Effects of vasomotor- and mediator-induced hypotension on bronchomotor tone in swine

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Abstract
We studied the sympathetic neural response on airways to hypotensive stimuli in 19 swine in vivo. The effects of pharmacologically induced hypotension with nitroprusside (NTP) and hypotension elicited by intravenous compound 48/80 (48/80), a mast cell degranulating agent, were compared after equivalent reductions in mean arterial blood pressure (MAP). Reduction of the MAP to 60% of base line with NTP in six swine caused an increase in plasma epinephrine (E) from 60 .+-. 28 to 705 .+-. 276 pg/ml (P = 0.032) and plasma norepinephrine (NE) from 270 .+-. 46 to 796 .+-. 131 pg/ml (P = 0.032). Comparable reduction in MAP elicited with 48/80 in six other swine caused a substantially greater increse in both plasma E (9,581 .+-. 4,147 pg/ml; P = 0.012 vs. NTP group) and plasma NE (2,239 .+-. 637 pg/ml; P = 0.041 vs. NTP group). Catecholamine secretion attenuated mediator-induced changes in lung resistance (RL). In animals receiving 48/80, RL increased from 2.97 .+-. 0.31 to 7.44 .+-. 0.56 cmH2O .cntdot. l-1 .cntdot. s. In animals having ganglionic blockade with 7.5 mg/kg iv hexamethonium and .beta.-adrenergic blockade with propranolol (4.0 mg/kg iv followed by 40 .mu.g .cntdot. kg-1 .cntdot. min-1), comparable doses of 48/80 caused an increase in RL to 18.6 .+-. 4.55 cmH2O 1. l-1 .cntdot. s (P < 0.04 vs. swine receiving neither nexamethonium nor propranolol). Ganglionic and .beta.-adrenergic blockade did not alter catecholamine secretion caused by hypotension after 48/80, indicating that mediator induced hypotension elicited autonomic secretion by a route that bypassed normal reflex mechanisms. We demonstrate that mediator-induced hypertension in swine elicits substantially greater catecholamine secretion by a different mechanism than for comparable hypotension elicited by vasodilation alone. This degree of E secretion is sufficient to attenuate substantially the bronchoconstriction caused by endogenously released mediators. Secretion of E is a direct postganglionic effect of circulating mediator.