Abstract
We have designated the hindquarter (or terminal aortic) vascular resistance (HQR) of the rat as hindquarter compensator (HC) because it increases after such hypotensive interventions as pentobarbital anesthesia and nitrate administration, presumably due to reflex excitation of regional vasoconstrictor fibers. The aim of the present study was to observe whether the HC mechanism is also mobilized in response to hemorrhage. Rats were implanted with a 1.5 or 2 mm diameter electromagnetic flow probe at the terminal aorta for measurement of hindquarter flow (HQF). An indwelling catheter was placed in the right common carotid artery to measure arterial pressure (AP) and withdraw blood. Experiments were performed in conscious rats two or three days after implantation. HQR was calculated by dividing AP by HQF. About 10 min after withdrawing blood (0.3 ml/100 g body weight), ganglionic blockade with hexamethonium bromide significantly decreased HQR, which indicated a mobilization of the HC mechanism, a change not observed with superior mesenteric resistance. A quantitatively similar change was observed in HQR after withdrawing double the amount of blood, i.e., 0.6 ml/100 g body weight, suggesting that the HC mechanism is activated almost fully by the relatively small amount of blood loss of 0.3 ml/100 g body weight.
