Depressor response during experimental portal hypertension in dog.
Elevation of splanchnic portal pressure in dogs results in an apparently reflexic response manifest as an active reduction in mean arterial pressure (AP). The results from 14 dogs separated into a tachycardic (TACH) heart rate (HR) response (P less than 0.005, n = 6) group and a bradycardic (BRAD) HR response (P less than 0.005, n = 8) group. Both groups showed similar reductions in AP and cardiac output (CO); however, stroke volume (SV) was reduced to a greater extent (P less than 0.029) in the TACH group. Atropine eliminated or reversed the bradycardia in the BRAD group and propranolol blocked the tachycardia in the TACH group. When portal hypertension was repeated in the BRAD group after atropine, similar reductions (P less than 0.01) were observed in AP, SV, and CO but total peripheral resistance (TPR) no longer increased. Reductions in SV or CO due to reduced venous return only partially explain the AP changes. These data suggest the reflex activation of several mechanisms that contribute to rather than completely oppose the reduction in AP anticipated with a reduction in venous return. They include an atropine-sensitive negative chronotropic effect and a negative inotropic effect as well as adjustments in TPR. We thus propose a reflex mechanism that is activated by increased splanchnic pressure and contributes to an active lowering of mean arterial pressure.
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D004195:Disease Models, Animal; D004285:Dogs; D006339:Heart Rate; D006975:Hypertension, Portal / Q000503:physiopathology*; D012018:Reflex; D013318:Stroke Volume; D014655:Vascular Resistance