Myocardial buffering capacity and high-energy phosphate utilization during hypothermic circulatory arrest and recovery in the newborn lamb in vivo.

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.

Cardiopulmonary effects of fentanyl-droperidol, nitrous oxide, and atropine sulfate in dogs.

The cardiopulmonary effects of droperidol-fentanyl, nitrous oxide, and atropine were evaluated in 12 adult male Beagle dogs. All dogs were surgically instrumented with a cardiac output thermistor and arterial and venous catheters and were prepared with a chronic tracheostomy. Each dog was used as its own control, and data obtained when dogs were nonanesthetized and nonmedicated were compared with data recorded after the test drugs were administered. The dogs were randomly allotted to 3 groups of 4 dogs each. Group I dogs were given droperidol-fentanyl alone intravenously (IV); group II dogs were given droperidol-fentanyl IV with 67% nitrous oxide; and group III dogs were given atropine sulfate intramuscularly followed by droperidol-fentanyl IV with 67% nitrous oxide. Minute volume was decreased in the 3 groups of dogs for 3 to 5 minutes after droperidol-fentanyl was injected. This resulted in respiratory and metabolic acidosis in all dogs, as indicated by increased arterial carbon dioxide tension, decreased pH, and increased base deficit. In addition, droperidol-fentanyl given alone caused a decrease in systolic pressure and a slight decrease in heart rate. Group 1 dogs were sensitive to auditory stimulation. Cardiovascular changes were not seen when nitrous oxide was added; however, analgesia and muscle relaxation were improved. Premedication with atropine sulfate resulted in increased cardiac output, heart rate, and diastolic pressure, and subsequent administration of droperidol-fentanyl with nitrous oxide caused a transient increase in mean arterial and systolic pressure. This last anesthetic regimen, along with assisted or controlled respiration, seems to provide an excellent anesthetic state with minimal cardiopulmonary depression.

Technique for measuring the area of canine articular surfaces.

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.

Mixed venous oxygen tension as an estimate of cardiac output in anesthetized horses.

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.

Streptokinase treatment of cats with experimentally induced aortic thrombosis.

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.

Cardiovascular effects of gallamine triethiodide and succinylcholine chloride during halothane anesthesia in the dog.

The cardiovascular effects of gallamine triethiodide and succinylcholine chloride were studied in Beagle dogs during controlled halothane anesthesia. Small but significant increases in heart rate and mean arterial presssure were observed 1 minute after intravenous injection of succinylcholine chloride. Intravenous injection of gallamine triethiodide did not produce significant cardiovascular changes.

Effect of dobutamine in postperfusion cardiac failure in the dog.

The effect of dobutamine on cardiac function of dogs was investigated. Sixteen dogs were submitted to cardiopulmonary bypass. The aorta of each dog was cross-clamped for 1 hour; attempt was not made to perfuse the heart. After 1 hour, 8 of the 16 dogs were randomly selected and treated with dobutamine (5 mug/kg/min). The other 8 dogs were designated the control group and were given placebo. Postperfusion failure and death were used as end point criteria. Dogs given dobutamine responded remarkably well, with significantly decreased postperfusion low output syndrome. Evidence of cardiac function 5 minutes after the removal of the bypass was the criterion used to determine survival of the surgical cross-clamp procedure; however, this did not necessarily indicate survival of the dog. Of the 8 dogs given dobutamine, 6 (75%) survived the surgical cross-clamp, whereas of the 8 dogs not given dobutamine, 3 (37.5%) survived the surgical procedure. Seemingly, the effect of dobutamine is not mainly chronotropic, but is rather a direct aid to myocardial strength.

Double-chambered right ventricle in two dogs.

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.

Aortic regurgitation in the dog.

In a review of aortic regurgitation in 12 dogs, breed or sex predilection was not found. Clinical signs included decreased exercise tolerance and diastolic murmur. Associated anomalies included ventricular septal defect and aortic stenosis. It was concluded that when aortic regurgitation develops secondary to a ventricular septal defect, the prognosis should be grave.

Patent ductus arteriosus in the dog: characteristics of occurrence and results of surgery in one hundred consecutive cases.

The results of surgical repair of patent ductus arteriosus (100 dogs) were compared with the results of nonsurgical treatment of this defect (14 dogs). The death rate for dogs surgically treated was 8%, with 2 deaths at surgery and 6 late postoperative deaths. In the nonsurgical group, 64% died within one year of the examination. The increased survival rate for the surgically treated group was significant ( P less than 0.001). Surgical death rate was high for dogs more than 2 years old and weighing more than 23 kg. It was concluded that surgery is the preferred method of treatment and that early surgery increases the survival rate of dogs with patent ductus arteriosus, compared with the survival rate for older, heavier dogs with the defect.

Use of an extracardiac conduit in the repair of supravalvular pulmonic stenosis in a dog.

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.

Interruption of aortic arch in two foals.

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.

Aorticopulmonary septal defect in a dog.

A 2-year-old Brittany Spaniel ahd clinical signs of pulmonary diseases and pulmonary hypertension, with cardiac murmur and congestive heart failure. Aorticopulmonary septal defect was detected by means of cardiac catheterization. Attempted surgical correciton was unsuccessful.

Aortic interruption in a dog.

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.

Efficacy of digoxin administration in dogs with idiopathic congestive cardiomyopathy.

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.

Pulmonary artery banding for ventricular septal defect in dogs and cats.

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.

Comparison of plasma aldosterone concentration among clinical status groups of dogs with chronic heart failure.

The plasma aldosterone concentration (PAC) among clinical status groups of 23 dogs with chronic heart failure was compared at various times after diagnosis of the problem. Eighteen dogs admitted in New York Heart Association (NYHA) class IV clinical status had significant elevations in PAC (P<0.0001), when compared with clinically normal dogs. Five dogs admitted in NYHA class III status and 4 dogs that responded with a change to NYHA class III status had significant elevations in PAC (P<0.01), when compared with clinically normal dogs. In patients with NYHA class IV status, the PAC was significantly greater (P<0.01) than in patients in NYHA class III status. For patients with the poorest prognosis, ie, severe signs of NYHA class IV status, the PAC was not markedly different, when compared with that for patients with a favorable prognosis, ie, recent onset of signs of NYHA class IV status. Patients treated with captopril had significantly lower PAC after therapy (P<0.01), whereas patients treated with hydralazine had significantly higher PAC (P<0.05) after therapy. It was concluded that heart failure in the dog increases PAC, most likely because of renin-angiotensin-aldosterone-system activation, and that the increase is related directly to the clinical status of the patient. Further, it was concluded that treatment of dogs in heart failure with captopril causes a decrease in circulating PAC, whereas treatment with hydralazine causes an increase in circulating PAC.

Myocardial function in small dogs with chronic mitral regurgitation and severe congestive heart failure.

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.

Congenital pericardial diaphragmitic hernia and multiple cardiac defects in a litter of collies.

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.

Mitral valve prosthesis for correction of mitral regurgitation in a dog.

Mitral regurgiation with atrial fibrillation in a 3-year-old St. Bernard dog was corrected by digitalization, placement of a mitral valve prosthesis, and direct current cardioversion. The atrial fibrillation eventually returned and became refractory to cardioversion.