Regional blood flow and vascular resistance in response to oxytocin in the pregnant sheep and dog

1961 ◽  
Vol 16 (6) ◽  
pp. 1087-1092 ◽  
Author(s):  
N. S. Assali ◽  
L. Holm ◽  
H. Parker

The effects of oxytocin on regional blood flow and regional vascular resistance were investigated in a group of pregnant ewes and bitches not in labor and in another group in early labor. Single injections or intravenous drip infusion did not change significantly arterial pressure, cardiac output, electrocardiogram, and renal, iliac, femoral, and carotid blood flows in any of the animals studied. The effects on the pregnant uterus were negligible before the onset of spontaneous labor. Only when the animal was in labor did oxytocin produce an increase in uterine contractions accompanied by a significant decrease in uterine blood flow. The data indicate that in the pregnant sheep and dog the circulatory action of oxytocin is limited to the pregnant uterus in labor and that the decrease in blood flow is probably due to an increase in intramural vascular resistance caused by the contracting myometrium around the uterine arterioles. Submitted on May 5, 1961

1989 ◽  
Vol 257 (1) ◽  
pp. H17-H24 ◽  
Author(s):  
C. R. Rosenfeld ◽  
R. P. Naden

The uteroplacental vasculature is more refractory to angiotensin II (ANG II) than the systemic vasculature as a whole. To ascertain the differences in responses between reproductive and nonreproductive tissues that account for this, we infused ANG II (0.573, 5.73, and 11.5 micrograms/min) in pregnant sheep (137 +/- 5 days of gestation) and monitored arterial pressure (MAP), heart rate, and uterine blood flow (UBF); cardiac output and regional blood flows were measured with radiolabeled microspheres. Dose-dependent changes in MAP, UBF, and systemic (SVR) and uterine (UVR) vascular resistance occurred (P less than 0.05); systemic responses exceeded uterine (P less than 0.05), except with 11.5 micrograms/min, when % delta UVR = % delta SVR, % delta UVR greater than % delta MAP, and UBF fell 29%. Although a dose-dependent rise in placental resistance occurred, blood flow was unaffected except at 11.5 micrograms ANG II/min, falling 16.8 +/- 3.5% (P = 0.059). In contrast, endometrial perfusion decreased 68 +/- 4.2 and 81 +/- 1.8% (P less than 0.01) with 5.73 and 11.5 micrograms ANG II/min, respectively. Myometrial responses were intermediate, thus placental flow increased from 75 to greater than 90% of total UBF. Adipose, renal, and adrenal glands were extremely sensitive to ANG II, with blood flows decreasing maximally at 0.573 micrograms/min (P less than 0.05). Maximum adipose vascular resistance occurred at 0.573 micrograms/min, greater than 400% (P less than 0.001), exceeding responses in all tissues (P less than 0.05). The placenta is less responsive to ANG II than other uterine and most nonreproductive tissues, resulting in preferential maintenance of uteroplacental perfusion and protecting the fetus from the effects of this vasoconstrictor.


1961 ◽  
Vol 201 (3) ◽  
pp. 485-491 ◽  
Author(s):  
Bjorn Westin ◽  
N. Sehgal ◽  
N. S. Assali

Changes in regional blood flow and regional vascular resistance during hypothermia in dogs with intact or abolished shivering mechanisms were measured with sine-wave electromagnetic flowmeters. In animals with shivering intact, cooling produced a fall in renal and carotid blood flows, despite a rise or no change in cardiac output. The fall was caused by an increase in renal and carotid vascular resistances. Femoral blood flow increased because of a decrease in vascular resistance. In animals with shivering abolished, cooling evoked a fall in the cardiac output and in renal and femoral blood flows, due to an increase in the vascular resistance. Upon rewarming, femoral flow immediately rose to values far above control. Carotid flow increased during cooling because of a decline in carotid resistance. Such a decline might have been related to the elevated blood Pco2 observed in the nonshivering animals.


1994 ◽  
Vol 77 (1) ◽  
pp. 165-172 ◽  
Author(s):  
W. Shen ◽  
M. Lundborg ◽  
J. Wang ◽  
J. M. Stewart ◽  
X. Xu ◽  
...  

The contribution of endothelium-derived relaxing factor (EDRF) to the regulation of regional vascular resistance and tissue blood flow at rest and during acute moderate exercise was studied in chronically instrumented conscious dogs. Radioactive microspheres were injected before and during exercise to measure regional blood flow. An infusion of nitro-L-arginine (L-NA), an analogue of L-arginine, was used to inhibit the synthesis of EDRF and resulted in a significant increase in mean arterial pressure, associated with significantly elevated vascular resistance in heart, skeletal muscle, renal and splanchnic circulations and with decreases in tissue blood flow in those regions at rest. Acute exercise caused a typical redistribution of blood flow, in which there was vasodilation in heart and working skeletal muscles, accompanied by vasoconstriction in kidney and splanchnic circulations. L-NA resulted in significantly elevated vascular resistance during vasodilation in heart and working skeletal muscles and also significantly increased vasoconstriction in renal cortex, stomach, pancreas, liver, and colon during exercise. Blood flows during exercise were largely unaffected by L-NA treatment. Our results suggest that whereas EDRF functions to regulate basal vascular tone and vascular resistance during exercise, EDRF has a minor role in determining the pattern of the redistribution of tissue blood flow during exercise.


1976 ◽  
Vol 231 (3) ◽  
pp. 754-759 ◽  
Author(s):  
JH Rankin ◽  
TM Phernetton

The effect of PGE2 on regional blood flows in the chronically catheterized near-term pregnant sheep was investigated using radioactive microspheres. The injection of 20 mug PGE2 per kilogram into the left ventricle of eight sheep resulted in no change in maternal brain and noncotyledonary uterine flow. The renal blood flow increased from 692 to 892 ml/min (P less than 0.004). The uterine blood flow decreased from 673 to 317 ml/min (P less than 0.001). The trium was bypassed by injecting 7 mug PGE2 per kilogram of sheep into a fetal venous catheter and permitting it to reach the placental vasculature after placental transfer. Eleven sets of observations were made in eight animals. We observed no change in the intrauterine pressure, maternal brain flow, and noncotyledonary uterine blood flow secondary to this procedure. The maternal renal blood flow changed from 592 to 669 ml/min (P less than 0.007). The uterine blood flow increased from 762 to 853 ml/min (P less than 0.02). The uterine vascular resistance decreased from 0.124 to 0.115 mmHg x min/ml (P less than 0.04). It was concluded that 1) PGE3 crosses the placenta quite readily, and 2) PGE3 causes dilatation of the maternal placental vascular bed.


1985 ◽  
Vol 249 (6) ◽  
pp. R781-R786 ◽  
Author(s):  
R. W. Lappe ◽  
J. A. Todt ◽  
R. L. Wendt

Previous studies have demonstrated that infusion of synthetic atriopeptin II (AP II) lowered arterial pressure, reduced regional blood flow, and increased total peripheral and regional vascular resistances in conscious spontaneously hypertensive rats (SHR). This study was designed to examine the mechanism(s) involved in regional vasoconstrictor responses to AP II. In these experiments, hemodynamic actions of AP II were examined in control, 6-hydroxydopamine-treated (chemically sympathectomized), and renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1 microgram X kg-1 X min-1) caused similar reductions in mean arterial pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/- 2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and hindquarters (-18 +/- 10%) blood flow and increased regional vascular resistance in all three beds. Chemical sympathectomy prevented the fall in renal blood flow (RBF) and significantly abolished the regional vasoconstrictor responses to AP II infusion. In unilateral renal-denervated groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in contralateral-innervated kidneys. This study demonstrated that chemical or surgical destruction of renal sympathetic nerves abolished AP II-induced increases in RVR. These data further indicate that in conscious SHR the regional vasoconstrictor responses to AP II infusion appear to be mediated by increases in sympathetic tone rather than through direct vascular actions of AP II.


1958 ◽  
Vol 195 (3) ◽  
pp. 614-620 ◽  
Author(s):  
N. S. Assali ◽  
K. Dasgupta ◽  
A. Kolin ◽  
L. Holms

Uterine blood flow has been measured with a chronically implanted miniature electromegnetic flow meter in unanesthetized pregnant sheep and dogs during spontaneous and oxytocin induced labor and followed in the same animal for several postpartum days. In either spontaneous or oxytocin induced labor, uterine contractions are accompanied by a significant decrease in uterine blood flow and relaxations by the return of the flow to or higher than control values. The decrease is roughly proportional to the intensity of uterine contraction. When the contraction is of a tetanic nature and not followed by relaxation, uterine ischemia is so severe that the fetus might succumb. After the delivery of the fetus and before the expulsion of the placenta, uterine blood flow falls slightly. However, after separation and expulsion of the placenta, uterine blood flow falls precipitously. Thereafter, a very slight and progressive decrease continues for several days paralleling uterine involution.


1988 ◽  
Vol 65 (1) ◽  
pp. 165-172 ◽  
Author(s):  
C. M. Blatteis ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
T. A. Mashburn

To determine whether the reported absence of fever in full-term-pregnant ewes might be associated with shifts of regional blood flows from thermogenic tissues to placenta during this critical period, fevers were induced twice by injections of Escherichia coli lipopolysaccharide (LPS, 0.25 microgram/kg iv) into each of six Merino ewes from 8 to 1 days prepartum, and their regional blood flow distribution was measured with radioactive, 15-microns-diam microspheres before and during the rise in fever (when their rectal temperature had risen approximately 0.4 degree C). Unexpectedly, fever always developed, rising to heights not significantly different at any time before parturition [4-8 days prepartum = 0.81 +/- 0.23 degree C (SE); 1-3 days prepartum = 0.75 +/- 0.17 degree C) and similar to those in three wethers treated similarly (0.90 +/- 0.10 degree C). Generally, during rising fever, blood flow in the ewes shifted away from heat loss tissues (e.g., skin, nose) to heat production tissues (e.g., shivering muscle, fat) and cardiac output increased; blood flow through redistribution organs (e.g., splanchnic bed) decreased. The reverse occurred during defervescence. Utero-placental blood flow remained high in the febrile ewes. These regional blood flow distributions during febrigenesis and lysis are essentially the same as those during exposures to ambient cold and heat, respectively. Some differences in the responses of cardiac output and its redistribution, however, were apparent between wethers and pregnant ewes. We conclude that 1) the previously reported "absence of fever in the full-term-pregnant sheep" should not be regarded as a general phenomenon and 2) full-term-pregnant sheep support fever production without sacrificing placental blood flow.


1979 ◽  
Vol 237 (1) ◽  
pp. R52-R57
Author(s):  
D. Caton ◽  
C. Crenshaw ◽  
C. J. Wilcox ◽  
D. H. Barron

Normal sheep were studied at intervals of 3-5 days during the last weeks of pregnancy in order to evaluate variability in rate of O2 consumption (QO2) of the uterus in relation to several variables involved in delivery of O2 to the organ. Among-animal differences of uterine QO2 were statistically significant and directly related to birthweight of the lamb. Among-animal differences of uterine blood flow (UBF) and uterine arteriovenous O2 content difference [C(a-v)O2] also were statistically significant, though neither was related to birthweight, presumably since they tended to vary inversely with one another. In a given ewe relative magnitude of UBF and of C(a-v)O2 was related to maternal arterial O2 content (CaO2), day of pregnancy, and whether the animal carried singlets or twins. Variability in QO2 was most closely related to UBF, although its relations to C(a-v)O2 and CaO2 were significant also. These data suggest there are systematic relationships among variables involved in the delivery of O2 to the uterus of pregnant sheep.


1986 ◽  
Vol 60 (5) ◽  
pp. 1759-1764 ◽  
Author(s):  
A. W. Bell ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
R. B. King

Radioactive microspheres were used to measure cardiac output and blood flow to most major tissues, including those in the pregnant uterus, in late-pregnant ewes at rest and during treadmill exercise (approximately 3-fold increase in metabolic rate for 30 min) in thermoneutral (TN) (dry bulb temperature (Tdb) = 13 degrees C, wet bulb temperature (Twb) = 10 degrees C) and mildly hot (MH) (Tdb = 40 degrees C, Twb = 27 degrees C) environments. Exercise caused major increases in blood flow to respiratory muscles, nonrespiratory limb muscles, and adipose tissue, and flow was decreased to some gastrointestinal tissues, spleen, pancreas, and to placental and nonplacental tissues in the pregnant uterus. Heat exposure had relatively little effect on these exercise-induced changes, except that flow was further increased in the respiratory muscles. Results are compared with those of a similar study on nonpregnant sheep in which changes in muscle, skin, and visceral flows during exercise were attenuated by heat exposure. It is suggested that redistribution of blood flow from the pregnant uterus, which in resting ewes took 22% of cardiac output, is a significant buffer against the potentially deleterious effects of combined exercise and heat stress on blood flow to exercising muscles and thermoregulatory tissues.


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