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

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.

METHODS

18 noninfected control and 9 heartworm-infected dogs.

METHODS

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(-5)M)-induced contraction of the pulmonary vascular smooth muscle, carbamylcholine chloride (CCh, 10(-6)M) 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(-5)M), and in reversed dose-dependent manner by L-arginine (10(-4) to 3 x 10(-2)M). Sodium nitroprusside (10(-8) to 10(-5)M) caused a dose-dependent relaxation in all vessels, and there was no significant difference in the relaxation responses in both groups except at 10(-7)M for vessels with intact endothelium from noninfected dogs.

CONCLUSIONS

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.