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We investigated the time course and possible mechanisms by which the maternal cardiovascular system adapts to the demands of pregnancy. Control, 20-, 40-, and 60-day gestation guinea pigs (total 68 days) and nonpregnant virgin female guinea pigs chronically dosed with cholesterol (control), estrogen (17beta-estradiol), progesterone, and estrogen plus progesterone were studied. In vivo heart rates, pressures, cardiac outputs, blood volumes, and in vitro left ventricular pressure-volume relations were measured. There was no difference in heart rate, mean arterial, right atrial, or left ventricular end-diastolic pressures, or left ventricular weights between the various pregnant animals or hormone-dosed animals and their respective controls. By 20 days gestation blood volume (24%, P less than 0.005), cardiac output (22%, P less than 0.005), and stroke volume (22%, P less than 0.05) were increased, whereas uterine blood flow was unchanged. Chronic estrogen administration resulted in similar increases in cardiac output (24%, P less than 0.05), stroke volume (31%, P less than 0.05), and blood volume (13%, P less than 0.05). In vitro left ventricular pressure-volume relations were shifted to the right in all pregnant and hormone-dosed groups. Increases in left ventricular size and output occur before changes in uterine blood flow in guinea pig pregnancy, and these adaptations can be elicited by chronic sex steroid administration.

To determine the normal maternal heart rate and stroke volume response to exercise and the role of the autonomic nervous system in this response, pregnant and non-pregnant pygmy goats were studied at rest, during and following treadmill exercise, and after autonomic blockade. Resting heart rates, stroke volumes and cardiac outputs were 10%, 60%, and 76% higher in pregnant compared to non-pregnant animals (P less than 0.05, 0.001, and 0.001 respectively). During exercise, heart rate and stroke volume rose in both pregnant and non-pregnant animals by similar amounts. Immediately post-exercise, stroke volume in pregnant animals dropped precipitously below resting levels by 15% (P less than 0.005) but cardiac output was preserved by heart rate. This fall in stroke volume was not seen in control animals. Autonomic blockade lowered resting and exercise heart rates in both groups without changing stroke volume. The elevations in heart rate and stroke volume in pregnancy are not primarily mediated via the autonomic nervous system. Although the maternal cardiac output response to exercise appears normal, the post-exercise fall in stroke volume, presumed secondary to a reduction in preload, could potentially be harmful to both mother and fetus.

The effect of acute hypoxaemia on right and left ventricular function was investigated in 8 fetal sheep (137-140 days gestation). Fetuses were instrumented with electromagnetic flow sensors on the ascending aorta and the main pulmonary artery. After 8 days recovery, hypoxaemia was achieved by reducing the maternal ewe's inspired O2 concentration to 13.1 +/- 1.5%. Control and hypoxaemic arterial blood values were pH 7.37 +/- 0.04 (SD) and 7.35 +/- 0.06, PCO2 48.0 +/- 2.8 and 47.6 +/- 5.1 mmHg, PO2 19.9 +/- 2.2 and 11.4 +/- 1.5 mmHg, haematocrit 37.5 +/- 1.2 and 39.5 +/- 2.2, respectively. Arterial pressure increased insignificantly with acute hypoxaemia (50.2 +/- 3.9 to 53.6 +/- 8.1 mmHg). Left and right ventricular performance was assessed by generating biventricular function curves relating stroke volume to mean atrial pressure. All function curves were composed of steep ascending and plateau limbs that intersected at a breakpoint. Comparing control and hypoxaemia function curves, the left ventricular stroke volume breakpoints were 0.79 +/- 0.20 and 0.78 +/- 0.21 ml/kg, respectively, while the right ventricular stroke volume breakpoints were 0.99 +/- 0.11 and 0.88 +/- 0.21 ml/kg (n.s.). In 4 fetuses, acute hypoxaemia was associated with significant increases in arterial blood pressure (P less than 0.05). In these fetuses, the right ventricular function curve was shifted significantly downward compared to the control right ventricular curve. When nitroprusside was given to these hypertensive fetuses to return blood pressure to control levels, the right ventricular function curve returned to baseline. We conclude that even under conditions of extreme hypoxaemia, ventricular function is well preserved in the normotensive fetal sheep. However, when increases in arterial pressure also accompany hypoxaemia, detectable changes in right ventricular function can be accounted for by changes in arterial pressure.

We investigated the relationship between mean circulatory filling pressure (MCFP) and blood volume in nonpregnant (NP), estrogen-treated (E), and pregnant (P) guinea pigs. Reversible circulatory arrest was produced by rapid ventricular pacing or acetylcholine in unanesthetized animals remote from surgery. MCFP (mmHg) was higher for E (7.1 +/- 0.3) than for NP (5.8 +/- 0.5) or P (5.3 +/- 0.4). The gradient for venous return, the difference between MCFP and right atrial pressure (mmHg), did not differ in NP- (6.0 +/- 0.5), P- (5.8 +/- 0.5), or E- (5.8 +/- 0.4) treated animals. Capacitance, the blood volume (ml/kg) at an MCFP of 6 mmHg, was increased in P (84 +/- 6) and E (89 +/- 7), compared with NP (64 +/- 5) animals. Compliance, the ratio of the change in volume to change in pressure in the range of 6-12 mmHg (ml.kg-1.mmHg-1), was greater in P (4.4 +/- 0.3) than NP (3.5 +/- 0.3) animals. Hexamethonium blockade did not affect MCFP, capacitance, or compliance. We conclude that the effect of blood volume expansion on the circulation in pregnancy cannot be predicted from knowledge of MCFP-blood volume relationships in the nonpregnant animal, because capacitance and compliance are altered. Estrogen administration to nonpregnant animals reproduces some of these effects.

Progesterone-induced hyperventilation has thus far not been reported in animals other than humans. Accordingly we investigated the effects of chronic progesterone treatment on ventilation in guinea pigs. Virgin female guinea pigs were divided into those treated with cholesterol as controls (C), progesterone (P), or estrogen plus progesterone (E&P). All hormones were administered in silastic capsules placed subcutaneously for 28 days. On day 28 arterial blood gases and respiratory rates were determined. Arterial pH was elevated in P- and E&P-treated animals compared with controls (7.43 +/- 0.04 and 7.43 +/- 0.03 vs 7.39 +/- 0.05, respectively, P less than 0.05). Arterial PCO2 was reduced in both progesterone-treated groups compared to controls (33.9 +/- 5.8 (P), 33.1 +/- 2.8 (E&P), 38.0 +/- 4.3 (C)), and was correlated with systemic progesterone concentrations in animals receiving E&P (r = -0.85, P less than 0.01) but not in animals receiving P alone (r = -0.07, P = N.S.). Arterial [HCO-3], PO2 and respiratory rates were not different between groups. We conclude that chronic progesterone administration produces hyperventilation in guinea pigs, and that estrogen facilitates this action of progesterone.

The resting hemodynamics were determined in 8 guinea pigs after they were anesthetized with ketamine/xylazine. Measurements were made of blood pressure, heart rate, cardiac output, arterial blood gases, and pH. These measurements were obtained initially at 4 to 5 hours after an injection (IM) of ketamine HCl (25 mg) and xylazine (0.15 mg) was given to anesthetize the animals for catheterization (period 1), again 5 days after the operation (period 2), and finally 4 to 5 hours after a 2nd injection of ketamine/xylazine (period 3). There were no differences in heart rates, respiratory rates, or cardiac outputs among the 3 study periods. However, arterial blood pressure was slightly, but significantly, lowered after, and presumably due to, instrumentation (62 +/- 4 mm of Hg, P less than 0.05) when compared with the 5-day postoperative period (67 +/- 7 mm of Hg) or after the readministration of anesthetics (66 +/- 7 mm of Hg). The partial pressure of carbon dioxide in the arterial blood was slightly lower (4 mm of Hg, P less than 0.05) in both acutely postanesthetic periods (period 1 and period 3) than in the same animals at postoperative day 5 (period 2). This study has demonstrated that resting hemodynamics measured shortly after this anesthesia with ketamine/xylazine are not largely different from those in chronically instrumented animals.

An asymptomatic intrarenal arteriovenous fistula was incidentally discovered by color flow and duplex ultrasonography approximately 2 weeks after a percutaneous biopsy of a renal allograft. On the basis of information obtained from the color flow image and pulsed Doppler analysis, the vascular communication could be characterized without the need for angiographic correlation. The patient was managed successfully with close observation aided by serial ultrasound examinations. Spontaneous resolution of the fistula occurred within 4 weeks after the biopsy and was evident on a follow-up ultrasound examination. Duplex ultrasonography in conjunction with color flow imaging proved to be a valuable noninvasive technique for diagnosing and monitoring this postbiopsy vascular complication.

We investigated the relationship between left atrial (LA) and pulmonary capillary wedge pressure (PCW) in order to define the clinical settings in which PCW may be used to approximate LA pressure and to determine the cause and significance of difference between LA and PCW pressures. Nineteen patients who at cardiac catheterization had LA, PCW, and left ventricular (LV) pressures recorded, had mitral valve gradients and areas determined. Mean PCW and LA pressures correlated well (r = 0.94). Phasic PCW consistently overestimated the MV gradient and underestimated the MV area compared to LA pressure, (8 +/- 4 versus 4 +/- 3 mm Hg, p less than 0.001, 1.3 +/- 0.3 versus 1.6 +/- 0.3 cm2, p less than 0.005, respectively). Three patients had abnormal MV prosthesis function assessed by PCW pressure but not by LA pressure. Diastolic MV gradients between PCW and LV were caused or increased by a slowed y descent in the PCW tracing. Using the PCW pressure may falsely elevate MV gradients and falsely reduce MV areas and lead to incorrect clinical action.

The effect of ritodrine hydrochloride tocolytic therapy on left ventricular size and performance was studied during pregnancy by M-mode echocardiography. Ritodrine therapy increased heart rate, calculated stroke volume, ejection fraction, and cardiac output. Left ventricular end-diastolic dimension and systemic arterial pressure were unchanged. Left ventricular velocity of circumferential fiber shortening was markedly augmented. Ritodrine, as currently used for tocolytic therapy, has potent inotropic and chronotropic effects on the maternal heart. These effects suggest that ritodrine tocolytic therapy should be used with caution in patients with latent or manifest heart disease.