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J D Dewey

Publications and source records attributed to J D Dewey.

10 recordsLinked to original sources
PubMed1987

Effects of isoflurane on coronary arteries and coronary arterioles in the intact dog.

To determine the site of isoflurane-associated coronary vasodilatation, the authors measured epicardial coronary artery diameter and examined the effects of isoflurane on coronary arteriolar tone. Angiograms of the left coronary system were obtained in seven fentanyl-pentobarbital anesthetized dogs and quantitated with a computerized analysis system. Cross-sectional areas of the proximal, mid, and distal left anterior descending and proximal circumflex coronary arteries were obtained at three arterial pressures, and then the measurement repeated following administration of 0.75%, 1.5%, and 2.25% end-tidal isoflurane. At the same time coronary blood flow was measured using a 123Xe washout technique. Isoflurane was found to have no effect on epicardial coronary artery dimensions. No dilatation was observed throughout the range of isoflurane concentrations and coronary perfusion pressures investigated. However, despite the absence of epicardial coronary effects, coronary arterioles were dilated by both 1.5% and 2.25% isoflurane. Coronary blood flow corresponding to a myocardial oxygen consumption of 7.5 ml oxygen X 100 gm-1 X min-1 was calculated as 99 +/- 17 ml X 100 gm-1 X min-1 (mean +/- SD) during control conditions, and it increased to 150 +/- 26 ml X 100 gm-1 X min-1 at 1.5% isoflurane (P less than .004) and to 197 +/- 35 ml X 100 gm-1 X min-1 at 2.25% isoflurane (P less than .001). Although higher concentrations of isoflurane dilated intramyocardial arterioles, isoflurane had no effect on epicardial coronary arteries.

Animals↗
PubMed1986

Effects of thromboxane analog U46619 on endothelial damaged canine coronary arteries in vivo.

We studied the effects of the thromboxane analog, U46619, infused into the left anterior descending (LAD) artery of intact dogs before and after producing endothelial denudation of the mid portion of the LAD. Proximal artery cross-sectional area (CSA) decreased by 47% with 0.1 microgram/min infusion of U46619 with intact and denuded endothelium, while resting CSA reduced spontaneously following denudation. Coronary resistance vessels demonstrated a marked constrictor response to U46619 with a rise in resistance and a fall in flow and myocardial O2 consumption. U46619 produces significant narrowing of proximal epicardial coronary arteries as well as resistance coronary vessels. This effect could cause ischemia in patients with moderate coronary atherosclerosis.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1985

Proximal coronary vasomotor reactivity after exercise training in dogs.

The effects of exercise on large coronary vasoreactivity were determined in eight dogs trained by treadmill running for 8 weeks. Six nontrained dogs comprised the control group. The trained group showed a significant reduction in heart rate during graded submaximal exercise testing when compared with the controls, and resting plasma levels of norepinephrine (nontrained group, 331 +/- 99 pg/ml; trained group, 142 +/- 30 pg/ml; p less than .05) and epinephrine (nontrained, 424 +/- 105; trained, 258 +/- 45 pg/ml; p less than .05) were reduced significantly in the trained group. Epicardial coronary responses to intracoronary infusion of serotonin and phenylephrine were evaluated by quantitative coronary angiography, and myocardial blood flow was measured with 15 microns radioactive microspheres. Left ventricular/body weight ratio was similar in the trained (4.81 +/- 0.24 g/kg) and nontrained groups (4.79 +/- 0.17), and no differences were noted in resting myocardial oxygen consumption or coronary arteriovenous oxygen difference. The constriction of the proximal left anterior descending artery (LAD) in response to serotonin infusion was not different in the two groups, but the LAD and circumflex artery constrictor responses to phenylephrine were attenuated in the trained when compared with the nontrained dogs. The data indicate that endurance exercise diminishes the large epicardial coronary vasoconstrictor response to alpha-adrenergic stimulation, but not to serotonin. The blunted constrictor response in the trained animals suggests that exercise may be useful in reducing epicardial coronary vasoconstriction, which is thought to be important in some patients with coronary artery disease.

Angiography↗
PubMed1984

Increased conjugated dopamine in plasma after exercise training.

To evaluate the effect of endurance exercise on plasma catecholamines, we exercise trained eight dogs (group T) by treadmill running for 8 weeks. Six sedentary dogs constituted a nontrained control group (group NT). Heart rate response to a graded submaximal stress test was reduced in group T dogs (p less than 0.05), but mean resting aortic blood pressure (NT, 84 +/- 5 mm Hg; T, 82 +/- 4 mm Hg) and heart rate (NT, 87 +/- 1 bpm; T, 84 +/- 2 bpm) were unchanged by exercise, and no cardiac hypertrophy occurred after exercise. Plasma norepinephrine and epinephrine levels were reduced in group T at rest and during a fixed exercise workload. Plasma conjugated dopamine showed a marked increase in group T dogs (NT, 1398 +/- 130 pg/ml; T, 11346 +/- 1291 pg/ml; p less than 0.01) at rest, and no change in conjugated dopamine occurred in either group after short-term exercise stress. No intergroup differences were noted in resting coronary flow or coronary arteriovenous oxygen, or in myocardial oxygen consumption. The data verify previous findings of lower plasma levels of norepinephrine and epinephrine after training, and indicate that a marked rise in conjugated dopamine occurs after training. These findings suggest that norepinephrine and epinephrine metabolism is shifted toward conjugated dopamine by exercise training, thereby reducing active catecholamines in plasma, but retaining a large pool of usable metabolite.

Animals↗
PubMed1983

Effects of serotonin and histamine on proximal and distal coronary vasculature in dogs: comparison with alpha-adrenergic stimulation.

The effect of several vasoactive agents on epicardial conductance arteries and distal resistance arteries was studied in intact dogs using a special catheter system to infuse vasoactive mediators directly into the left anterior descending coronary artery of intact dogs. Serotonin produced significant epicardial vasoconstriction (42% cross-sectional area reduction, p less than 0.01), whereas histamine had no effect on proximal coronary arteries. Phenylephrine, an alpha-adrenergic agonist, produced an 11% reduction in cross-sectional area. Distal coronary vascular resistance (pressure/flow) changes were small for serotonin and phenylephrine, whereas histamine significantly dilated the peripheral vascular bed and caused flow measured by xenon-133 washout to increase from 30.4 +/- 4.0 to 72.4 +/- 12.6 ml/min . 100 g (p less than 0.05). These results show that vasoactive mediators can have different actions on coronary resistance and conductance vessels. Serotonin is a potent vasoconstrictor of epicardial coronary arteries but does not produce significant constriction of coronary resistance vessels.

Adrenergic alpha-Agonists↗
PubMed1980

Failure of interventions to maintain mitochondrial function in ischemic myocardium.

The purpose of this study was to investigate whether pyruvate (2.5 mmol/kg), the combination of glucose (3.9 mmol/kg) and insulin (0.13 unit/kg) with potassium (9.27 meq/kg), or sodium dichloroacetate (120 mg/kg) infused for 15 minutes before and 20 minutes after ligation of the left anterior descending coronary arterv in anesthetized dogs restricted the depression in mitochondrial respiratory function induced by ischemia. Myocardial blood flow after ligation in the three groups was o.2 ml/min per gram or less in ischemic subendocardium and was similar to that in saline-infused controls that had also undergone coronary artery ligation. The depressions induced in mitochondrial respiratory control index and state 3 respiration by ischemia in the subendocardium and subepicardium of the three treatment groups, when compared with corresponding nonischemic tissue, were not significantly improved from the control values. It was concluded that these three interventions fail to preserve mitochondrial respiration in ischemic myocardium.

Animals↗