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Biomedical subjects

J D Folts

Publications and source records attributed to J D Folts.

90 records · Page 5Linked to original sources
PubMed1975

Effects of partial obstruction on phasic flow in aortocoronary grafts.

Phasic blood flow recorded in five unobstructed dog aortocoronary bypass grafts to the left coronary artery was similar to that of normal coronary arteries, with a high diastolic-to-systolic flow ratio which averaged 2.7 +/- 0.4. With an average of 52 +/- 7% and 72 +/- 6% stenosis in the coronary artery distal to the graft, the phasic graft-flow pattern was altered, with a decrease in the diastolic-to-systolic flow ratio to 1.9 +/- 0.4 and 1.2 +/- 0.4, respectively. Phasic patterns recorded in 42 human saphenous vein grafts to branches of the left coronary artery subsequently shown to be patent by postoperative coronary arteriography were similar to those of a normal coronary artery, with an average diastolic-to-systolic flow ratio of 2.3 +/- 0.83 and an average flow of 76 +/- 48 ml/min. Phasic flow measured in 20 grafts shown to be occulded at restudy had an average diastolic-to-systolic flow of 1.3 +/- 0.45, with an average flow of 72 +/- 33 ml/min and a phasic graft flow which was similar to that obtained from partially obstructed coronary arteries. We conclude that partial obstruction of the graft or the distal coronary artery alters the flow pattern, and this partial obstruction may lead to closure of the graft.

Animals↗
PubMed1975

Role of adenine nucleotide translocase in metabolic change caused by ischemia.

Inhibition of adenine nucleotide translocase by elevated levels of long chain acyl-CoA esters has been shown to occur during the onset of ischemia in experiments conducted on dogs. Other findings indicate that, as a consequence of translocase inhibition, the production of mitochondrial creatine phosphate was abolished and, in this manner, respiration was slowed to state 4 or an ischemic-like condition. A variety of biochemical, hemodynamic, and ultrastructural evidence further suggest that this inhibition of adenine nucleotide transport in and out of the heart mitochondria may be the initial and key disturbance which "triggers" the more drastic metabolic changes known to occur as the degree of ischemia becomes more severe. The mitochondrial "damage" caused by long chain acyl-CoA ester inhibition of adenine nucleotide translocase appears to be reversible by carnitine.

Adenosine Diphosphate↗
PubMed1975

Inhibited adenine nucleotide translocation in mitochondria isolated from ishcemic myocardium.

Experiments conducted in healthy mongrel dogs indicate that acyl-CoA levels are raised and adenine nucleotide translocase is inhibited during ischemia. The biochemical findings are accompanied by ultrastructural evidence of myocardial cell damage. These results raise the possibility that the inhibition of adenine nucleotide translocase may be a key disturbance in cellular metabolism.

Animals↗
PubMedDate not supplied

Systemic and coronary hemodynamic effects of Abbott (40557) and its interaction with aminophylline.

Adenosine is a naturally occurring substance with potent coronary vasodilator action. However, its action is of short duration due to its rapid inactivation in blood and other tissues (1). If used for therapeutic purposes a prolonged duration of action might be desirable. A recent adenosine derivative (Abbott 40557) ethyl-adenosine-5'-carboxylate hydrochloride1) has marked and prolonged coronary vasodilator activity (2,3). The present report concerns the coronary and systemic hemodynamic and metabolic effects of A 40557 and attempts to determine whether, like adenosine, its action is enhanced by dipyridamole (4,5), hexobendine (6), and Cassella 7657 (7) or inhibited by aminophylline (8,9).

Adenosine↗
PubMedDate not supplied

Coronary blood flow measurement using an angiographic first pass distribution technique: a feasibility study.

Due to the well-documented problems associated with visual interpretation of coronary angiograms, more physiologic means of assessing coronary artery stenosis are being investigated. One physiologic parameter that has been suggested is coronary flow reserve (CFR). A digital subtraction angiographic technique based on first pass distribution analysis (FPA) is proposed as a means of measuring CFR and absolute coronary flow. The theory of the FPA method is first outlined, and the implementation of a preliminary version of the FPA algorithm is described. Experiments verifying the utility of this algorithm for measuring absolute flow through a flow phantom, and through the canine circumflex artery are reported. It was determined that the preliminary FPA algorithm is capable of measuring canine coronary flow ratios (R) with accuracy and precision characteristics meeting or exceeding those reported for the parametric imaging technique (RFPA = 0.933.Rtrue, SEE = 0.16, r = 0.984). Accurate absolute flow (Q) measurements were obtained in all of the phantom experiments (QFPA = 1.054.Qtrue, r = 0.993), and in one of the three dogs that were studied (QFPA = 0.977.Qtrue, r = 0.935). The difficulty encountered in the other two dog experiments is attributed to the effects of system temporal lag, and would likely be corrected through the use of improved cameras. The feasibility of the general FPA method for measuring relative flow is established, and the potential for routine, absolute flow measurement is demonstrated.

Algorithms↗
PubMedDate not supplied

Ischemic-like change produced in canine heart by atractyloside: a chemical model.

Experiments were conducted in two canine models. Intracoronary infusion of atractyloside resulted in physiological, biochemical, and ultrastructural changes similar to those seen with ischemia. The fact that atractyloside, a specific inhibitor of adenine nucleotide translocase produces this change in vivo suggests that this inhibition in the key disturbance that initiates the metabolic derangements seen with ischemia. This chemical model seems to provide unique opportunities to study the possible factors that may reverse adenine nucleotide translocase inhibition and thus possibly prevent cell injury.

Animals↗