Vasomotor center controls of the hepatic circulation during blood pressure oscillation in rabbits.
Changes in hepatic hemodynamics during blood pressure oscillations caused by the side pressure exertion procedure (SPEP) were studied in anesthetized rabbits. The brain was excluded from systemic circulation except for one of the common carotids, which was compressed with stepwise elevated pressure. In normovolemia, the hepatic arterial flow (HAF) increased as the systemic arterial pressure (SAP) rose up to 140 mmHg, and then decreased as SAP rose further. With the rise of SAP, the portal venous flow (PVF) initially rose slightly, followed by a nearly constant decrease. Hemorrhaging influenced slightly the changes of HAF and PVF with the SAP rise. After volume loading, SAP and PVF markedly increased but HAF changed little. However, the initial increase in HAF with the SAP rise was markedly depressed by volume loading. PVF conspicuously decreased without initial increase with the rise in SAP. The hepatic vascular bed has a mechanism that prevents expected decrease of blood flow after hemorrhaging and during neurogenic hypertension. The interaction among HAF, PVF, and PVP may be involved in this mechanism.
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002545:Brain Ischemia / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D005260:Female; D006439:Hemodynamics; D006470:Hemorrhage / Q000503:physiopathology; D006499:Hepatic Artery / Q000294:innervation; D008102:Liver Circulation; D008297:Male; D011169:Portal Vein / Q000294:innervation; D011311:Pressoreceptors / Q000503:physiopathology; D011817:Rabbits; D014655:Vascular Resistance; D014666:Vasomotor System / Q000503:physiopathology*