TY - JOUR
T1 - The effect of acute hypoxaemia on ventricular function during beta-adrenergic and cholinergic blockade in the fetal sheep
AU - Reller, M. D.
AU - Morton, M. J.
AU - Giraud, G. D.
AU - Reid, D. L.
AU - Thornburg, K. L.
PY - 1989
Y1 - 1989
N2 - 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<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.
AB - 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<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.
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M3 - Article
C2 - 2558132
AN - SCOPUS:0024444191
SN - 0141-9846
VL - 11
SP - 263
EP - 269
JO - Journal of Developmental Physiology
JF - Journal of Developmental Physiology
IS - 4
ER -