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Pulmonary edema associated with transient airway obstruction was detected in 3 horses. The cause of obstruction was different in each horse, but after relief of the obstruction, clinical signs and radiographic abnormalities were indicative of pulmonary edema. In 2 of the 3 horses, pink frothy fluid was evident in the airways. The horses were treated with furosemide, nasal insufflation of O2, anti-inflammatory agents, and anti-biotics. Of the 3 horses examined, 1 horse died acutely, 1 horse recovered fully, and 1 developed pleuritis and was subsequently euthanatized.

The purpose of this study was to determine the effects of cocaine on vasoreactivity in the swine model. Eight miniature pigs underwent regional endothelial denudation of the left anterior descending coronary artery and were then fed a high cholesterol diet. Cross-sectional area (CSA) of coronary arteries was measured by quantitative angiography. Before denudation, intravenous cocaine (1, 3, and 10 mg/kg) decreased CSA of epicardial vessels by 19-44%. At 3 mo after the denudation, the percent reduction in CSA of the denuded vessels induced by the 10 mg/kg dose was significantly augmented compared to nondenuded vessels (59 +/- 5% vs. 48 +/- 4%, P less than 0.05). Under in vitro conditions where isometric force of isolated ring segments was measured, methoxamine (an alpha 1 agonist) or BHT-920 (an alpha 2 agonist) produced similar degrees of contraction of denuded and control vessels; however, cocaine in concentrations up to 3 x 10(-3) M did not produce contraction. These responses were unaffected by removal of the endothelium. Histologically, myointimal thickening was noted at the denuded site. The present study demonstrates an enhanced vasoreactivity of atherosclerotic coronary arteries to cocaine in vivo, the mechanism of which appears to be mediated by endogenous vasoactive substances rather than by a direct action of cocaine on vascular smooth muscle.

Milrinone, a positive inotropic drug with vasodilating properties, was administered at doses of 0.5 to 1 mg/kg orally twice daily to 29 dogs with moderate to severe congestive heart failure (CHF). Significant echocardiographic improvement in ventricular systolic function was observed after 3 days of administration of milrinone and at the patients' last echocardiographic observation (day 21 in 25 subjects, day 7 in 2 subjects, and day 3 in 2 subjects). Echocardiographic shortening fraction at the initial measurement had a median increase of 6.14% (P less than 0.001), and for the last observation a 2.83% increase (P less than 0.005). Most patients also showed improvement in their clinical signs as assessed by the veterinarian (72%) and by owner's evaluation (81%). No consistent problem or adverse reaction to milrinone was observed, except for a small number of clinically manageable ventricular dysrhythmias. Milrinone appears in this trial to be effective for the treatment of advanced CHF in dogs.

Six horses (five males) aged three months to fourteen years had endocarditis at necropsy. Two of the horses had a clinical diagnosis of valvular endocarditis with negative blood cultures. Single or complex valvular involvement was present in five horses. One horse had non-infectious thrombi associated only with the chordae tendineae. Mitral valves were affected in four horses, and aortic semilunar valves were affected in two. Infarcts had occurred in the kidneys and the myocardium of four horses. Bacteria were isolated postmortem from the valvular vegetations of two horses; Candida parapsilosis was isolated and demonstrated morphologically in a third horse.