TY - JOUR
T1 - Plasma protein concentration and control of coronary vascular resistance in isolated rat heart
AU - Avolio, A. P.
AU - Spaan, J. A E
AU - Laird, J. D.
PY - 1980
Y1 - 1980
N2 - Isolated externally paced (300 beats/min) rat hearts were perfused at constant pressure (70 mmHg) using a modified Krebs-Henseleit solution with (n = 52) and without (n = 15) washed bovine red cells. Albumin concentration varied from 1 to 10 g/dl. With increasing albumin concentration in blood-perfused hearts, wet-to-dry weight ratio, peak reactive hyperemic flow, and control geometric resistance were decreased, whereas oxygen consumption, control flow, and minimal geometric resistance remained constant. For plasma-perfused hearts, there was a decrease in both control and peak flow, and the other results were similar to the blood-perfused hearts. These results indicate the following. 1) Increase in interstitial fluid volume is not sufficient to cause a significant increase in minimal vascular resistance. 2) Increase in blood viscosity is compensated by vasodilation maintaining steady flow constant. 3) Minimal vascular resistance is determined by physical geometry of the vascular bed. 4) Regulation of coronary flow is postulated to be achieved by smooth muscle response to interstitial osmolarity, with a negative feedback signal coming from variation of capillary arterial pressure to variations in flow.
AB - Isolated externally paced (300 beats/min) rat hearts were perfused at constant pressure (70 mmHg) using a modified Krebs-Henseleit solution with (n = 52) and without (n = 15) washed bovine red cells. Albumin concentration varied from 1 to 10 g/dl. With increasing albumin concentration in blood-perfused hearts, wet-to-dry weight ratio, peak reactive hyperemic flow, and control geometric resistance were decreased, whereas oxygen consumption, control flow, and minimal geometric resistance remained constant. For plasma-perfused hearts, there was a decrease in both control and peak flow, and the other results were similar to the blood-perfused hearts. These results indicate the following. 1) Increase in interstitial fluid volume is not sufficient to cause a significant increase in minimal vascular resistance. 2) Increase in blood viscosity is compensated by vasodilation maintaining steady flow constant. 3) Minimal vascular resistance is determined by physical geometry of the vascular bed. 4) Regulation of coronary flow is postulated to be achieved by smooth muscle response to interstitial osmolarity, with a negative feedback signal coming from variation of capillary arterial pressure to variations in flow.
UR - http://www.scopus.com/inward/record.url?scp=0018819524&partnerID=8YFLogxK
M3 - Article
C2 - 7377317
AN - SCOPUS:0019004914
SN - 0363-6135
VL - 238
SP - H471-H480
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 4
ER -