Vascular responses to many physiological stresses are abnormal in heart failure. Increased peripheral resistance and a reduction in the vasodilator response to exercise and ischemia are examples of this abnormal vascular control. Such abnormal vascular control in heart failure is a result of interplay between neural, hormonal, and local vascular factors. This study was designed to test the hypothesis that a specific local mechanism, endothelium-dependent relaxation to acetylcholine (ACh), is depressed in experimental heart failure. Experiments were performed on 11 purebred beagles. Experimental heart failure was induced by rapid ventricular pacing for approximately 30 days. Femoral artery diameter was measured by sonomicrometry, and dose-response relationships to ACh, norepinephrine (NE), and nitroglycerin (NTG) were done before and after inhibition of cyclooxygenase by indomethacin. Heart failure resulted in a significant depression of ACh relaxation at all concentrations. In dogs with heart failure, indomethacin enhanced the dilation response to low concentrations of ACh. Constriction to NE and dilation to NTG were unchanged by heart failure. These data demonstrate that in the canine femoral artery endothelium-dependent dilation to ACh is depressed in experimental heart failure. Depression of endothelium-dependent vasodilation represents one local mechanism for abnormal control of the vasculature in congestive heart failure.

Results suggest that for horses in a therapeutic riding program, being ridden by physically or psychologically handicapped individuals is no more stressful for the horses than is being ridden in the same setting by recreational riders. However, at-risk children caused more stress to the horses, suggesting that the time horses are ridden by at-risk children should be limited both daily and weekly.

We investigated regional differences of in vitro responses of pulmonary arteries (6-mm OD) from the dorsocaudal (top) and cranioventral (bottom) lung regions to endothelium-dependent vasodilators (methacholine, bradykinin, and calcium ionophore A-23187). Methacholine relaxed endothelium-intact top vessels; however, in bottom vessels, a small relaxation preceded a profound contraction. In top vessels, removal of endothelial cells converted relaxation to contraction, and in bottom vessels it abolished relaxation and enhanced contraction. Bradykinin and A-23187 were more potent and caused greater endothelium-mediated relaxation in top than in bottom arteries. The endothelium-independent vasodilator sodium nitroprusside caused similar relaxations in all rings. Nomega-nitro-L-arginine and NG-monomethyl-L-arginine and methylene blue abolished relaxation of top and bottom arteries to methacholine; meclofenamate had little effect. We conclude that regional differences in endothelium-mediated relaxation are caused by differences in the magnitude of the endothelial release of nitric oxide. Similar differences in endothelium-dependent flow-mediated vasodilation and endothelial nitric oxide release may result in preferential perfusion of caudodorsal lung regions.

Among healthy dogs from the lower peninsula of Michigan, > 20% have antibodies against leptospiral serovars historically considered uncommon but more recently incriminated as causing clinical canine leptospirosis. Wildlife and livestock may be of increasing importance as reservoirs for canine leptospirosis as urbanization continues to occur. Expanded vaccination strategies may partially mitigate these trends.

Degree of viremia induced during BVDV infection is associated with severity of clinical disease. Isolates of BVDV that induce a high degree of viremia may be more capable of inducing clinical signs of disease. Strategies (eg, vaccination) that reduce viremia may control clinical signs of acute infection with BVDV.