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Biomedical subjects

A S Wechsler

Publications and source records attributed to A S Wechsler.

At least 19 recordsLinked to original sources
PubMed1979

The effects of hypothermia on myocardial oxygen consumption and transmural coronary blood flow in the potassium-arrested heart.

Hypothermia remains the primary adjunct employed to lower cellular metabolism during various cardiac procedures. In these experiments, left ventricular myocardial oxygen consumption (MVO2) and transmural blood flow (TBF) were measured during cardiopulmonary bypass with the range of temperatures used clinically. Determinations were made in empty beating normothermic hearts and after potassium cardioplegia at 37, 32, 28, 22, 18, and 15 degrees (K+ = 15--37 meq/L: Hct 25 volumes %). Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer (vs Van Slyke, R = 0.98). Transmural blood flow was measured at each temperature using microspheres (8 microns), and perfusion was maintained at 80 mmHg. Asystole (37 degrees) alone decreased MVO2 from 5.18 +/- 0.55 to 1.85 +/- 0.20 ml O2/min/100 g of left ventricle or approximately 65% (p less than 0.001). With progressive cooling to 15 degrees an additional 82% decrement in oxygen uptake occurred during asystole (p less than 0.001). During asystole at 37 degrees the decrease in MVO2 was reflected mainly by a large decrement (p less than 0.01) in TBF (1.27 +/- 0.19 to 0.74 +/- 0.17 ml/min/g of mean left ventricular flow). However, with cooling below 32 degrees, the arteriovenous oxygen difference narrowed progressively (p less than 0.001) while TBF paradoxically returned to control levels. Endocardial/epicardial flow ratios were not altered by cooling. These data not only confirm earlier reports describing a sequential drop in MVO2 with incremental myocardial cooling, but also establish MVO2 levels for perfused hearts arrested by potassium at lower temperatures (18--15 degrees). Moreover, as transmural blood flow becomes independent of metabolic necessity during hypothermia, coronary autoregulation appears to be impaired, possibly affecting detrimental tissue over perfusion.

Animals↗
PubMed1979

Protection of mitochondrial function during ischemia by potassium cardioplegia: correlation with ischemic contracture.

The effect of potassium cardioplegia on mitochondrial function was evaluated in the ischemic isolated rat heart. Mitochondrial function as well as adenosine triphosphate (ATP) levels were determined at the initiation of ischemic contracture, at the completion of ischemic contracture, and 20 minutes following contracture completion. Group I received no cardioplegia prior to ischemia, while Group II received potassium cardioplegia prior to the onset of ischemia. The respiratory control index (RCI), which is the primary measure of the intactness of mitochondrial function, was calculated with both a NAD (nicotinamide adenine dinucleotide)-linked substrate and a FAD (flavin adenine dinucleotide)-linked substrate. Potassium cardioplegia significantly delayed ischemic contracture initiation and completion. Although the RCI and ATP levels decreased significantly at successive levels of contracture, there was no difference in the RCI or ATP content between Group I and Group II at contracture initiation or completion. Unlike previous investigations that have used a time-base to examine mitochondrial function and acute cardiac ischemic injury, we correlated mitochondrial function with the measurable physiologic event ischemic contracture. The data indicated that potassium cardioplegia preserved ATP content and mitochondrial function, and that contracture initiation and completion correlate well with specific ATP levels and mitochondrial respiratory control. The relationship between mitochondrial function and ATP content indicates that the beneficial effect of potassium cardioplegia on mitochondrial function may be secondary to the preservation of high-energy phosphate levels which provide energy for mitochondrial maintenance.

Adenosine Triphosphate↗
PubMed1979

Regional myocardial dimensions following coronary artery bypass grafting in patients. Relationship of functional deterioration to graft occlusion.

The direct relationship between graft flow and regional midwall myocardial function has not been documented in patients. Therefore, the present study was designed to quantitate the effects of coronary artery bypass grafting on regional myocardial mechanics distal to a coronary artery obstruction. Twenty-one patients with subtotal or total occlusion of the left anterior descending (LAD) coronary artery underwent coronary artery bypass grafting. Following completion of the aortic and coronary anastomoses, two miniature ultrasonic dimension transducers (2.5 mm. diameter) were positioned within the minor axis of the anterior left ventricular free wall and were allowed complete freedom of movement. The transducers were placed at midwall depth, and areas of clinically apparent myocardial fibrosis were not utilized as sites of implantation. During control, 30 minutes following the termination of cardiopulmonary bypass, regional myocardial dimensions, pulmonary artery diastolic pressure, arterial pressure, and heart rate were recorded with all saphenous vein grafts open and after 30 seconds of single vein graft occlusion. These measurements were repeated during atrial pacing at a rate of 128 +/- 4 beats per minute. Data are mean +/- the standard error of the mean. During control, graft occlusion resulted in a regional decrease in systolic excursion from 1.3 +/- 0.1 to 1.0 +/- 0.2 mm. (p less than 0.01), as well as a decrease in the rate of shortening from 8.7 +/- 0.2 to 6.2 +/- 1.1 mm. per second (p less than 0.05); heart rate, mean arterial pressure, and diastolic pulmonary artery pressure remained unchanged. Graft occlusion with atrial pacing resulted in an exaggerated decrease in both regional systolic excursion, from 1.2 +/- 0.2 to 0.6 +/- 0.2 mm. (p less than 0.01), and rate of shortening, from 9.4 +/- 1.5 to 4.4 +/- 0.2 mm. per second (p less than 0.01). For the group of patients studied, end-diastolic lengths were unchanged with graft occlusion during control and atrial pacing. Moreover, with graft occlusion, isolated patients demonstrated regional dyskinesia as evidenced by holosystolic bulging. These studies in patients have documented for the first time that, despite a constant preload, afterload, and heart rate, regional myocardial function following coronary artery bypass grafting is dependent upon adequate graft flow, especially during stress.

Cardiac Pacing, Artificial↗
PubMed1979

Effects of phenylephrine on transmural distribution of myocardial blood flow in regions supplied by normal and collateral arteries during cardiopulmonary bypass.

Cardiopulmonary bypass is frequently accompanied by decreased peripheral vascular resistance with resultant hypotension that is unresponsive to increased flow rates. Alpha adrenergic agonists are routinely used to increase peripheral vascular resistance and augment blood pressure. In this study, the effects of the alpha adrenergic stimulant phenylephrine on blood flow distribution during cardiopulmonary bypass in myocardium supplied by normal and collateral arteries were studied in eight mongrel dogs. Microsphere determinations of blood flow were made following augmentation of perfusion pressure with phenylephrine and were compared with intraoperative normotensive and hypotensive control levels. With systemic flow rates held constant, phenylephrine was infused in doses adequate to raise perfusion pressure to normotensive levels following hypotension. In the normal region (NR), blood flow was returned to normotensive control levels with flow favoring the subendocardium. In the region supplied by collateral vessels (CR), however, phenylephrine infusion failed to return flow to the normotensive control level in the subendocardial layer, and the flow imbalance present during hypotension was not corrected. An analogue model of the calculable resistances in the CR is presented, which indicates that phenylephrine increased resistance in the collateral vessels. Associated with this inflow restriction is decreased resistance or vasodilatation of the intramyocardial vessels supplied by collateral coronary arteries.

Animals↗
PubMed1978

Maintenance of permanently implanted cardiac pressure catheters in experimental animals.

Two techniques for maintaining permanently implanted cardiac catheters in experimental animals are described. Polyvinylchloride catheters are coated with TDMAC-Heparin, a polymer complex currently used clinically to prevent thrombogenesis in vascular shunts. Long-term catheter obstruction and thrombus formation have been obviated by using this method. Also, to assure multiple, painless studies in awake animals, a somewhat different technique for pressure catheter access has been developed and is detailed in this report.

Animals↗
PubMed1978

The effects of intermittent ischemic arrest on the perfusion of myocardium supplied by collateral coronary arteries.

Six weeks after placement of an ameroid constrictor on the circumflex coronary artery, blood flow in a collateral region was compared with flow in myocardium supplied by normal arteries during cardiopulmonary bypass (80 mm Hg). Myocardial blood flow was determined using radionuclide-labeled microspheres (8 to 10 mu) before 10 minutes of ischemic arrest and after 1, 5, and 10 minutes of reperfusion. The retrograde circumflex pressure was monitored continuously and served as an additional index of perfusion of the collateral region. During reperfusion, endocardial flow in the collateral region remained unchanged despite a threefold increase in a similar layer having normal arteries (p less than 0.01). Following ischemic arrest, mean transmural and subendocardial hyperemic responses both persisted for longer than 10 minutes in normal regions. Simultaneously, peripheral circumflex pressures decreased at 1 and 5 minutes of reperfusion (p less than 0.001) but returned to control within 10 minutes. Persistently elevated endocardial flow in the normal arteries and the absence of a hyperemic response in the collateral region during an associated decrement in retrograde circumflex pressure may indicate incomplete flow repayment even after 10 minutes of reperfusion. Marked transmural flow imbalances despite adequate coronary perfusion pressures suggest that intermittent ischemic arrest may cause cumulative ischemia, and this occurrence may be detrimental especially in collateral regions of myocardium.

Animals↗
PubMed1978

A reproducible model of moderate to severe concentric left ventricular hypertrophy.

A reproducible model for the production of moderate to severe concentric left ventricular hypertrophy has been developed in this laboratory. Coarctation-banding of the ascending aorta was performed successfully in 10 puppies. There were no late deaths related to aortic rupture, and in the dogs surviving for 1 yr no evidence of congestive heart failure was present. A second operative procedure was performed in seven dogs for chronic instrumentation, and all survived. Severe supravalvular aortic stenosis with a marked peak systolic pressure gradient was noted in each dog. Postmortem examination revealed a substantial increase in left ventricular mass and in the ratio of left ventricular to body weight.

Animals↗
PubMed1978

Pressure-flow characteristics of the coronary collateral circulation during cardiopulmonary bypass. Effects of ventricualr fibrillation.

Even though ventricular fibrillation is used frequently during cardiopulmonary bypass (CPB), the effects of fibrillation on myocardial regions supplied by collateral vessels have not been determined. To study these effects, nine dogs with left ventricles (ameroid model) consisting of a region of myocardium supplied by collateral vessels (CR) and a region supplied by normal coronary arteries (NR) were subjected to normothermic CPB at two perfusion pressures. In both the empty beating heart (EBH) and empty fibrillating heart (EFH) regional myocardial flow was determined by tracer microspheres. Retrograde coronary pressure was measured via cannulation of the circumflex artery distal to the ameroid induced occlusion. When perfusion pressure was maintained at 80 mm Hg, retrograde coronary pressure was similar in the EBH (46 +/- 4 mm Hg) and in the EFH (48 +/- 3 mm Hg). During fibrillation subendocardial flow in the CR was unchanged, while flow in the NR increased (P less than 0.02). In addition, the endo/epi was greater in the NR than in the CR (P less than 0.01), a difference which did not exist in the EBH. The flow response to fibrillation in the CR could be produced in the NR by reducing the perfusion pressure to 50 mm Hg. These data suggest that during CPB, fibrillation exaggerates existing subendocardial perfusion deficits in collateral regions and the impaired flow response appears to be related to a low regional intravascular pressure.

Animals↗
PubMed1978

Myocardial blood flow distribution in concentric left ventricular hypertrophy.

Regional myocardial blood flow during both control conditions and ischemia-induced vasodilatation was studied in eight chronically instrumented awake dogs. Seven of these animals had coarctation-banding of the ascending aorta performed at 6 wk of age, and the other dog had congenital subvalvular aortic stenosis. The mean left ventricular weight for the group was 157+/-7.6 g, and the left ventricular body weight ratio was 8.76+/-0.47 g/kg. None of the animals exhibited signs of congestive heart failure. During the control state, the mean left ventricular systolic pressure was 249+/-12 mm Hg and the left ventricular end-diastolic pressure was 11.5+/-0.5 mm Hg. The aortic diastolic pressure was 74+/-6 mm Hg. Mean left circumflex coronary artery blood flow was 71+/-6 cm(3)/min. In the animals with coarctation-banding, 52+/-6% of the flow occurred during systole. In the dog with congenital subvalvular aortic stenosis, 5% of the coronary flow was systolic. Mean transmural blood flow during resting conditions was 0.97+/-0.08 cm(3)/min per g, and the ratio of endocardial to epicardial flow (endo/epi) was 0.88+/-0.07. During reactive hyperemia, the mean transmural blood flow increased to 3.5+/-0.30 cm(3)/min per g; however, the endo/epi decreased to 0.52+/-0.06.THESE STUDIES DOCUMENT A DIFFERENCE IN TRANSMURAL BLOOD FLOW DISTRIBUTION BETWEEN THE NORMAL AND THE HYPERTROPHIED LEFT VENTRICLE: during resting conditions, in the normal ventricle, the highest flow occurs in the endocardial layer, whereas in the hypertrophied ventricle, the highest flow is in the middle layers with the endocardial flow less than the epicardial flow. During ischemia-induced vasodilatation, the abnormal endo/epi becomes accentuated markedly. These data demonstrate that, in situations requiring high flow, the endocardial layer of a heart with marked concentric left ventricular hypertrophy may not be perfused adequately.

Animals↗