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Biomedical subjects

K G Lurie

Publications and source records attributed to K G Lurie.

15 recordsLinked to original sources
PubMed1992

Active compression-decompression. A new method of cardiopulmonary resuscitation. Cardiopulmonary Resuscitation Working Group.

OBJECTIVE: To describe and compare with standard cardiopulmonary resuscitation (CPR) in humans a new form of CPR that involves both active compression and active decompression of the chest. DESIGN: Patients in cardiac arrest in whom standard advanced cardiac life support failed were randomized to receive 2 minutes of either standard or active compression-decompression (ACD) CPR using a custom, hand-held suction device, followed by 2 minutes of the alternate technique. The ACD device was applied midsternum and used to perform CPR according to the guidelines of the American Heart Association: 80 compressions per minute, compression depth of 3.8 to 5 cm, 50% duty cycle, and constant-volume ventilation. Mechanical Thumper CPR was also compared in five patients. End-tidal carbon dioxide (ETCO2) concentrations and hemodynamic variables were measured. Transesophageal Doppler echocardiography was used to assess contractility, the velocity time integral (an analogue of cardiac output), and diastolic myocardial filling times. RESULTS: Ten patients were enrolled. The mean +/- SD ETCO2 was 4.3 +/- 3.8 mm Hg with standard CPR and 9.0 +/- 3.9 mm Hg with ACD CPR (P less than .0001). Systolic arterial pressure with standard CPR was 52.5 +/- 14.0 mm Hg and with ACD CPR, 88.9 +/- 24.7 mm Hg (P less than .003). The velocity time integral increased from 7.3 +/- 2.6 cm with standard CPR to 17.5 +/- 5.6 cm with ACD CPR (P less than .0001), and diastolic filling times increased from 0.23 +/- .09 seconds with standard CPR to 0.37 +/- .12 seconds with ACD CPR (P less than .004). Mechanical Thumper CPR consistently underperformed both standard and ACD CPR. Minute ventilation obtained in four patients during ACD CPR without endotracheal ventilation was 6.6 +/- 0.9 L/min. After 1 hour of standard CPR failed, three of 10 patients randomized to ACD CPR rapidly converted to a hemodynamically stable rhythm following 2 minutes of ACD CPR. CONCLUSION: ACD CPR is a simple manual technique that improved cardiopulmonary circulation in 10 patients during cardiac arrest. Although ACD CPR may have produced a return of spontaneous circulation in three patients refractory to standard measures, its impact on survival when used early in cardiac arrest remains to be determined.

Adult↗
PubMed1992

Active compression-decompression resuscitation: a novel method of cardiopulmonary resuscitation.

Chest compression is an important part of cardiopulmonary resuscitation (CPR), but it only aids circulation during a portion of the compression cycle and has been shown to only minimally increase blood flow to vital organs. The purpose of this study was to quantitate the short-term hemodynamic effects of CPR with a hand-held suction device that incorporates both active compression and decompression of the chest. The suction device was applied to the middle of the sternum and compared with standard manual CPR in eight nonventilated anesthetized dogs. Coronary perfusion pressure, systolic and diastolic aortic pressures, right atrial diastolic pressure, and the velocity time integral (an analog of cardiac output), which were obtained by means of transesophageal pulsed wave Doppler echocardiography from the main pulmonary artery, were measured every 30 seconds during CPR. Minute ventilation was measured over the last minute of each CPR technique. Both active compression-decompression CPR and standard CPR were sequentially performed for 2 minutes in random order 30 seconds after induced ventricular fibrillation. The CPR techniques consisted of 100 compressions per minute, with a compression depth of 1.5 to 2 inches and a 50% duty cycle. Coronary perfusion pressure, velocity time integral (cardiac output analog), minute ventilation, and systolic arterial pressure were all significantly improved by active compression-decompression CPR when compared with standard CPR. We conclude that active compression-decompression CPR is a simple technique that appears to improve coronary perfusion pressure, systolic arterial pressure, cardiac output, and minute ventilation in nonventilated animals when compared with standard CPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Curative percutaneous catheter ablation using radiofrequency energy for accessory pathways in all locations: results in 100 consecutive patients.

Patients with accessory pathway-mediated supraventricular tachycardia have typically been treated with drugs or surgery. Although catheter ablation using high voltage direct current shocks has been used to treat patients with drug-refractory supraventricular tachycardia, there are associated disadvantages, including damage due to barotrauma as well as the need for general anesthesia. Recently, transcatheter radiofrequency energy has evolved as an alternative to direct current shock or surgery to ablate accessory pathways. Percutaneous catheter ablation of 109 accessory pathways with use of radiofrequency energy was attempted in 100 consecutive patients. Patient age ranged from 3 to 67 years. The patients had been treated for recurrent tachycardia with a mean of 2.7 +/- 0.2 antiarrhythmic agents that either proved ineffective or caused unacceptable side effects. In seven patients previous attempts at accessory pathway ablation with use of direct current shock had been unsuccessful. Forty-five (41%) of the pathways were left free wall, 43 (40%) were septal and 21 (19%) were right free wall. Eighty-nine (89%) of the 100 patients had successful radiofrequency ablation at the time of hospital discharge. In all but 12 patients the ablation was accomplished in a single session. Complications attributable to the procedure, but not to the ablation itself, occurred in four patients (4%). No patient developed atrioventricular block or other cardiac arrhythmias. Over a mean follow-up period of 10 months, nine patients had some return of accessory pathway conduction; a repeat ablation procedure was successful in all five patients in whom it was attempted. It is concluded that a catheter ablation procedure using radiofrequency energy can be performed on accessory pathways in all locations. The procedure is effective and safer, less costly and more convenient than cardiac surgery and can be considered as an alternative to lifelong medical therapy in any patient with symptomatic accessory pathway-mediated tachycardia.

Adolescent↗
PubMed1992

Regional distribution of ECS in contractile and conductive elements of rat and rabbit heart.

By adaptation of recently developed quantitative microanalytic techniques, the size of the extracellular space (ECS) was measured regionally in the rat and rabbit cardiac conductive and contractile tissues. When inulin and sucrose were measured as extracellular markers in rabbit heart, the ECS in the atrioventricular (AV) node was found to be, respectively, 2.4 and 2.2 times larger than that of adjacent ventricular muscle. By use of inulin, the ECS in the rabbit His bundle was found to be 1.8 times larger than the adjacent ventricular tissue. Similarly, when inulin was used in rat, the ECS of the AV node, His bundle, right bundle branch, and right atrium was found to be, respectively, 2.5, 1.9, 1.8, and 1.2 times larger than that of left and right ventricular muscle. Similarly, significant regional differences in ECS were also observed in rat heart with sucrose. By use of glucose as an ECS marker, these results also revealed a 2.5-2.9 times larger ECS in rat and rabbit AV node compared with contractile elements. In contrast, ATP content, measured as an intracellular marker, was the same in both AV nodal and ventricular muscle tissue from both rat and rabbit. These data demonstrate that there are significant regional variations in ECS within the cardiac conduction system. Collectively, the data obtained with all extracellular markers indicate that the size of the ECS of the conduction system is markedly larger than the adjacent contractile muscle.

Adenosine Triphosphate↗
PubMed1991

Radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia: results and long-term follow-up.

Seven of 120 consecutive patients with inducible sustained ventricular tachycardia (from September 1, 1988 to January 1, 1991) had bundle branch reentrant tachycardia and underwent percutaneous radiofrequency ablation of the right bundle branch. The seven patients had been unsuccessfully treated with a mean of 3 +/- 1 drugs. Four patients presented with syncope and three with aborted sudden death. The baseline electrocardiogram revealed a left bundle branch block pattern in three patients and an intraventricular conduction defect in four. The baseline HV interval was prolonged in each case (79 +/- 2 ms). With use of programmed ventricular extrastimuli, sustained bundle branch reentrant tachycardia was inducible in all patients at a mean cycle length of 283 +/- 17 ms (range 230 to 350). Bundle branch reentrant tachycardia characteristics included atrioventricular dissociation, a His deflection that preceded each QRS complex and spontaneous His to His variation that preceded changes in ventricular tachycardia cycle length. A quadripolar catheter was positioned across the tricuspid valve with the distal electrode tip of the catheter near the right bundle branch. One to three applications of continuous unmodulated radiofrequency current at 300 kHz between the distal electrode and a large posterior skin patch resulted in complete right bundle branch block in all patients, after which none had inducible bundle branch reentrant tachycardia on restudy. On restudy, three of the seven patients had ventricular tachycardia of myocardial origin (not bundle branch reentry). One patient required no therapy; drug or defibrillator therapy was used in the others.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Implantable cardioverter defibrillator proarrhythmia: case report and review of the literature.

A 31-year-old man who received an automatic cardioverter defibrillator subsequently underwent exercise testing. During exercise, a sinus tachycardia resulted above his device detect rate prompting two shocks, the second of which produced an unstable polymorphous ventricular tachycardia. In this article, we review the literature on automatic cardioverter defibrillator-induced ventricular tachyarrhythmias as well as the management of exercise testing in patients with these devices.

Adult↗
PubMed1991

Measurement of extracellular space in the rabbit AV node.

We used quantitative histochemistry to measure the size of the extracellular space (ESC) in various regions of the rabbit heart. When inulin, sucrose, and sorbitol were used as ECS markers, the ECS of the AV-nodal tissue was found to be, respectively, 2.4, 2.2, and 2.5 times larger than that of left ventricular muscle. Glucose was also measured over a 50-fold serum concentration range as an extracellular marker for AV-nodal tissue, left ventricular muscle, and Purkinje fibers. Measurements with glucose also revealed that the ECS of the AV node was 2.5-2.8 times larger than that of ventricular muscle. In contrast, the ECS of the AV node was the same as that of Purkinje fibers when glucose was used as an extracellular marker. ATP content, measured as an intracellular marker, was similar in both AV-nodal and contractile tissue. Collectively, the data obtained with all extracellular markers indicate that the ECS of the AV-nodal region is approximately 2.5 times larger than that of adjacent contractile tissue. Differences in the size of the ECS in various regions of the heart probably have functional significance and should be considered appropriately during the interpretation of data obtained by biochemical and densitometric approaches.

Acetylcholinesterase↗
PubMed1990

Diabetes and the myo-inositol paradox.

To test the general applicability of the hypothesis that diabetes mellitus causes increased polyol pathway activity, decreased tissue free myo-inositol, and resultant pathological changes in tissues susceptible to the ravages of diabetes, we measured glucose, sorbitol, and myo-inositol with quantitative histochemical techniques in layers of the cornea, the aortic myointima, the cardiac left ventricle and atrioventricular node (AVN), and retina and kidney after 19 days or 2 mo (mildly diabetic non-insulin-treated [MD] and severely diabetic insulin-treated [SD] groups) in the alloxan-induced diabetes model. In the aqueous humor, glucose rose linearly with increased serum glucose, sorbitol was markedly increased in the MD and SD groups, and myo-inositol did not change in any diabetic group. There was no change in glucose or sorbitol in aortic myointima in any group, but myoinositol was decreased in 19-day diabetic rabbits by 26%, unchanged in MD rabbits but paradoxically increased by 60% in SD rabbits. Glucose, sorbitol, and myo-inositol increased in all three corneal layers in SD rabbits but only in epithelium and stroma in 19-day and MD rabbits. AVN glucose and sorbitol did not change in 19-day diabetic, MD, or SD diabetic rabbits. AVN myo-inositol was three times higher than ventricular myo-inositol and did not appear to change in SD rabbits. Retinal pigmented epithelium myo-inositol was decreased 30% in SD rabbits. Glomerular myo-inositol was also decreased, but not significantly, in SD rabbits. We conclude that the paradoxical increase in corneal and aortal myo-inositol raises fundamental questions about the general applicability of the myo-inositol-depletion hypothesis.

Animals↗
PubMed1988

6-Hydroxydopamine mediated cardiotoxicity in rabbits.

Weekly injections of the catecholamine depleting agent 6-hydroxydopamine (6-OHDA) were used to denervate rabbit hearts chemically. Analyses of morphology and beta-adrenergic receptor density were made at 1, 2, and 4 weeks. Changes resulting from subacute and chronic inflammatory processes were evident by light microscopy after 1 week. At that time, electron microscopy revealed marked increases in collagen, large myocytic vacuolizations in myocytes, widened gap junctions, and myofibrillar degeneration and dropout. Receptor density was marginally increased at 2 weeks but was decreased (p less than .05) at 4 weeks (maximal [3H]dihydroalprenolol (DHA) binding in fmol/mg: 69.6 +/- 5.4 in controls vs 49.2 +/- 5.1 in 6-OHDA-treated animals). Basal, isoproterenol-stimulated and F- -stimulated adenylate cyclase activities were decreased in the 6-OHDA-treated group at 4 weeks. We conclude that administration of 6-OHDA may cause severe myocardial damage, and that this process may involve loss of some functional components of the cell membrane.

Adenylyl Cyclases↗
PubMed1988

Cardiomyopathy in a rat model of pheochromocytoma. Morphological and functional alterations.

To investigate the cardiac muscle damage observed in pheochromocytoma, New England Deaconness Hospital rats were implanted subcutaneously with a transplantable pheochromocytoma. The tumor was evident 4 weeks after transplantation. Approximately 5-6 weeks after transplant, systolic blood pressure was significantly increased in tumor-bearing animals (183 +/- 13 vs 119 +/- 7 in controls). At this time a cardiomyopathy with the following features was apparent in the tumor-bearing animals: multifocal lesions of enhanced interstitial and replacement fibrosis; granularity of the cytoplasm and contraction band necrosis; and mixed inflammatory infiltrates. Using a morphological scoring system from 0 (no cardiac damage) to 3 (complete involvement of the ventricular cross section studied), the pheochromocytoma animals had a cardiomyopathy score of 1.8 +/- 0.1, which is significantly greater than that found in age- and sex-matched controls: 0.4 +/- 0.1, p less than .001. A significant increase in the wet heart weights (1.28 +/- 0.07 vs. 1.12 +/- 0.04 in controls) was also observed in these animals, indicating the possibility of cardiac hypertrophy in the pheochromocytoma rats. There was a marked decrease in sensitivity to isoproterenol in isolated, electrically driven left atrial strips from pheochromocytoma rats. Isoproterenol's EC50 increased eightfold from 1.5 +/- 0.6 x 10(-8) M in controls to 1.3 +/- 0.4 x 10(-7) M in left atrial strips from the pheochromocytoma rats. However, there was no difference in maximal contractile response to isoproterenol in either the left atrial strips or in right or left ventricular papillary muscle strips. Also, there was no change in responsiveness of either left atrial or right ventricular muscle strips from pheochromocytoma hearts to contraction induced by 3.75 mM calcium chloride. However, the contractile response to calcium was enhanced in left ventricular papillary muscle from tumor-bearing animals (808 +/- 195 vs 372 +/- 101 mg tension in controls, p less than 0.05). These results demonstrate a catecholamine-induced cardiomyopathy in hearts from pheochromocytoma-bearing rats. Furthermore, the results demonstrate a functional beta-adrenergic receptor desensitization in isolated left atrial strips from tumor-bearing rats, whereas maximal contraction of heart muscle, induced by either isoproterenol or calcium chloride, remains intact.

Animals↗
PubMed1987

Metabolism and electrophysiology in subendocardial Purkinje fibers after infarction.

Subendocardial Purkinje fibers (SEPF) have been implicated in the genesis of fatal arrhythmias that occur 24-48 h after infarction but little is known about the metabolic processes involved. Quantitative microchemical and electrophysiological studies were performed on normal and infarcted hearts removed 24 h after coronary artery occlusion. ATP, ADP, AMP, total adenine nucleotide content, phosphocreatine (PCr), and inorganic phosphate in superficial subendocardial Purkinje fibers from infarct preparations decreased approximately 30% compared with normal preparations. The phosphate potential decreased 45% in the infarct group. Similar changes were observed in adjacent contractile muscle between normals and infarcts. Action potentials of SEPF from infarct hearts had increased automaticity, markedly prolonged action potential durations at 50 and 90% repolarization (APD50 or APD90), but unchanged resting membrane potentials. The decrease in ATP, total adenine nucleotides, and the phosphate potential correlated linearly with APD50 and APD90. No correlation was found between PCr and APD90. This combined biochemical and electrophysiological approach provides a promising new way to further probe the biochemical basis of the abnormal electrical properties of subendocardial Purkinje fibers after myocardial infarction.

Action Potentials↗
PubMed1985

Decreased membrane fluidity and beta-adrenergic responsiveness in atherosclerotic quail.

The effects of increased cholesterol on erythrocyte membrane fluidity and beta-adrenergic function were studied in a quail model of atherosclerosis. Birds fed a cholesterol-supplemented diet developed severe atherosclerosis and hypercholesterolemia after 6 wk. This cholesterol-enriched diet led to a markedly elevated serum cholesterol and a 26% increase in the cholesterol-to-phospholipid ratio in erythrocyte membranes. Electron paramagnetic resonance spectra measured with 5- and 12-doxyl-stearic acid spin-label probes were used to estimate the order of quail erythrocyte membranes. Membrane preparations from cholesterol-fed birds were more highly ordered near the membrane leaflet surface, as well as deeper in the membrane interior, compared with controls. beta-Adrenergic receptor stimulation of adenosine 3',5'-cyclic monophosphate accumulation was blunted in erythrocytes from the hypercholesterolemic quail. There was no change in beta-receptor density or affinity in the cholesterol-enriched membranes. These studies demonstrate that cholesterol incorporation into erythrocyte membranes in vivo is associated with decreased membrane fluidity and decreased beta-adrenergic responsiveness. The atherosclerotic quail may serve as a useful model to further probe the sequelae of hypercholesterolemia on the function of integral membrane proteins.

Animals↗
PubMed1985

Desensitization of alpha-1 adrenergic receptor-mediated vascular smooth muscle contraction.

Desensitization of alpha-1 receptor-mediated smooth muscle contraction was studied in rabbit aorta. Incubation of rabbit aorta ring segments with epinephrine (10(-6) M) for 7 hr resulted in a 10-fold loss in sensitivity of the tissue to alpha-1 adrenergic receptor-mediated contraction with no change in maximal force of contraction. This loss in sensitivity was specific for alpha-1 receptor-mediated contraction because responses to histamine and serotonin were unchanged in these aortas. Conversely, prolonged exposure of vessels to histamine (10(-5) M) led to desensitization of histamine-mediated contraction without altering responses to alpha-1 receptor stimulation. Using [125I] BE2254, a potent alpha-1 receptor antagonist, the loss in sensitivity to catecholamines was found not to be mediated by down-regulation of alpha-1 receptors nor by a loss in their affinity for epinephrine. However, desensitization was associated with a blunting of alpha-1 receptor stimulation of phosphatidylinositol turnover. These results suggest that desensitization of alpha-1 receptor-mediated contraction in rabbit aorta does not appear to be mediated by changes in receptor number or affinity but may involve alterations in receptor coupling.

Adenylyl Cyclases↗