Effects of hemorrhage on regional blood flow distribution in dogs and primates

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Abstract

The effects of hemorrhage on arterial pressure, blood flows, and resistances in the coronary, mesenteric, renal, and iliac beds of healthy, conscious dogs and intact, tranquilized baboons were studied. Mild nonhypotensive hemorrhage (14±2 ml/kg) increased heart rate and mesenteric and iliac resistances slightly but significantly, and decreased renal resistance (-13±2%). Moderate hypotensive hemorrhage, 26±2 ml/kg, reduced mean arterial pressure (-23±2 mm Hg) and blood flows to the mesenteric (-56±3%), iliac (-58±5%), and coronary (-39±4%) iliac (-58±5%), and coronary (-39±4%) vascular beds, and increased heart rate (+89±9 beats/min) and resistances in the mesenteric (+73±15%), iliac (+102±19%), and coronary (+27±5%) beds. In contrast to the other beds, renal flow rose 11±6% above control and renal resistance fell 31±2% below control. Renal vasodilatation with hemorrhage was also observed in 5 baboons. The increases in mesenteric and iliac resistances were blocked almost completely by phentolamine, while the increase in coronary resistance was only partially blocked by phentolamine. The renal dilatation was not blocked by phentolamine, propranolol, atropine, or tripelennamine, but was prevented by indomethacin, suggesting that this dilatation was mediated by a prostaglandin like compound. Thus the peripheral vascular responses to hemorrhage involve intense vasoconstriction in the mesenteric and iliac beds. In the normal conscious dog and the intact, tranquilized primate, the renal bed does not share in the augmentation of total peripheral resistance with nonhypotensive and moderate hypotensive hemorrhage, but does with more severe hemorrhage. In fact, renal vasodilatation occurs with nonhypotensive or moderate hypotensive hemorrhage, which can be prevented by blockade of prostaglandin synthetase with indomethacin.

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APA

Vatner, S. F. (1974). Effects of hemorrhage on regional blood flow distribution in dogs and primates. Journal of Clinical Investigation, 54(2), 225–235. https://doi.org/10.1172/JCI107757

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