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The Acute Effects of A Non‐Selective β‐Adrenergic Blocking Agent in Hypertensive Pregnant Rats
Author(s) -
Karlsson Kirsten,
Lundgren Yen,
Ljungblad Ulf
Publication year - 1984
Publication title -
acta obstetricia et gynecologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.401
H-Index - 102
eISSN - 1600-0412
pISSN - 0001-6349
DOI - 10.3109/00016348409157129
Subject(s) - medicine , propranolol , cardiac output , blood pressure , hemodynamics , heart rate , cardiology , blood flow , anesthesia
. It is generally accepted that hypertensive cardiovascular complications can be prevented by treatment. However, during pregnancy, antihypertensive drugs might be hazardous in view of their influence on the fetus. Nevertheless, in spite of the diverging published results, even β‐blockers have been used in the pregnant patient. As our basic knowledge concerning the circulatory and fetal effects is minimal, we decided to elucidate the influence of the non‐selective β‐blocker, propranolol, on the haemodynamic circumstances in hypertensive pregnant rats. Renal hypertension was induced by clamping both renal arteries 4 weeks before pregnancy. Shortly before term, cardiac output was determined with the dye‐dilution technique and utero‐placental blood flow was determined with the microsphere technique, both before and after propranolol injection. Mean arterial pressure and heart rate were registered continuously. The acute propranolol injection reduced mean arterial pressure by 26%. This was due mainly to a 32% decrease in cardiac output, which in turn was due to a 24% decrease in stroke volume and a 6% decrease in heart rate. Both myometrial and placental blood flow decreased significantly, by 45 and 50%, respectively. It was furthermore of interest to observe the significant increase in blood flow resistance in both myometrium and placenta. In conclusion, it can be stated that the non‐selective β‐blocker propranolol, which lacks intrinsic stimulating activity, reduces mean arterial pressure mainly by a cardiac output decrease. The present results further indicate that the influence on peripheral blood flow might be caused by cardiac output changes as well as by direct effects on the utero‐placental vascular bed.

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