Beta 2-adrenergic vascular control in hemorrhage and its influence on cardiac performance.
Cardiac output (CO), heart rate, stroke volume (SV), and total peripheral resistance (TPR) were followed in anesthetized cats with intact and selectively blocked beta 2-adrenoceptors. SV and CO decreased and TPR increased initially after bleeding in both groups. After this, animals with intact beta 2-adrenoceptors showed gradual recovery of SV and CO and gradual restoration to control of the initially raised TPR. In beta 2-blocked animals SV and CO instead remained low and TPR high. These patterns of response occurred after mild, moderate, and severe bleeding. Separate experiments indicated that the restoration of TPR with intact beta 2-adrenoceptors mainly can be attributed to beta 2-adrenergic dilator interaction with the vasoconstrictor influences. The previously described beta 2-adrenergic control of plasma volume in hemorrhage (Acta Physiol. Scand. 116: 175-180, 1982) suggests that the increases in SV and CO with intact beta 2-adrenoceptors, in turn, probably are indirect effects on cardiac performance due to improved cardiac filling. A synthesis of present and previous findings thus suggests the existence of a beta 2-adrenergic vascular control in hemorrhage favoring tissue perfusion via decreased resistance and via increased plasma volume and hence SV and CO.
D000319:Adrenergic beta-Antagonists; D000818:Animals; D001808:Blood Vessels / Q000503:physiopathology*; D002196:Capillaries; D002302:Cardiac Output; D002415:Cats; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D006470:Hemorrhage / Q000503:physiopathology*; D008297:Male; D010953:Plasma Volume; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D013318:Stroke Volume; D014655:Vascular Resistance
D000319:Adrenergic beta-Antagonists; D011943:Receptors, Adrenergic, beta