Why the study?
Does chronic pindolol administration affect central hemodynamics and uteroplacental blood flow in pregnant renal hypertensive rats?
Does chronic pindolol administration affect central hemodynamics and uteroplacental blood flow in pregnant renal hypertensive rats?
In a rat model of pregnancy complicated by renal hypertension, chronic pindolol administration severely reduced uteroplacental blood flow despite maintaining cardiac output and mean arterial pressure.
Pindolol may reduce uteroplacental flow in hypertensive pregnancy models despite stable hemodynamics; leaves open beta-blocker effects in humans.
The aim of the present study on pregnant renal hypertensive rats was to investigate the effects on central hemodynamics and uteroplacental blood flow after chronic administration of pindolol, a nonspecific beta-adrenergic receptor blocking agent with intrinsic beta-stimulatory effect. Renal hypertension was induced by partial clamping of both renal arteries four weeks before pregnancy. Pindolol was administered with the food during the entire pregnancy period. Two to four days before expected delivery mean arterial pressure, heart rate, cardiac output, (dye-dilution technique) and utero-placental blood supply (microsphere technique) were determined. The chronic pindolol treatment reduced heart rate by 25 per cent while both mean arterial pressure and cardiac output remained unchanged. However, blood flow to uterus and placentae was reduced by 43 and 64 per cent, respectively, after pindolol treatment. Clinical as well as experimental studies (15, 16) demonstrate a reduced utero-placental blood supply when pregnancies are complicated by hypertension. As pregnancies with severe hypertension are associated with an increased frequency of intrauterine growth retardation and intrauterine asphyxia the present results indicate that the combination of hypertension and long-term treatment with beta-blockers might reduce utero-placental blood flow enough as to seriously interfere with fetal oxygen supply thereby increasing the risk of intra- and extra-uterine asphyxia.
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Lundgren et al. (1983) studied this question.
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