Effect of Dirofilaria Immitis on Canine Cardiopulmonary Physiology.
The effects of canine heartworm disease (CHD) were studied using in vitro and in vivo preparations to gain insight into the pathogenesis and pathophysiology of the characteristics lesions. The in vitro studies examined the contractile responses of pulmonary artery strips, bronchial spirals and lung parenchymal strips from normal and CHD dogs. Carbamylcholine failed to contract arteries and bronchial and parenchymal responses were the same for both groups. Decreased arterial responsiveness to histamine in both magnitude and number of strips responding was seen in the CHD group, suggesting tachyphylaxis of the histamine receptors. Enhanced responses were seen in the CHD pulmonary artery strips with norepinephrine and in the lung parenchymal strips with histamine. Chronically instrumented anesthetized dogs were hemodynamically observed before and after administration of beta adrenergic agonists for differences in pressure, flow, or pulmonary vascular resistance responses. Cardiac index values and heart rates were lower in the CHD dogs under baseline conditions. Both groups increased cardiac index and pulmonary perfusion pressures with isoproterenol and terbutaline. Terbutaline caused the same drop in pulmonary vascular resistance at a lower heart rate than isoproterenol. Hypoxia caused increased pulmonary perfusion pressures in the anesthetized dogs. Only heart rate changes and percent change in cardiac index differed. Half the control dogs decreased cardiac output more than 20% during hypoxia causing a mean reduction in cardiac index. Phentolamine did not alter response in either group significantly, although the CHD group showed less percent increase in perfusion pressure. Cardiac index was a significant covariant in perfusion pressure values in the first two minutes of hypoxia, and in total pulmonary vascular resistance at the time of maximal pressor response. Alpha 1 adrenergic receptors of the lung parenchyma were studied by radioligand binding using (H$\sp3$) prazosin. Low amount of specific binding necessitated the use of a single high concentration of ligand to determine receptor density. No differences in binding were seen. Similarity of lesion formation in CHD and human arteriosclerosis and a role for histamine in the pathogenesis were presented. Also noted were similarities of the pulmonary hypertension and cardiac limitations in CHD to primary pulmonary hypertension and cor pulmonale in humans.