Biomedical subjects
Publications and source records attributed to G E Eyster.
In summary, ASD and VSD sometimes do not require surgical intervention and have a good-to-excellent prognosis in animal patients in which surgical intervention is necessary. Animal patients with these diseases often do not show symptoms, but those that do and cannot be adequately managed medically are challenging but rewarding cardiac surgical cases.
UNLABELLED: The purpose of this study was to measure myocardial buffering capacity and adenosine triphosphate utilization rates in the newborn animal in vivo during hypothermic circulatory arrest and recovery. METHODS: These studies were performed with 31P magnetic resonance spectroscopic techniques, which supplied a 12- to 16-second time resolution, to monitor intracellular pH and phosphocreatine and adenosine triphosphate levels. All experiments were performed with a radiofrequency surface coil on the pericardium with the sheep centered inside a 4.7 T magnet. Newborn sheep (n = 5, aged 16 days +/- 2.4 standard error) were supported by cardiopulmonary bypass, cooled to 20 degrees C, and subjected to 20 minutes of circulatory arrest. RESULTS: During early ischemia, phosphocreatine hydrolysis progressed at a linear rate, 1.2 +/- 0.05 mumol/gm per minute, and was accompanied by intracellular alkalinization. Myocardial buffering capacity calculated from delta pH/delta phosphocreatine equals 25 +/- 3 mueq gm-1 delta pH-1, a value similar to that obtained from perfused heart studies. After the initial 4 minutes in ischemia, the decrease in phosphocreatine hydrolysis was accompanied by intracellular acidification, which is likely due to late induction of anaerobic metabolism. CONCLUSIONS: In these studies, early phosphocreatine hydrolysis rate is nearly equivalent to adenosine triphosphate utilization rate. During the early period of ischemia phosphocreatine hydrolysis serves a buffering function and is associated with intracellular alkalinization. These techniques and measurements can be used to compare effects of myocardial preservation techniques on intracellular pH and adenosine triphosphate kinetics.
A method for measuring the surface area of canine articular cartilage was developed. Ten pairs of humeri were harvested from fresh canine cadavers. The articular cartilage of each humeral head was covered with liquid rubber latex applied with a brush to the margins of the articular surface. The latex cast was removed from the cartilage after the latex dried. Radial cuts were made in the cast so it could be flattened into a 2-dimensional plane. The surface area of each cast was then measured, using a compensating polar planimeter.
The relationship between mixed venous O2 tension and cardiac output was studied in six anesthetized horses breathing 100% O2. Cardiac output, O2 consumption, mean arterial pressure, heart rate, and arterial and venous blood gases were measured after administration of xylazine or dobutamine to horses in lateral, sternal, and dorsal recumbencies. After approximately 3 hours, Escherichia coli endotoxin was administered while horses were in dorsal recumbency, and all measurements were repeated. Relationships between cardiac index (CI) and PVO2, heart rate, mean arterial pressure, jugular PVO2, and PVO2 of blood from a superficial limb vein were evaluated by linear regression analysis. Mean arterial pressure was significantly (P less than 0.05) correlated with CI in horses in all positions and after endotoxin administration. However, data points were poorly grouped. Heart rate and CI were significantly correlated in horses in all positions, but not after endotoxin administration. Correlations between jugular PVO2 and PVO2 of blood from a superficial limb vein were not significant in horses in sternal recumbency, and PVO2 of blood from a superficial limb vein was not significantly correlated with CI in horses in lateral recumbency. There was a significant and tight correlation between PVO2 and CI in horses in all positions and after endotoxin administration.
An investigation was initiated to determine the dosage of streptokinase (given IV) that would consistently produce systemic fibrinolysis, as determined by laboratory evaluation, and to determine the relative safety of this drug in the cat. Results indicated that a loading dose of 90,000 IU of streptokinase (given by continuous infusion over 20 to 30 minutes) and a maintenance dosage (IV) of 45,000 IU of streptokinase/hr predictably produced systemic fibrinolysis in the cat. There were no detectable adverse affects seen on physical examination, necropsy, or histopathologic examination. Using the foregoing dosage regimen, investigation was begun to evaluate the use of streptokinase for treatment of feline thromboembolism. Aortic thrombosis was created experimentally in 15 cats. There was no clearly predictable improvement in nonspecific venous angiograms or thermal circulatory indices for the cats given streptokinase, compared with the values for the control cats. After a total of 180 minutes of treatment, the mean weight of remaining clot removed at necropsy from the aortic trifurcation was 7.3 mg in the streptokinase-treated cats, compared with 13.4 mg in the control cats.
Digoxin administration (0.22 mg/m2 of body surface BID) to 10 large-breed dogs with congestive cardiomyopathy increased shortening fraction more than 5.5% in 4 of the dogs. This group of dogs lived longer than the group that did not have a positive inotropic response to digoxin. Heart rate decreased in both groups of dogs. Base-line jugular PVO2 were low in all dogs. Jugular PVO2 decreased significantly in the group that did not respond to digoxin, presumably because of decreased cardiac output. Jugular PVO2 consistently increased in dogs that had a positive inotropic response to digoxin. Base-line shortening fraction, heart rate, and PVO2 did not predict which dogs would respond to digoxin. Serum digoxin concentrations were consistently between 1.5 and 2.5 ng/ml. It was concluded that digoxin administration is not efficacious in all dogs with congestive cardiomyopathy and that the positive inotropic response is not predicted by base-line shortening fraction, heart rate, or jugular PVO2. Dogs that do respond to digoxin usually live longer than those that do not. Jugular PVO2 can be used to separate dogs that do respond from dogs that do not respond to digoxin as long as the base-line PVO2 is low. The negative chronotropic effects of digoxin may be detrimental to dogs that do not have a positive inotropic effect from digoxin.
Cell damage initiated during ischemia matures during reperfusion. Mechanisms involved during reperfusion include the effects of arachidonic acid and its oxidative products prostaglandins and leukotrienes, reperfusion tissue calcium overloading, and damage to membranes by lipid peroxidation. Lipid peroxidation occurs by oxygen radical mechanisms that require a metal with more than one ionic state (transitional metal) for catalysis. We have shown that cellular iron is delocalized from the large molecules where it is normally stored to smaller chemical species during postischemic reperfusion. Postischemic lipid peroxidation is inhibited by the iron chelator deferoxamine. Intervention in the reperfusion injury of membranes by chelation of transitional metals is a new and promising therapeutic possibility for protection of the heart and brain.
Systolic myocardial function was assessed in 16 dogs with severe congestive heart failure due to chronic mitral valve fibrosis. End-systolic diameters were measured on echocardiograms and end-systolic volume indices were calculated. Thirteen of the 16 dogs (81%) had normal or only mildly abnormal myocardial function. These data suggested that myocardial failure is not a prominent factor contributing to signs of heart failure in dogs with mitral regurgitation. Because of these data, the routine use of digitalis glycosides to increase cardiac contractility is seriously questioned in dogs with heart failure secondary to chronic mitral regurgitation.
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In 2 dogs (3 and 8 months old), double-chambered right ventricle was diagnosed by selective angiocardiography. In 1 dog, the systolic pressure in the outflow tract portion of the right ventricle and in the main pulmonary artery was 13 mm of Hg, whereas the systolic pressure in the right ventricle proximal to a constricting muscular ring was 80 mm of Hg. The absence of a valvular pressure gradient and the appearance of normal valves at surgery indicated that the right ventricular outflow obstruction was a congenital lesion. The 67-mm of Hg pressure gradient suggested the need for resection of the obstruction. The defect was corrected surgically and the dog was clinically normal when examined 1 1/2 years later. The 2nd dog was not considered for corrective surgery because of a clinically insignificant gradient in the right ventricular outflow tract. When the dog was examined at 11 months of age, the cardiac silhouette was bilaterally enlarged. However, inasmuch as the dog had not experienced any exercise intolerance or weakness and the electrocardiogram was normal, further diagnostic and therapeutic work was not done. When the dog was examined at 20 months of age, it appeared healthy.
A 3-month-old English Bulldog was found to have a discontinuity between the ascending and descending aorta. There were no signs of illness associated with the interruption. The descending aorta was supplied with blood by collateral circulation. An aortic graft of woven synthetic material was surgically implanted to connect the ascending and descending aorta. Without any restrictions on the dog's activity, the dog has lived for over 1 year and continues to do well.
Congenital supravalvular pulmonic stenosis was diagnosed in a dog. A pulmonary artery-to-pulmonary artery anastomosis of a Dacron arterial conduit restored continuity of blood flow around the obstruction in the main pulmonary artery. By the 6th day after surgery, right ventricular systolic pressure averaged 85 mm of Hg, a decrease of 90 mm from the preoperative value. Angiocardiography confirmed the patency of the conduit. At examination 6 months after surgery, the dog was clinically normal.
Two foals with a history of normalcy at birth developed a lack of exercise tolerance and weakness in the first few days of life. Weakness, inability to rise, and reluctance to suckle were common complaints. Physical examination of both foals revealed a cardiovascular abnormality, with a loud systolic murmur audible over both thoracic walls. Additional diagnostic techniques were blood gas analysis, radiography, cardiovascular catheterization, and necropsy. Necropsy findings were ventricular septal defect, atrial septal defect, patent ductus arteriosus, and congenital absence of the aortic arch. Additionally, 1 foal had anomalous drainage of the cranial vena cava into the left atrium.
Three young unrelated dogs were diagnosed as having the canine counterpart of Ebstein's anomaly, an eponymic term for a cardiac malformation in man. All of the dogs had systolic murmurs in the tricuspid area, and all had radiographic evidence of cardiac enlargement, particularly of the right atrium. Electrocardiography indicated atrial disease or right atrial enlargement and right ventricular conduction defects. The defect was confirmed by means of cardiac catheterization in all 3 dogs. Open heart surgery was performed on 2 of the dogs--plastic reconstruction of the tricuspid annulus and placement of a prosthetic valve in 1 and closure of an atrial septal defect in the other; both of these dogs died (1 day and 1 month after surgery).
Four Collie littermates had multiple cardiac and diaphragmatic anomalies. Ventricular septal defect was found in 3, pulmonic stenosis in 2, atrial septal defect in 1, mitral regurgitaion in 1, and pericardial diaphragmatic hernia in 3. Five additional littermates died within 72 hours of birth but were not necropsied. On the basis of available evidence, it was believed that the defects were congenital but not hereditary.
Five dogs and 1 cat had pulmonary artery banding for ventricular septal defect and congestive heart failure. An umbilical tape band constricted the pulmonary artery to one-third its original diameter, increased the right ventricular pressure, and decreased the left ot right shunt. Five animals had remission of clinical signs; 1 dog died of right ventricular failure due to a band that had been applied too tightly. The results indicated pulmonary artery banding is helpful in reduction of clinical signs, due to increased flow to the lungs from ventricular septal defect.
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