Beta 2-adrenergic vascular control in hemorrhage and its influence on cardiac performance

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Abstract
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 suggests that the increases in SV and CO with intact .beta.2-adrenoceptors probably are indirect effects on cardiac performance due to improved cardiac filling. A .beta.2-adrenergic vascular control evidently operates during hemorrhage, favoring tissue perfusion via decreased resistance and via increased plasma volume and hence SV and CO.