We investigated the extent to which sympathomimetic amines induced splenic contraction and associated increases in arterial O2 (Cao2) and how these mechanisms affected control of the coronary circulation by sympathomimetic amines in conscious dogs. Blood hemoglobin (Hb) and Cao2 increased by 16q2% and 18q2% respectively during norepinephrine (NE) infusion in the intact, conscious state following splenic contraction. Phenylephrine (PE)induced similar effects. After either `1-adrenergic receptor blockade or splenectomey, these effects were abolished. Isoproterenol also decreased splenic thickness, which was abolished after either ganglionic or ` or a1/a2-adrenergic blockade. Direct infusions of NE and PE into the splenic artery decreased splenic thickness and increased Hb and Cao2 while ISO had no effect. After splenectomy, NE, i.v., did not increase Cao2 but coronary blood flow increased more (73q6%) vs. before splenectomy (49q7%) without any differences before and after splenectomy in the responses of pressures, contractility and myocardial O2 consumption (Mvo2). In contrast, renal, mesenteric, and iliac artery blood flows were not significantly different in response to sympathomimetic amines before and after splenectomy. These data indicate that sympathomimetic amines induced splenic contraction either directly or reflexly via `-adrenergic stimulation. The consequent increase in hemoglobin and Cao2 allows for equivilent increases in Mvo2 but at a smaller increase in coronary blood flow.
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