Objective-To map canine mitochondrial proteins and identify qualitative and quantitative differences in heart mitochondrial protein expression between healthy dogs and dogs with naturally occurring and induced dilated cardiomyopathy (DCM). Sample Population-Left ventricle samples were obtained from 7 healthy dogs, 7 Doberman Pinschers with naturally occurring DCM, and 7 dogs with induced DCM. Procedures-Fresh and frozen mitochondrial fractions were isolated from the left ventricular free wall and analyzed by 2-dimensional electrophoresis. Protein spots that increased or decreased in density by greater than or equal to 2-fold between groups were analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry or quadrupole selecting, quadrupole collision cell, time-of-flight mass spectrometry. Results-Within narrow pH gradients of control canine heart mitochondrial samples, a total of 1,528 protein spots were revealed. Forty subunits of heart mitochondrial proteins that differ significantly from control tissues were altered in tissue specimens from dogs with naturally occurring and induced forms of DCM. The most affected heart mitochondrial proteins in both groups were those of oxidative phosphorylation (55%). Upregulation of manganese superoxide dismutase was suggestive of heart oxidative injury in tissue specimens from dogs with both forms of DCM. Evidence of apoptosis was associated with overexpression of the heart mitochondrial voltage-dependent anion channel-2 protein and endonuclease G in tissue specimens from dogs with induced DCM. Conclusions and Clinical Relevance-Alterations of heart mitochondrial proteins related to oxidative phosphorylation dysfunction were more prevalent in tissue specimens from dogs with induced or naturally occurring DCM, compared with those of control dogs.

A technique for transvenous endomyocardial biopsy of the right ventricle was developed and evaluated for safety and efficacy in anesthetized healthy cats positioned in left lateral recumbency. At least 6 endomyocardial biopsy specimens were obtained from the right ventricle or interventricular septum of 11 cats. In 4 cats, the right jugular vein was torn during attempts to pass the introducing catheter into the right ventricle; however, in only 1 cat did this preclude catheter passage. This cat's heart was biopsied via the left jugular vein. Except for damage to the jugular vein, complications were infrequent, and the biopsy procedure was well tolerated by all cats.

Nintey nonanesthetized 7- to 16-week-old pigs were studied, using 2-dimensional echocardiography that permits orientation of a targeted M-mode beam perpendicular to structures being studied and allows serial studies of the same cardiac regions. Normative data were obtained and included body weight and measurements of left atrial diameter, mitral valve excursion, aortic root diameter, left ventricular end-diastolic and end-systolic diameters, and left ventricular fractional shortening. A positive correlation was found between body weight and measurements of left atrial diameter, mitral valve excursion, aortic root diameter, left ventricular end-diastolic and end-systolic diameters, and fractional shortening. A correlation was found between body weight and age. Best-fit analysis resulted in all measurements fitting either a first- or second-degree polynomial.

Cardiopulmonary function values were determined before and after surgical removal of adult heartworms in 25 dogs with spontaneous and 4 dogs with drug-induced caval syndrome (CS). Fifteen dogs with spontaneous CS (recovery group) and 4 dogs with drug-induced CS (drug-induced CS group) recovered after removal, and 10 dogs with spontaneous cs were euthanatized or died (nonsurviving group). Before heartworm removal, injected radiographic contrast medium was regurgitated from the right ventricle to the right atrium. Mean pulmonary arterial pressure and total pulmonary resistance were not statistically different between the recovery and nonsurviving groups of dogs, but the end-diastolic right ventricular pressure (mean +/- SD, 6.9 +/- 9.1 mm of Hg) and the a (8.7 +/- 9.2 mm of Hg)- and v (6.3 +/- 8.5 mm of Hg)-waves of the right atrial pressure curve in the recovery group were less, respectively, than the end-diastolic right ventricular pressure (17.3 +/- 6.0 mm of Hg) and the a (15.8 +/- 6.1 mm of Hg)- and v (21.4 +/- 6.9 mm of Hg)-waves in dogs of the nonsurviving group. After heartworm removal, contrast medium regurgitation disappeared, and cardiac output of the right ventricle increased in dogs of the recovery (from 2.08 +/- 0.72 to 2.38 +/- 0.68 L/min; P < 0.05) and drug-induced CS (from 1.42 +/- 0.19 to 1.88 +/- 0.26 L/min, P < 0.05) groups. However, regurgitation remained, and cardiac output did not increase in some dogs of the nonsurviving group. Mean pulmonary arterial pressure decreased significantly (from 37.7 +/- 18.3 mm of Hg to 32.0 +/- 16.1 mm of Hg; P < 0.01) at 1 week after heartworm removal in dogs of the recovery group, but not in those of the nonsurviving group. Total pulmonary resistance (from 12,612 +/- 7,670 dynes.sec.cm-5.kg of body weight to 9,776 +/- 6,089 dynes.sec.cm-5.kg; P < 0.01) and right atrial pressure (a-wave: from 8.7 +/- 9.2 mm of Hg to 4.1 +/- 5.6 mm of Hg; v-wave: from 6.3 +/- 8.5 mm of Hg to 2.1 +/- 4.6 mm of Hg) decreased after heartworm removal in dogs of the recovery group. Total pulmonary resistance (from 20,309 +/- 9,682 dynes.sec.cm-5.kg to 15,970 +/- 6,798 dynes.sec.cm.5.kg; P < 0.05) and right atrial pressure (a-wave: from 15.8 +/- 6.1 mm of Hg to 10.1 +/- 6.3 mm of Hg; v-wave: from 21.4 +/- 6.9 mm of Hg to 11.1 +/- 3.7 mm of Hg) also decreased in dogs of the nonsurviving group. However, pressures in the right side of the heart and total pulmonary resistance after heartworm removal were greater in dogs of the nonsurviving group than in dogs of the recovery group. At necropsy pulmonary arterial emboli containing dead heartworms were found in almost all dogs with spontaneous CS, but not in dogs with drug-induced CS. The severity of pulmonary arterial embolism correlated significantly with mean pulmonary arterial pressure before (r = 0.710; P < 0.01) and 1 week after (r = 0.728; P < 0.01) heartworm removal.

The ventricular arrhythmogenic dose of epinephrine (ADE) was determined in 6 dogs anesthetized with halothane alone or with halothane after injection of tiletamine/zolazepam (TZ). Respiratory rate and tidal volume were controlled and sodium bicarbonate was administered to maintain arterial pH and blood gas values within reference range. Heart rate and arterial blood pressure were recorded during determination of the ADE. The ADE (mean +/- SD) was no different during anesthesia with use of halothane alone (8.9 +/- 4.3) than it was when injections of TZ preceded administration of halothane (6.7 +/- 2.8). Tiletamine/zolazepam was also administered IV immediately after determination of the ADE during halothane-induced anesthesia. The TZ administered in this manner did not alter the ADE. Blood pressure and heart rate were significantly greater during infusion of epinephrine than immediately prior to infusion. The administration of TZ did not alter blood pressure response. The ADE was also determined in 6 cats anesthetized with halothane preceded by administration of TZ. The ADE (mean +/- SD) was 0.7 +/- 0.23 microgram/kg, a value similar to that reported for cats during anesthesia with halothane alone.

Right atrial, pulmonary artery, pulmonary capillary, pulmonary artery wedge, and systemic blood pressures of strenuously exercising horses increase markedly. As a consequence, myocardial metabolic O2 demand in exercising horses must be high. Experiments were, therefore, carried out on 9 healthy, exercise-conditioned horses (2.5 to 8 years old; 481 +/- 16 kg) to ascertain the regional distribution of myocardial blood supply in the atria and ventricles at rest and during exercise. Blood flow was measured, using 15-micrometer-diameter radionuclide-labeled microspheres that were injected into the left ventricle while reference blood samples were being withdrawn at a constant rate from the thoracic aorta. Myocardial blood flow was determined at rest and during 2 exercise bouts performed on a high-speed treadmill at 8 and 13 m/s (0% grade). The sequence of exercise bouts was randomized among horses, and a 60-minute rest period was permitted between exercise bouts. There was considerable heterogeneity in the distribution of myocardial perfusion in the atria and the ventricles at rest; the right atrial myocardium received significantly (P < 0.05) less perfusion than did the left atrium, and these values were significantly (P < 0.05) less than those for the respective ventricular myocardium. The right ventricular myocardial blood flow also was significantly less than that in the left ventricle. With exercise, myocardial blood flow in all regions increased progressively with increasing work intensity and marked coronary vasodilation was observed in all cardiac regions. During exercise at 8 or 13 m/s, right and left atrial myocardial blood flows (per unit weight basis) were not different from each other. Although at treadmill speed of 8 m/s, left ventricular myocardial blood flow exceeded that in the right ventricle, this was not the case at 13 m/s, when perfusion values (per unit weight basis) became similar. These data suggested that, in exercising horses, myocardial metabolic O2 requirements increase markedly in all regions. However, the right atrial and right ventricular myocardial blood flows increased out of proportion to those in the left atrium and left ventricle, respectively.

Transcutaneous pulsed-wave Doppler echocardiography was used to obtain velocity signals from the aortic and pulmonary roots of clinically normal adult dogs tranquilized with acepromazine. Doppler-derived variables included peak ejection velocity, ejection time, and velocity-time integral. The cross-sectional areas of the left and right ventricular outflow tracts were estimated from diameters of the respective orifices measured from two-dimensional echocardiographic images. These data were used to calculate stroke volume and cardiac output for each ventricle. Linear, single variable regressions of ejection time, velocity-time integral, and peak velocity with body weight showed no significant correlations. Significant correlations existed between body weight and estimated left and right ventricular stroke volume and cardiac output. A close correspondence existed between pulmonary and aortic determinations of velocity-time integral, stroke volume, and cardiac output. These results provide an initial framework for interpretation of clinical data by veterinary cardiologists.