Decreased pulmonary arterial endothelium-dependent relaxation in heartworm-infected dogs with pulmonary hypertension

Abstract

Abstract Objective To investigate the contractility of pulmonary arterial smooth muscle and the relation between pulmonary hypertension and endothelium-derived relaxing factor in canine heartworm disease. Animals 18 noninfected control and 9 heartworm-infected dogs. Procedure Mean pulmonary arterial blood pressure was measured in vivo, and tension of pulmonary arterial strips was measured by use of the isometric tension method. Results After phenylephrine (10−5M)-induccd contraction of the pulmonary vascular smooth muscle, carbamylcholine chloride (CCh, 10−6M) caused more relaxation of the vascular smooth muscle of noninfected dogs than that of heartworm-infected dogs. Furthermore, the degree of CCh-induced relaxation was inversely correlated with mean pulmonary arterial blood pressure in the noninfected and the heartworm-infected dogs. The CCh-induced relaxation was inhibited by pretreatment with Ng-nitro-l-arginine methyl ester hydrochloride (10−5M), and in reversed dose-dependent manner by l-arginine (10−4 to 3 × 10−2M). Sodium nitroprusside (10−8 to 10−5M) caused a dosedependent relaxation in all vessels, and there was no significant difference in the relaxation responses in both groups except at 10−7M for vessels with intact endothelium from noninfected dogs. Conclusion The depression of endothelium-dependent relaxation is correlated with the pulmonary arterial blood pressure in heartworm-infected dogs, suggesting that the decrease is one of the essential factors for the genesis of pulmonary hypertension in canine filariasis. (Am J Vet Res 1997;58:171–174)