriction that we observe. In other phases of the cycle, vessel tone and blood flow data are difficult to correlate, especially because changes in tone in the uterine and ovarian arteries are not always in sync with one another. Although it is appealing to link the rise and fall in flow and diameter to estradiol levels (11, 35), the temporal relationship between estradiol, resistance artery diameter, and measured ovarian blood flow also are not wholly consistent.
Neural influences on cyclical changes in utero-ovarian blood flow have been considered. Estrous cycle-linked changes in uterine innervation have been documented in the rat (38). However, the axonal degeneration and regeneration observed was isolated to the uterine myometrium and was observed not to affect uterine vascular innervation. In the hamster, the majority of uterine sympathetic innervation is indeed directed at the vasculature (28), but we are unaware of any reports of cyclical changes in uterine innervation in the hamster.
A broad variety of locally produced hormones and chemical mediators have been linked to utero-ovarian vascular control. Estrous cycle-dependent, estradiol-linked changes in nitric oxide production and the rise and fall of uterine production of PGF2 (12, 18, 23), a potent vasoconstrictor, are the most likely humoral determinants of the cyclical variations in resistance artery tone. Estrogen has been shown to decrease arteriolar basal tone and increase flow-induced vasodilation (15). As is true in other species, estrogen peaks in the hamster in the preovulatory period (35); it then falls abruptly as the end of cycle day 4 is approached. Upregulation of eNOS has been shown to occur in the uterine artery during the follicular phase, as ovulation in approached (34), and this has been linked to greater uterine artery endothelial NO production in response to agonists (37). Countercurrent exchange of PGF2 from the uterine vein and lymphatics (12, 18, 23) may maintain the reduction in artery diameter on day 2, when the ovarian artery diameter is peaking. We plan to investigate these potential control mechanisms in an isolated vessel model of the utero-ovarian resistance arteries, which will provide a more appropriate setting for dissecting the local mechanisms controlling resistance artery tone.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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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.
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REFERENCES |
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in the rabbit ovary. Am J Obstet Gynecol 117: 381–385, 1973.[Web of Science][Medline]
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Significantly different from mean diameter on cycle day 3.