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radionuclide-labeled microspheres that were injected into the left ventricle while reference blood samples were being withdrawn at a constant rate from the thoracic aorta.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.

Although ovine cysticercosis is not a zoonotic problem, it results in substantial economic losses due to the condemnation of infected tissues or entire carcasses. This study aimed to record preliminary data on the prevalence, and phylogenetic diversity of Cysticercus ovis isolates from slaughtered sheep in the province of Sulaymaniyah, Iraq. From January to September 2020, 6, 411 slaughtered sheep were examined for C. ovis by routine meat inspection. The amplification and sequence analysis of the COX1 gene for up to 35 specimens of C. ovis was performed using conventional PCR. The overall prevalence rate was 1.3%, and the prevalence was significantly higher in older sheep (>1 year) than younger ones (<1 year) (P< 0.05). The cardiac muscle showed a higher tendency to carry C. ovis infection compared to other examined muscles. Sequence analysis of the COX1 gene revealed six haplotypes, and the level of pairwise nucleotide diversity between individual haplotypes was 1–2%. Five out of six of the Taenia ovis haplotypes recovered could have been recorded for the first time globally. Phylogenetic interpretation indicated that all the T. ovis haplotypes clustered in a single clade, and it also indicated an extremely close similarity to Iranian and New Zealand isolates. Globally, this report adds new data on C. ovis genetic diversity, which provide an extremely useful molecular background with regard to future preventive as well as control strategies.

Objective: To compare mitochondrial complex I and complex IV activity in myocardial mitochondria of clinically normal dogs, clinically normal dogs exposed to inhalation anesthesia, and dogs affected with dilated cardiomyopathy. Sample: Myocardial samples obtained from 21 euthanized dogs (6 clinically normal [control] dogs, 5 clinically normal dogs subjected to inhalation anesthesia with isoflurane prior to euthanasia, 5 dogs with juvenile-onset dilated cardiomyopathy, and 5 dogs with adult-onset dilated cardiomyopathy). Procedures: Activity of mitochondrial complex I and complex IV was assayed spectrophotometrically in isolated mitochondria from left ventricular tissue obtained from the 4 groups of dogs. Results: Activity of complex I and complex IV was significantly decreased in anesthetized dogs, compared with activities in the control dogs and dogs with juvenile-onset or adult-onset dilated cardiomyopathy. Conclusions and Clinical Relevance: Inhalation anesthesia disrupted the electron transport chain in the dogs, which potentially led to an outburst of reactive oxygen species that caused mitochondrial dysfunction. Inhalation anesthesia depressed mitochondrial function in dogs, similar to results reported in other species. This effect is important to consider when anesthetizing animals with myocardial disease and suggested that antioxidant treatments may be beneficial in some animals. Additionally, this effect should be considered when designing studies in which mitochondrial enzyme activity will be measured. Additional studies that include a larger number of animals are warranted.

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.

Effects of endotoxemia on left ventricular contractility and systemic hemodynamics were determined in pentobarbital-anesthetized swine. A multielectrode conductance (volume) catheter and a high-fidelity pressure transducer catheter were passed retrograde into the left ventricle to continuously measure pressure and volume. End-systolic pressure-volume relationships were determined during transient (8 to 10 s) caudal vena caval balloon occlusion. Lactated Ringer's solution was administered at a rate sufficient to maintain left ventricular end-diastolic pressure > 6 mm of Hg. Following baseline measurements, Escherichia coli endotoxin (O55-B5) was infused IV at 2.5 micrograms/kg of body weight/h for 3 hours. Left ventricular end-systolic elastance (Ees), the slope of the end-systolic pressure-volume relationship; end-systolic elastance normalized for left ventricular end-diastolic volume (Ees norm); the rate of increase of left ventricular pressure (dP/dtmax); and preload recruitable stroke work (PRSW, stroke work-to-end-diastolic volume relationship) did not change in endotoxemic swine, compared with baseline measurements or with values from control (physiologic saline solution-treated) swine. Left ventricular pressures and volumes had marked pig-to-pig variability in the control and endotoxin-treated groups. Determination of Ees, Ees norm, and PRSW was further confounded by development of frequent premature ventricular contractions during caudal vena caval balloon occlusion. Endotoxin significantly (P < 0.05) decreased left ventricular end-diastolic pressure, compared with that in control swine, and significantly (P < 0.01) decreased left ventricular end-diastolic volume, compared with baseline. Endotoxin decreased cardiac index and arterial blood pressure, whereas heart rate, central venous pressure, and mean pulmonary arterial pressure increased. Endotoxin did not decrease myocardial contractility, as measured by Ees, Ees norm, dP/dtmax, or PRSW in anesthetized swine.

Twenty-three clinically normal Beagles were inoculated with North American Trypanosoma cruzi isolates from an opossum (Tc-O), an armadillo (Tc-A), or a dog (Te-D). The dogs were grouped according to the clinical outcome of inoculation. Group 1 consisted of 7 dogs inoculated with Tc-O or Tc-A that died or were euthanatized during acute stages of disease. Group 2 consisted of 5 dogs inoculated with Tc-O or Tc-A, that also developed acute disease, but survived to develop chronic disease. Group 3 consisted of 7 dogs inoculated with Tc-D neither developed acute nor chronic disease. Group 4 consisted of 4 dogs and served as noninoculated controls. In group 1, the gross lesions were diffusely pale myocardiums with right ventricular enlargement, hepatomegaly, and a moderate amount of modified transudate in the abdominal cavity. Severe diffuse granulomatous myocarditis with large numbers of pseudocysts and minimal fibrosis characterized the tissues from all cardiac chambers and septum. The lesions were most severe in the right atrium and ventricle. Mild multifocal myositis and pseudocysts were observed in skeletal muscles and smooth muscles of the urinary bladder and small intestine. Multifocal encephalitis and pseudocysts were in the cerebral cortex, cerebellum, and brain stem. In group 2, the gross lesions were biventricular enlargement and thinning of the ventricular free walls. The right ventricle contained the most severe microscopic changes. There were mild multifocal interstitial lymphohistiocytic cellular infiltrates, perivasculitis, and marked fibrosis in all areas of the myocardium. Mild myositis and multifocal encephalitis were seen in the skeletal muscles and brains. Pseudocysts were not observed in any tissues. In group 3, there was mild biventricular dilatation, minimal inflammation with fibrosis in cardiac tissues, and a multifocal myositis in most skeletal muscles. Multifocal encephalitis was seen in the brain stem. Pseudocysts were not observed in any tissues. Lesions were not found in group 4. Our results indicated heterogeneity between North American T cruzi isolates in lesion development in dogs, and there appeared to be a temporal relationship between acute and chronic trypanosomiasis in Tc-O- and Tc-A-inoculated dogs and the 3 phases of Chagas disease in human beings.

An in vitro bioassay system was used to study the effects of cyclopiazonic acid (CPA) mycotoxin on cardiac muscle. Acute exposure to 6 microgram of CPA/ml of modified Krebs-Henseleit solution significantly (P < 0.05) decreased 5 in vitro turkey cardiac muscle performance criteria: maximal weight a muscle could lift; maximal contraction velocity; relaxation velocity; time to peak contraction; and total time for muscle contraction and relaxation. The effect on these 5 criteria appeared to result from intracellular changes partially associated with calcium availability and were irreversible, suggesting that physiologic changes had developed after acute exposure to CPA.

To differentiate the origin of high total lactate dehydrogenase (LD) activity in canine sera, a spectrophotometric method based on the preferential inhibition of cardiac LD isoenzymes by pyruvate was performed. Comparison with the electrophoretic separation of LD isoenzyme activities and determination of the hydroxybutyrate dehydrogenase-to-LD ratio indicated that the method proposed gave a better discrimination between cardiac and hepatic LD activities than did the other tests.

The Langendorff isolated heart preparation was adapted to determine the effect of furazolidone (0.5 and 2 migrogram/ml of perfusate) on hearts of 3-week-old broiler chickens. Following 115 minutes of perfusion, both concentrations of furazolidone caused approximately a two-fold increase in myocardial vascular resistance and a six-fold increase in myocardial vascular resistance and a six-fold increase in lactate dehydrogenase release into the effluent fluid, compared with a control perfused group of isolated hearts (P less than 0.01). Ultrastructural alteration differences were not found between the drug-treated and control groups. It was concluded that: (i) furazolidone, at concentrations only moderately above therapeutic plasma concentrations, caused detrimental changes in myocardial vascular resistance and lactate dehydrogenase release and (ii) the isolated chicken heart preparation is an example of a cost-effective, reliable laboratory tool for screening potential cardiotoxins.

Sarcocystis cruzi, newborn calves (exper.), correlation of development of Sarcocystis with the resulting lesions