Thromboxane mimics the pulmonary but not systemic vascular responses to bolus HCl injections in broiler chickens

Bolus i.v. injections of 1.2 N HCl elicit a rapid but transient pulmonary v asoconstriction in broiler chickens. In mammals, the pulmonary vasoconstric tive response to bolus acid injection depends on increased synthesis of thr omboxane A(2); however, the vascular responsiveness of domestic fowl to thr omboxane previously had not been evaluated. In the present study, we tested the hypothesis that, if HCl triggers pulmonary vasoconstriction by stimula ting thromboxane A(2) synthesis in broilers, then bolus i.v. injections of the potent thromboxane A(2) mimetic U44069 (9,11-dideoxy-9 alpha,11 alpha-e poxy-methanoprostaglandin F-2 alpha; 1 mu mol/mL; 0.5 mt injected volume) s hould trigger hemodynamic responses similar to these elicited by HCl (1.2 N ; 1.5 mL injected volume). Both HCl and the thromboxane mimetic elicited tw ofold or greater increases in pulmonary vascular resistance, which in turn increased pulmonary arterial pressure by 50% despite concurrent reductions in cardiac output. The reductions in cardiac output were associated with re ductions in stroke volume but not heart rate. The thromboxane mimetic also increased the total peripheral resistance, which minimized the reduction in mean systemic arterial pressure associated with the decrease in cardiac ou tput. In contrast, HCl injections did not increase total peripheral resista nce; consequently, the reduction in cardiac output caused the mean systemic arterial pressure to decrease by 30 mm Hg. Mannitol (2.5%; 1.5 mt) was inj ected i.v. as a volume central, and had no influence on any of the variable s. This study provides the first direct evidence that thromboxane is a pote nt pulmonary vasoconstrictor in broilers, and provides support for the hypo thesis that thromboxane mediates the pulmonary vasoconstrictive response to bolus i.v. injections of HCl. The differential response of the systemic va sculature to the thromboxane mimetic and HCl may indicate that cardiopulmon ary responses to HCl injections are not mediated solely via thromboxane pro duction. Alternatively, a direct dilatory effect of elevated hydrogen ion c oncentrations on the systemic vasculature may have counteracted any tendenc y for simultaneously evolved endogenous thromboxane to elicit systemic vaso constriction.