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Biomedical subjects

J D Folts

Publications and source records attributed to J D Folts.

At least 73 records · Page 4Linked to original sources
PubMed1981

Myocardial revascularization of the canine circumflex coronary artery using retrograde internal mammary artery flow without cardiopulmonary bypass.

A new surgical technique using perfusion of the circumflex coronary artery with retrograde blood flow of the internal mammary artery (IMA) is described. This project was undertaken because the IMA is uniquely well supplied with blood: proximally through is attachment to the subclavian artery, along the sternum by the intercostal arteries to the aorta, and distally from the iliac artery by the epigastric and musculophrenic arteries. In this experimental study, the IMA in 16 dogs was ligated and divided at the subclavian artery, then dissected free down along the sternum to obtain sufficient length. The large subclavian end was then anastomosed to the circumflex coronary artery using a metal cannula technique to perfuse the circumflex bed while the anastomosis was being done. In all 16 dogs, the retrograde flow of the IMA was adequate to maintain the circumflex bed. It is postulated that this technique may have some limited use in man.

Animals↗
PubMed1980

The effect of exercise on the granulocyte response to isoproterenol in the trained athlete and unconditioned individual.

Many factors will influence the tissue response to catecholamine stimulation. Isolated human granulocytes (PMNs) release the lysosomal enzyme beta-glucuronidase following incubation with complement-activated zymosan particles. Isoproterenol, histamine, and prostaglandin E1 (PGE1) inhibit this PMN release of beta-glucuronidase. The effect of exercise on this in vitro granulocyte response was studied in two groups: highly conditioned marathon runners (n = 6) and unconditioned subjects (n = 7). A 13-km run did not produce leukocytosis in the highly conditioned marathon runners and the granulocyte response to isoproterenol was unchanged in cells obtained immediately following the run. In contrast, the seven unconditioned subjects exercised to a maximal response on the treadmill. Following exercise there was an increase in plasma catecholamines, a significant leukocytosis, and granulocytes from the immediate postexercise period responded less well to isoproterenol.

Adult↗
PubMed1979

Phasic changes in human right coronary blood flow before and after repair of aortic insufficiency.

We have shown previously that acute aortic insufficiency in chronically instrumented dogs reverses the normally high ratio of diastolic to systolic coronary blood flow. Phasic blood flow in the dominant right coronary artery was measured directly with an electromagnetic flow meter during surgery in eight patients with severe aortic insufficiency before and after relacement of the aortic valve. Before the insufficiency was eliminated, right coronary flow average 116 +/- 37 ml./minute and the diastolic to systolic flow ratio was 0.88 +/- 17. Mean arterial blood pressure averaged 106 +/- 17 mm. Hg, heart rate 84 +/- 19 beats/minute, and mean diastolic pressure averaged 67 +/- 10 mm. Hg. After the aortic valve was replaced with an average heart rate of 90 +/- 15 and mean blood pressure of 103 +/- 13 mm. Hg, the average right coronary blood flow increased to 180 +/- 40 ml./minute with a D/S ratio of 2.18 +/- 0.8. In all cases the right coronary blood flow increased after the aortic insufficiency was eliminated surgically. Right coronary flow probably increased because of the improved diastolic perfusion pressure and the change from predominantly systolic to diastolic coronary flow.

Aortic Valve Insufficiency↗
PubMed1977

Non-polarographic blood gas analysis. II. In vivo evaluation of gas chromatograph system.

Evaluation of a new system, based on gas chromatography, providing arterial blood gas tensions without requiring drawn blood samples is continued in an animal model. A series of in vivo dog experiments is discussed evaluating flow dependence and other performance characteristics. Results confirm the laboratory bench performance reported earlier; clinical trials are now indicated.

Animals↗
PubMed1977

Hemodynamic effects of controlled degrees of coronary artery stenosis in short-term and long-term studies in dogs.

Coronary and aortic blood flow, aortic and distal coronary blood pressure were measured with electromagnetic flowmeters and pressure gauges in 15 anesthetized dogs with the chest left open. Increasing degrees of known, fixed, partial coronary artery obstruction were applied with concentric plastic cylinders 3 mm. in length and with varying internal diameters. Because these plastic cylinders are radiolucent and can also be permanently implanted, postoperative arteriograms were taken to evaluate the degree of stenosis produced. At necropsy the degree of obstruction was checked by ligating and removing the narrowed vessel and examining a histologic section of a stenosed portion. The reactive hyperemic response to a 20 second complete occlusion was recorded with amounts of obstruction varying from 10 to 90 per cent. The reactive hyperemia began to decrease with an average of 36 +/- 10 per cent stenosis. A pressure gradient of 10 mm. Hg across the obstruction occurred with an average of 57 +/- 8 per cent stenosis. The reactive hyperemic response was abolished with an average of 75 +/- 6 per cent stenosis, and with greater degrees of stenosis the total flow began to decrease below control levels. The phasic coronary flow pattern was also altered with increasing amounts of fixed partial obstruction. As the per cent of stenosis was increased, the ratio of diastolic to systolic coronary flow decreased. When reactive hyperemia was abolished, very little diastolic-to-systolic variation remained.

Animals↗
PubMed1976

Platelet aggregation in partially obstructed vessels and its elimination with aspirin.

In 35 open chest anesthetized dogs coronary and aortic blood flow were measured with electromagnetic flowmeters while aortic and distal coronary blood pressure and an epicardial ECG were recorded. A fixed amount of stenosis (60-80%) was produced in the coronary artery by an externally applied plastic cylinder. In 24 of the 35 dogs the coronary blood flow showed cyclical reductions to near zero, with a sudden spontaneous return to near control levels. During reduced flow the epicardial ECG showed ST-segment depression suggestive of ischemia, and ventricular premature beats were often noted. Six animals died acutely during episodes of reduced flow. After 35 mg/kg of aspirin were given intravenously the cyclical reductions in coronary blood flow were abolished and the in vitro platelet aggregations were reduced from a control of 62.1 +/- 15 units (Born technique) to an average of 23.7 +/- 12 units. Histologic sections of the narrowed coronary artery obtained when coronary flow was reduced show an amorphous mass in the lumen which was thought to be a platelet aggregate. Perhaps a similar process of platelet aggregation occurs in the stenosed coronary arteries in man, producing acute coronary obstruction, ischemia, and sudden death.

Animals↗
PubMed1976

Ultrastructural and physiological changes induced by atractylate in the canine myocardium.

The myocardial cellular response to the cardiac glycoside atractylate, a known inhibitor of mitochondrial adenine nucleotide translocation, was examined physiologically, morphologically, and morphometrically in eight dogs. An isolated in situ segment of left ventricular tissue was employed in these experiments to eliminate collateral flow and the potential for large sampling error. It was found that atractylate infusion rapidly induced physiological and morphological changes suggestive of a loss of membrane regulation of ion flux in the arteriole, capillary endothelium, and myocardial cell. Also mitochondrial changes suggestive of adenine nucleotide translocase inhibition were observed. As these responses are similar to those induced by acute myocardial ischaemia, it is suggested that ischaemia and atractylate induce cell injury by similar mechanisms.

Animals↗
PubMed1976

Control of energy production in myocardial ischemia.

Long chain fatty acyl-CoA esters are potent in vitro and in vivo inhibitors of adenine nucleotide translocation in heart mitochondria. Within a short time following production of myocardial ischemia, the dog heart exhibits an increased concentration of long chain acyl-CoA esters associated with a decrease in adenine nucleotide translocase activity. In contrast to liver, the tricarboxylate carrier system for citrate and phosphoenolpyruvate is rather low in heart mitochondria. Phosphoenolpyruvate-stimulated calcium egress from heart mitochondria may, therefore, result from transport of this anion on the adenine nucleotide translocase. During myocardial ischemia effective modulation of these metabolite trasnport systems are disrupted by accumulation of long chain acyl-CoA esters which leads to a decrease in the overall energy charge of the cell.

Animals↗
PubMed1976

Prostaglandin-like substances in coronary venous blood following myocardial ischemia.

Twelve anesthetized open chest dogs received an intracoronary infusion of 20 muCi of 3H-arachidonic acid through the left anterior descending coronary artery. A control blood sample was then taken from the great cardiac vein. The left anterior descending coronary artery was occluded for 10 minutes and then released. A second cardiac vein blood sample was obtained during the coronary reactive hyperemic response. The pre-and postocclusion blood samples were analyzed for prostaglandin (PG)-like substances using thin-layer chromatography and analysis for radioactivity. There was an increase in PGE2- and PGA2-like substances, and arachidonic acid found in the postocclusion samples. PGE2 appears to be the predominant prostaglandin formed. Three animals received 10 mg/kg of indomethacin intravenously 1 hour before the 3H-arachidonic acid infusion. Pretreatment with indomethacin abolished the release of PGE2 and PGA2-like substances but no arachidonic acid and reduced the reactive hyperemic response in magnitude and duration. Reactive hyperemia after a 10-minute occlusion was studied in five dogs before and 1 hour after the intravenous administration of 10 mg/kg of indomethacin. The control coronary flow and peak reactive hyperemic response were significantly reduced by the indomethacin. These studies suggest that myocardial ischemia promotes the synthesis and release of PG-like substances which may play a role in reactive hyperemia.

Animals↗
PubMed1975

The role of beta-adrenergic activity in the production of cardiac and aortic arch anomalies in chick embryos.

The sympathomimetic amines isoproterenol, epinephrine, norepinephrine, and phenylephrine are structural derivatives of beta-phenylethylamine and have proportionately different effects on alpha- and beta-adrenergic receptors. Chick embryos in ovo were each administered a single dose of one of these compounds at concentrations ranging from 0.4 times 10(-9) to 20 times 10(-9) mol/5 mul saline during Hamburger and Hamilton stages 20-27. In other experiments embryos were pretreated with the beta-antagonist propranolol and subsequently administered isoproterenol. 743 cardiovascular anomalies were produced. The production of cardiovascular anomalies was proportional to the degree of beta-adrenergic activity of each drug. The frequency of anomalies was significantly reduced by pretreatment with propranolol. At all concentrations tested the anomaly rate was greater in chick embryos receiving an experimental compound than in controls. The general types of anomalies included aortic arch defects, ventricular septal defect, double outlet right ventricle, aortic hypoplasia, and truncus arteriosus. These results demonstrate that activation of the beta-adrenergic receptor mechanism is directly related to the cardiovascular anomalies produced in the chick embryos.

Abnormalities, Drug-Induced↗
PubMed1975

Systemic and coronary haemodynamic effects of ketamine in intact anaesthetized and unanaesthetized dogs.

Ten intact anaesthetized dogs breathing room air spontaneously (Group A) were compared with ten artificially ventilated dogs (Group B). All were given a bolus of ketamine 2 mg/kg followed by a 20-min infusion of ketamine 0.1 mg/kg/min. In Group A, coronary sinus blood flow, measured with a thermodilution flowmeter, increased by 90% while coronary vascular resistance decreased by 28% and coronary sinus oxygen content decreased by 27%. Heart rate increased by 47%, and arterial pressure by 9%. Cardiac output, calculated by the dye dilution method, increased by 29%, while the left ventricular work index decreased by 50%. Minute ventilation rate decreased by 55%. The Group B dogs were studied as described above, except that they were artificially ventilated. The haemodynamic ahanges were less in Group B, possibly because of improved arterial oxygenation. Heart rate increased by 24%, cardiac output by 21% and arterial pressure by 2%. The coronary sinus blood flow increased by 12% while coronary vascular resistance decreased by 11%. Coronary sinus oxygen concentration decreased by 15%. Five unanaesthetized dogs with electromagnetic flowmeter probes chronically implanted on the aorta and circumflex coronary artery, and an indwelling arterial catheter were studied before, during and after the intravenous administration of ketamine 2, 4, and 8 mg/kg. A dose of 8 mg/kg produced increases in cardiac output, heart rate and arterial pressure of 21%, 44% and 24%, respectively, while coronary blood flow increased 47%. We conclude that, in healthy dogs, ketamine produces an increase in heart rate and cardiac work. A significant increase in coronary blood flow appears to be insufficient to meet the metabolic demands of the myocardium, as the coronary sinus oxygen content decreased.

Anesthesia, General↗
PubMed1975

Acyl-CoA inhibition of adenine nucleotide translocation in ischemic myocardium.

The translocation of adenine nucleotides across the inner mitochondrial membrane and the tissue concentration of long-chain acyl-CoA esters were studied in dog heart after experimental myocardial ischemia. Ligation of the anterior coronary artery initiated events leading to an early decrease in adenine nucleotide translocase activity. A reciprocal increase in the concentration of heart tissue long-chain acyl-CoA esters was also observed. Adjacent nonischemic tissue showed changes intermediate between that of ischemic and normal heart tissue. It is postulated that a decrease in fatty acid oxidation after myocardial ischemia would lead to an accumulation of long-chain acyl-CoA esters, which in turn would inhibit adenine nucleotide translocation. The net result would be a lowering of the energy charge of the cell, adversely affecting muscle contraction and electrical conduction.

Acetyl Coenzyme A↗