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Biomedical subjects

S Einzig

Publications and source records attributed to S Einzig.

At least 55 records · Page 3Linked to original sources
PubMed1984

Effect of early propranolol treatment in an animal model of congestive cardiomyopathy: I Mortality and Ca2+ transport in sarcoplasmic reticulum.

Young turkeys inbred for congestive cardiomyopathy were treated with propranolol prior to the development of cardiac enlargement. One-day-old inbred and commercial turkeys received propranolol, 2 mg X kg-1 X day-1 for 1 month. Propranolol treated inbred birds showed a significantly reduced mortality from 5 to 15 days of age when compared with untreated inbred birds. However, by 28 days of age, cumulative mortality in the treated inbred birds was equal to that in the untreated inbred birds, 29 and 32%, respectively. Propranolol-treated and untreated commercial birds have a 28-day cumulative mortality of 5%. Ca2+ transport in isolated cardiac sarcoplasmic reticulum was studied at 10 and 28 days of age. At 10 days of age Ca2+ uptake and Ca2+ binding in propranolol-treated birds was reduced to 56% and 83%, respectively, of values in untreated inbred birds. By 28 days of age Ca2+ uptake and Ca2+ binding in treated and untreated inbred birds were similar. Ca2+-stimulated ATPase activity was significantly elevated in treated inbred birds compared with age-matched untreated inbred birds at 10 and 28 days of age. Ca2+ transport in isolated cardiac SR from propranolol-treated commercial control birds was not significantly different from the values in untreated commercial birds at 10 or 28 days of age. Improvement in early mortality may be due to the prevention of arrhythmias. Propranolol alters Ca2+ transport in isolated cardiac SR from inbred birds by uncoupling Ca2+-stimulated ATPase. Whether this is due to a direct effect of propranolol on the SR membrane or occurs from its beta-adrenergic blocking action is unclear.

Animals↗
PubMed1984

Effect of early propranolol treatment in an animal model of congestive cardiomyopathy. II. beta-adrenergic receptors and left ventricular function.

Young turkeys inbred for congestive cardiomyopathy (CCM) were treated with propranolol prior to the development of cardiac enlargement. One-day-old inbred CCM and commercial turkeys received 2 mg X kg-1 X day-1 of propranolol for 1 month and were compared with untreated age matched inbred CCM and commercial turkeys. Heart weight, body weight, and binding characteristics of cardiac beta-adrenergic receptors, using (-)3H-dihydroalprenolol as a ligand, were determined at 10 and 28 days. Left ventricular shortening fraction was determined at 28 days and at 32 days, 4 days after propranolol was discontinued, in treated and untreated inbred CCM and commercial turkeys. Propranolol did not prevent the development of cardiac hypertrophy in inbred CCM turkeys at 28 days of age and did not effect body weight or heart weight in either inbred CCM or commercial turkeys at 10 or 28 days of age. In the inbred CCM turkeys, the maximum number of binding sites (Bmax) and the binding affinity (Kd) of beta-adrenergic receptors were not changed by propranolol treatment. In the propranolol-treated commercial turkeys, Bmax the of beta-receptors was increased at 28 days of age compared with untreated age matched controls, 382 vs 194 fmol X mg-1 (p less than 0.05). Untreated inbred CCM turkeys when compared with untreated age matched commercial turkeys show a significant reduction of binding affinity of beta-receptors at both 10 and 28 days of age, Kd = 10.4 vs 6.2 nmol X litre-1 at 10 days and 11.3 vs 5.2 nmol X litre-1 at 28 days (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Role of ischemia in contrast-induced renal damage: an experimental study.

Total and regional cortical blood flow was measured in dogs by the radioactive microsphere technique after renal damage of varying severity had been induced by combining selective injection of diatrizoate, iopamidol, or normal saline with a 10 min occlusion of the renal artery. There was extensive tubular and glomerular damage in the kidneys exposed to diatrizoate, but not in the kidneys exposed to saline. Iopamidol caused intermediate changes. Average cortical blood flow was reduced from baseline levels in all groups 5 min after perfusion was restored. After 1 hr the flow had returned to the baseline level. Analysis of variance did not show a statistically significant difference among the groups. A tendency for redistribution of flow from outer to inner cortical layers was seen, but this was present in all groups. The flow changes detected in this study cannot explain the varying severity of renal damage.

Animals↗
PubMed1984

Effect of prostaglandin inhibition on the renal vascular response to ionic and non-ionic contrast media in the dog.

In an attempt to study the role of prostaglandins in the renal vascular response to contrast media in mongrel dogs, renal arterial injections of 6 ml of either the non-ionic contrast medium Iopamidol or the ionic medium diatrizoate meglumine/Na+ were performed, before and after intravenous injection of a buffered solution of acetylsalicylic acid (10 mg/kg) (ASA). Renal blood flow was recorded using non-occluding electromagnetic flow probes. The resting renal blood flow was significantly reduced after ASA. The usual biphasic response to contrast injection was observed both before and after ASA, and using either contrast medium. Analysis of the results failed to show any difference in degree of vasodilation or vasoconstriction after ASA. We conclude that prostaglandins may affect the resting level of renal blood flow but are not mediators of the instantaneous changes in response to contrast injection.

Animals↗
PubMed1984

Comparison of catecholamine effects on canine myocardial metabolism and regional blood flow during and after cardiopulmonary bypass.

The acute metabolic and hemodynamic effects of dopamine, dobutamine (both at 10 micrograms . kg-1 . min), and isoproterenol (at 0.05 or 0.1 micrograms . kg-1. min) were determined in dogs following 20 minutes of normothermic global myocardial ischemia. The catecholamines were started 10 minutes before cardiopulmonary bypass (CPB) was discontinued and were continued for 1 hour after bypass. Regional myocardial and systemic blood flow distribution was measured by means of the radioactive microsphere technique. On bypass all catecholamines sharply increased heart rate, myocardial oxygen consumption, and left ventricular blood flow (p less than 0.01). Because the hearts were unloaded, these data suggest that velocity of contraction is an important component of myocardial oxygen consumption. Although these drugs did not lower myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) levels, the significant rise in oxygen consumption suggested that inotropic treatment on bypass may not be beneficial. Furthermore, renal blood flow was diminished in dobutamine-treated dogs (p less than 0.01) and tended to decrease with isoproterenol infusion. No change was seen with dopamine infusion. After bypass, dobutamine treatment increased cardiac output (p less than 0.01) and stroke volume (p = 0.017) with no change in heart rate, myocardial oxygen consumption, high-energy phosphate levels, and total or transmural distribution of left ventricular blood flow. Dopamine infusion did not change cardiac output but did increase oxygen consumption (p less than 0.01). Isoproterenol showed a slight inotropic effect, but frequent ventricular arrhythmias were present during weaning from bypass. In all treatment groups, blood flow in the other systemic beds (cerebral, gastrointestinal, and renal) was similar to that in control dogs. These data suggest that dobutamine is the most efficient of the drugs tested for support of the heart following global myocardial ischemia but, when given during bypass, it appears to decrease renal blood flow.

Adenosine Triphosphate↗
PubMed1984

Brain damage in profound hypothermia. Perfusion versus circulatory arrest.

To investigate brain changes in induced deep core hypothermia (18 degrees C) with or without circulatory arrest, four groups of dogs were subjected to cardiopulmonary bypass (CPB) under the following conditions: (1) differential head perfusion with pulsatile flow and simultaneous circulatory arrest to the rest of the body; (2) differential perfusion to the head with a nonpulsatile flow; (3) total circulatory arrest; and (4) continuous hypothermic perfusion. Parameters analyzed were: (1) blood flow distribution; (2) creatine kinase isoenzyme (CK-BB) elevation in the cerebrospinal fluid (CSF) and in the brain venous return; and (3) microscopy of the brain in animals killed at 30 minutes, 24 and 48 hours, 1 and 2 weeks, and 1 month. Although minor brain tissue flow differences were found at 37 degrees C among the groups, flows equalized at 18 degrees C. A significant seven-fold brain flow increase followed the period of circulatory arrest in Group III. Rise of CK-BB levels occurred in brain venous return but not in CSF in all groups. Microscopic cellular damage appeared in all groups with an equal degree of severity, regardless of the method of hypothermia and perfusion implemented.

Animals↗
PubMed1983

Vessel wall arachidonate metabolism after angioplasty: possible mediators of postangioplasty vasospasm.

The mechanism of postangioplasty vasospasm is uncertain. It was postulated that a reduction in vasodilator prostaglandin I2 (PGI2) or prostaglandin E2 (PGE2) or an increase in vasoconstrictor hydroperoxy acids might contribute to spasm of a dilated artery. Twelve mongrel dogs were anesthetized, intubated, and mechanically ventilated. Heart rate and aortic pressures were continuously monitored and arterial blood gases maintained within physiologic limits. A single carotid artery was dilated in each animal (4 atm X 1 minute X 3) using nonexpandable polyethylene balloon catheters with inflated balloon diameters 50 to 100% larger than the internal arterial lumen. The opposite carotid artery served as a control. In 4 animals, aspirin (10 mg/kg, intravenously) was injected 30 minutes before dilation. Sixty minutes after dilation, animals were heparinized and the carotid arteries carefully removed. The in vitro conversion of carbon-14(14C)-arachidonic acid (AA) to 6-keto PGF1 alpha (PGI2), PGE2, and 12L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE) was determined using thin-layer radiochromatography. Angioplasty caused a 70% decrease in vessel wall PGI2 production and a 44% decrease in PGE2 production (n = 4, p less than 0.05). Reductions in in vitro conversion of 14C-AA to PGI2 and PGE2 induced by angioplasty were comparable to that produced by cyclooxygenase inhibition with aspirin. Angioplasty, in addition, caused a 104% increase in vessel wall HETE production (n = 4, p less than 0.05). Therefore, angioplasty results in a local derangement of AA metabolism characterized by decreases in vasodilator prostaglandins and increases in vasoconstrictor hydroperoxy acids. These local changes may contribute, in part, to sudden arterial occlusion after angioplasty.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1983

Isolated cleft mitral valve: a variety of congenital mitral regurgitation identified by 2-dimensional echocardiography.

Nine children with isolated cleft mitral valve, aged 1 day to 12 years, were studied. The electrocardiogram showed a normal QRS axis in 5 subjects. Cardiac catheterization was performed in 4 patients and demonstrated severe mitral insufficiency in 3 but failed to clearly demonstrate a cleft mitral valve or gooseneck deformity. The mitral cleft was confirmed at operation in 2 patients. Two-dimensional echocardiography demonstrated a cleft dividing the anterior mitral leaflet into 2 portions in each patient. The mitral anulus was normally positioned and the atrioventricular septum present. Atrial and ventricular septa were intact. Features similar to anatomic studies such as accessory chordae and thickening of the edges of the cleft with increasing age were also seen. Two-dimensional echocardiography is the only method available to reliably diagnose isolated cleft of the mitral valve.

Cardiac Catheterization↗
PubMed1983

Maximal postextrasystolic potentiation following multiple extrasystoles: a simple means of myocardial assessment.

To obtain consistent, reproducible postextrasystolic potentiation (PESP), a single closely coupled extrasystole (ES) must be introduced using transvenous pacing. We hypothesized that multiple ES (spontaneous or catheter induced) produce maximal PESP at all coupling intervals (CI). Differences in PESP between single and double ES were assessed in dogs at varying CI by two different methods [systolic time intervals--PEP/LVET, and endocardial markers--ejection fraction (EF)]. Single ES produced variable decreases in PEP/LVET (-8.6 +/- 2.7% (SE) to -22.9 +/- 4.0%) depending on the CI duration. Double ES produced maximal decreases (-26.0 +/- 1.2%) at all CI. A similar relationship was noted for EF following single ES (8.6 +/- 2.7% to 43.0 +/- 4.0%) and double ES (42.9 +/- 1.3%). Double ES produced maximal PESP at all CI. This finding may allow simple myocardial assessment during routine left ventricular catheterization without simultaneous right ventricular catheterization.

Animals↗
PubMed1983

Prevention of ATP catabolism during myocardial ischemia: a preliminary report.

The enhancement of ATP regeneration following global myocardial ischemia in dogs by both ATP catabolic enzyme blockade and precursor infusion was investigated. The breakdown of AMP to adenosine is catalyzed by 5'-nucleotidase and this enzyme was inhibited during the ischemic period with either concanavalin A (Con A, 3 mg/kg) or alpha, beta-methyleneadenosine 5'-diphosphate (AMP-CP, 250 microM). To provide additional ATP precursors, adenine (30 mg/kg) and ribose (25 mg/kg) (A/R) were also infused into the coronary vasculature during ischemia and recovery on cardiopulmonary bypass. Left ventricular myocardial ATP levels in control animals decreased to 52% of preischemic values during aortic cross clamping, but ATP levels in dogs treated with AMP-CP + A/R fell to only 67% of preischemic values (P less than 0.05). During reperfusion, ATP levels in Con A + A/R (3.43 +/- 0.26 mumol/g wet wt) and AMP-CP + A/R (3.77 +/- 0.42) treated animals were higher than values found in control dogs (2.73 +/- 0.16, P less than 0.05). Infusions of A/R alone without enzyme inhibition did not increase ATP regeneration. The adenine nucleotide energy charge ratio was also increased by enzyme blockade with either inhibitor when combined with precursor infusion. On bypass, left ventricular myocardial blood flow (measured by the microsphere technique) was increased by 140% (P less than 0.01) over control values in all groups receiving A/R; therefore, enhanced ATP levels were not merely the result of increased flow. Renal blood flow was not adversely affected by this combination of drugs as has been previously found with adenosine infusion and inhibition of adenosine catabolism.

Adenosine↗
PubMed1983

The vasa vasorum and angioplasty.

Interruption of flow in the vasa vasorum may lead to medial necrosis and aneurysm formation. The purpose of this study was to determine whether angioplasty produces significant alterations in the morphology or blood flow of the vasa vasorum of the dilated artery. The morphology of the canine vasa vasorum was studied before and after angioplasty; in a separate experiment vessel wall blood flow (VWBF) in canine carotid arteries was measured after angioplasty to determine whether physiologic regulation of the blood flow was disrupted by arterial dilation. No morphologic changes could be demonstrated in the vasa vasorum of the dilated artery; however, VWBF was increased by 1194 +/- 215% (mean +/- standard error, p less than 0.01) between 90 and 120 minutes after angioplasty. VWBF in the adjacent nondilated arterial segment was also increased (720 +/- 177% between 10-30 minutes, p less than 0.01) but returned toward normal after 60 minutes. Adenosine caused a "paradoxical" decrease in VWBF (p less than 0.05) of the dilated arterial segment while causing increased VWBF (p less than 0.05) in the thoracic aorta. Angioplasty appears to produce persistent hyperemia in the dilated arterial wall. A paradoxical response to adenosine suggests that vasa vasorum in the dilated arterial segment are maximally vasodilated. This may be due to mechanical disruption of vasomotor tone or to release of vasoactive substances.

Adenosine↗
PubMed1983

Prostaglandins and angioplasty. An experimental study in canine arteries.

To prevent platelet aggregation following percutaneous transluminal angioplasty (PTA), cyclooxygenase inhibitors such as acetylsalicylic acid (ASA) and indomethacin are recommended. However, ASA blocks both the proaggregating effects of thromboxane (TXA2) and the antiaggregating and vasodilating effects of prostacyclin (PGI2). The authors measured the contractile response of dilated canine carotid arteries in situ and in vitro using an isometric force transducer. Following PTA, contraction of the arterial wall was significantly reduced (p less than 0.01). By blocking cyclooxygenase with indomethacin (3 micrograms/ml), contraction was greatly improved (p less than 0.001). These results suggest that PTA may result in marked release of prostacyclin by the damaged arterial wall, which could account for the decreased responsiveness of the artery to exogenous norepinephrine.

Angioplasty, Balloon↗
PubMed1983

Resting and exercise renal blood flows in immature ovine aortic coarctation. Impact of gradient relief.

The primary purpose of this study was to determine whether a neonatally induced thoracic aortic coarctation reduces renal blood flow during physiological stress (treadmill exercise), and whether relief of the gradient returned renal blood flow during exercise to normal. Two ancillary questions were also addressed: dose a coarctation after the responses of enteric and other visceral vascular beds to treadmill exercise? Eight newborn lambs that underwent sham thoracotomy with placement of left atrial lines served as controls; in seven lambs we also created a recently described form of dilatable juxtaductal coarctation. This preparation is unique in that, like human coarctation, the obstruction does not get worse as the animal grows. Rest and exercise vascular pressures and regional blood flows were determined 2-2 1/2 months after surgery. Coarctations were relieved with balloon dilation angioplasty catheters, inserted percutaneously. Postdilation rest and exercise hemodynamic studies were performed, at the same level of exercise, 24 hours after dilation. Renal blood flow did not change with exercise in the control animals. In lambs with coarctation, renal blood flow fell (-22%, P less than 0.01) during exercise. Unexpectedly, an exercise-induced fall in renal blood flow (-22%, P less than 0.001) persisted even after effective relief of the coarctation (descending aortic blood pressure fell 25% with exercise predilation, but remained unchanged with exercise postdilation). Blood flow to the terminal ileum and cecum followed a qualitatively similar pattern to that of renal blood flow in control, predilation, and postdilation lambs, and this pattern was distinct from that of other enteric and visceral organ flows. These results demonstrate an expected abnormality in the regulation of exercise renal blood flow in lambs with coarctation of the aorta; however, the persistence of this abnormality after effective gradient relief does not support the previously advanced theory that postcoarctation hypertension is largely nonrenal in origin. The apparent similarity between ileocecal and renal blood flow control under these circumstances may provide a clue to the known predilection of the terminal ileum to suffer ischemic injury.

Animals↗
PubMed1983

Pulmonary vascular effects of amrinone in conscious lambs.

The direct pulmonary vascular effects of amrinone, a nonglycoside, noncatechole cardiotonic agent were studied in conscious newborn lambs using a double-flow probe preparation that allows separation of direct and indirect pulmonary vascular effects. Amrinone was found to be a direct pulmonary vasodilator with a threshold dose of 0.3 mg/kg. Amrinone also increased cardiac output and decreased aortic pressure at somewhat higher threshold doses (1.0 mg/kg and 3.0 mg/kg, respectively). Amrinone's peak effect on pulmonary resistance appeared greater than its peak systemic effects. These effects were noted in both normoxia and hypoxia, and were not changed by pretreatment with propranolol.

Aminopyridines↗
PubMed1983

Effect of aspirin on angioplasty-induced vessel wall hyperemia.

Angioplasty produces a persistent 20-fold increase in blood flow through mural vasa vasorum. To assess the role of prostaglandins in this phenomenon, vessel wall blood flow in experimentally dilated carotid arteries of aspirin treated dogs was measured. Aspirin (10 mg/kg, intravenously) significantly attenuated the increase in blood flow produced by dilation (+283 +/- 91% SE, n = 6) when compared to non-aspirin-treated controls (+2356 +/- 885% SE, n = 10). This suggests that aspirin, by interfering with arachidonate metabolism, may decrease local vasodilation after angioplasty. The effect of aspirin therapy on the long-term success of angioplasty requires further study.

Angioplasty, Balloon↗
PubMed1982

The pulmonary vascular response to oxygen and its influence on operative results in children with ventricular septal defect.

The ratio of pulmonary vascular resistance to systemic resistance was determined before and after oxygen administration in 25 children with an isolated large ventricular septal defect and elevated pulmonary vascular resistance (pulmonary/systemic resistance ratio, Rp/Rs greater than 0.25). A fall of 30% or more in the Rp/Rs, after 20 minutes of oxygen inhalation (FiO2 greater than 0.90), was considered a positive response to oxygen. In the 6 children with Down's syndrome, the Rp/Rs fell significantly more in oxygen (52%) than it did in the 19 children without Down's syndrome (31%, p less than 0.05). No other clinical or baseline hemodynamic finding was predictive of vascular responsiveness. Seventeen children underwent closure of the ventricular septal defect. Three of 11 children who responded to O2 expired shortly after operation; each of the 6 children who did not respond to O2 survived operation. Two of the deaths (occurring less than 12 hours after closure) were from low cardiac output; a third child died suddenly 5 days postoperatively. Thirteen children, 7 who responded to oxygen and 6 who did not, were restudied by cardiac catheterization an average of 2.0 years following successful closure of the ventricular septal defect. While the Rp/Rs in room air fell following closure of the defect in both groups, the decrease was 22% in responders and 28% in nonresponders. The results of this study, unlike similar studies performed at higher altitudes, suggest that the preoperative responsiveness of the pulmonary vasculature to oxygen does not predict either operative survival or postoperative pulmonary vascular resistance.

Child↗