摘要:

ABSTRACTTo examine the relationship between the defibrillation threshold and the strength of shocks that induce ventricular fibrillation during the vulnerable period, we determined the defibrillation threshold in 22 open-chest dogs using epicardial defibrillation electrodes with the cathode at the ventricular apex and the anode at the right atrium. We also determined whether there was an upper limit of shock strength that induces fibrillation in the vulnerable period by giving shocks of various energy through these same electrodes during the repolarization phase of paced rhythm. The above determinations were also made with the anode at the ventricular apex and the cathode at the right atrium in eight of the dogs and with the cathode at the ventricular apex and the anode at the left atrium in another eight of the dogs. In all dogs for all electrode configurations, there was an upper limit to the shock strength that induced ventricular fibrillation during the vulnerable period. Depending on the electrode combination, this upper limit of ventricular vulnerability either was not significantly different from or was slightly lower than the defibrillation threshold. The correlation coefficient between the two was highly significant for all three electrode configurations. These results support the hypothesis that successful defibrillation with epicardial electrodes requires a shock strength that reaches or exceeds the upper limit of ventricular vulnerability and that shocks slightly lower than the defibrillation threshold fail because they reinitiate ventricular fibrillation by stimulating portions of the myocardium during their vulnerable period.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTAblation of atrioventricular conduction is now widely accepted in the management of supraventricular arrhythmias. Reports of high temperatures, high pressures, and gas production suggest that there may be adverse effects on the blood, the electrode, and the cardiovascular system. In this investigation, using samples of fresh, heparinized pig blood, we measured hemolytic damage, the liberated gas volume and composition, and electrode erosion associated with high-energy electrical ablation. The blood was tested in a 10 liter tank at room temperature. Impulses of 10 to 400 J were applied to new USCI No. 6F bipolar pacing electrodes using both positive and negative polarities. Voltage and current waveforms were recorded. The volume of gas liberated with cathodal electrodes was 0.50,ul/J up to 50 J and 0.29 gl/J above 100 J. It was composed predominantly of hydrogen and nitrogen, with carbon dioxide and oxygen. With positive electrodes, the gas volume was linearly related to energy at 4.34 gVIJ up to 200 J and also contained carbon monoxide. The hemolysis was directly proportional to impulse energy for both cathodal and anodal electrodes, being 1.37 gl/J and 4.48 ul/J, respectively. Electrode erosion was substantial but clinically acceptable. We conclude that there are marked differences in the energy conversion processes and, where the same energy can achieve a comparable clinical effectiveness, there are advantages in using a cathodal electrode polarity. It is also advisable to use lower energies.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTWe studied the effect of an isolated increase in preload on isovolumetric relaxation in the intact dog heart and isometric relaxation in isolated cardiac muscle (dog and rat) preparations. In eight anesthetized dogs, 8 to 12 ml of blood was infused into the left ventricle during a single diastole. The exponential time constant (T) of isovolumetric relaxation was measured in single-beat experiments in which the left ventricular systolic pressure increased (112 ± 2 to 128 ± 3 mm Hg; p < .05, n = 62). In a second series of experiments, left ventricular systolic pressure was held constant (109 ± 2 to 107 + 2 mm Hg; p = NS, n = 23) by simultaneous ventricular infusion and aortic unloading. In the first protocol, T increased from 28.0 ± 0.4 to 30.7 ± 0.4 msec (p < .05), whereas in the second protocol (constant systolic pressure) there was no change in T. The time course of isometric relaxation was also studied in six rat left ventricular papillary muscles and four dog right ventricular trabecular muscles. Preload was varied from 30% to 100% of the peak of the isometric length-tension curve in each muscle. Over this wide range of preload, the isometric force decline recordings were superimposable as long as the comparisons were made at equal levels of total load. Thus an isolated increase in preload does not influence the time course of isovolumetric relaxation.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTWe studied left ventricular performance and contractility after volume loading in lambs at 122 days (group I, n = 9) and 139 days gestational age (group IL, n = 9) and in 8-day-old full-term lambs (group III, n = 7). All were mechanically ventilated; each preterm lamb was treated with surfactant to stabilize pulmonary function and the ductus arteriosus was occluded with an inflated catheter balloon. Cineangiograms, left ventricular and vascular pressures, and the isovolumetric index of contractility, first derivative of left ventricular pressure (dP/dt), were recorded before and after three successive whole blood volume infusions of 10 ml/kg (total 30 ml/kg). The left ventricular enddiastolic volume per kilogram and stroke volume per kilogram increased significantly in all groups after volume infusion; these measurements and heart rate and systemic vascular resistance did not differ significantly between the groups either before or after the infusions. The left ventricular peak dP/dt did not change significantly within the groups during the volume infusions. The left ventricular stroke work was greatest in full-term animals and increased significantly in all groups after volume infusion. Thus, the left ventricles of the preterm and full-term lambs had quantitatively similar Frank-Starling responses and there was no increase in contractility during the infusions of whole blood. However, the left ventricle of the full-term lamb is capable of generating greater stroke work than that of the preterm lamb. These findings may contribute to the understanding of developmental aspects of postnatal circulatory adaptation.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTPulmonary arterial pressure (PAP)-flow coordinates were obtained in 14 anesthetized dogs before and after pulmonary hypertension was induced with autologous blood clots. Cardiac output (CO) was altered by systemic arteriovenous fistulas. The PAP-CO coordinates were always rectilinear.Before emboli, the mean vascular closing or outflow pressure (the pressure intercept of the PAP-CO line) was 8.8 2.1 (SD) mm Hg. Emboli increased PAP (15.1 + 1.6 to 36.5 + 3.5 mm Hg; p < .001) and decreased CO (3.8 + 0.6 to 2.4 + 0.8 liters min-'; p < .001). Incremental resistance (the slope of the PAP-CO line) only increased slightly. On the other hand, the marked increase in PAP was predominantly due to an increase in effective outflow pressure (from 8.8 + 2.1 to 28.6 ± 3.6; p < .001). Hydralazine was administered in a dose sufficient to double CO. This did not affect PAP and caused an inconsistent and small decrease in incremental resistance. However, a consistently significant decrease in effective outflow pressure, averaging 23%, was observed. In this canine preparation of pulmonary hypertension the predominant effect of hydralazine appears to be a decrease in the mean vascular closing or outflow pressure.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTTo explain the progression from infectious viral myocarditis to congestive cardiomyopathy an infection/immune hypothesis has been proposed stating that the primary viral process incites an excessive or disordered immunologic response against the myocardium. To test whether one form of immunosuppressive therapy might ameliorate this process, we used cyclosporine in a murine preparation of infectious myocarditis (encephalomyocarditis [EMC] virus), which has been shown to result in a congestive cardiomyopathy pathologically similar to that seen in man. Eight-week-old male DBA-2 mice were infected with EMC virus and randomized to a treatment or control group. Cyclosporine (25 mg/kg/day) was administered subcutaneously for 3 weeks, starting (1) at 1 week after infection during viral replication, and (2) at 3 weeks after infection, after the period of active viral replication. In mice treated during viral replication there was a significantly higher mortality rate compared with that of control mice (15/21 vs 9/29, p = .01). There was no evident reduction in myocardial pathology (inflammation, necrosis, or calcification) in the treated compared with the control groups. In mice treated after the period of viral replication, there was no improvement in mortality (8/22 vs 2/19, NS) compared with control. Treated mice showed no reduction in myocardial histopathologic lesions. Furthermore, treated mice had significantly greater heart weight/body weight ratios (1.3 ± 0.4% vs 1.0 ± 0.3%, p < .005), lung weight/body weight ratios (1. 1 ± 0.5% vs 0.8 ± 0.3%, p < .05), and liver weight/body weight ratios (6.0 ± 0.8% vs 5.4 ± 0.6%, p < .005) than control mice, suggesting more severe myocardial failure. Thus, the use of immunosuppressive therapy with cyclosporine in this murine preparation of acute viral myocarditis was associated with greater mortality when administered early in the illness, and greater myocardial failure when administered during the early recovery period, without evident reduction in pathologic indexes of myocardial injury to suggest possible longer term benefit. Clinical trials of cyclosporine therapy for inflammatory myocarditis secondary to an acute viral infection should be carried out with great caution and only in the setting of a carefully controlled clinical trial.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTSuperoxide dismutase (SOD) and catalase (CAT), enzymes that degrade superoxide anion and hydrogen peroxide, respectively, reduce size of infarction in anesthetized, open-chest dogs subjected to coronary occlusion followed by reperfusion. To evaluate potential protective effects of these enzymes in conscious animals, three groups of dogs were instrumented at sterile surgery with a hydraulic occluder on the left circumflex (LCX) coronary artery, sonomicrometers to measure regional wall thickness, and catheters to monitor arterial and left ventricular pressures. Ten to 14 days after surgery, the animals were sedated with morphine sulfate (0.5 mg/kg). The LCX artery was occluded for 3 hr by inflation of the hydraulic cuff. Infusions of SOD (n = 7), CAT (n = 6), or saline (control group, n = 7) were begun 15 min before reperfusion and lasted for 45 min of reperfusion. The doses of SOD and CAT were 5 mg/kg, dissolved in 60 ml of saline, and infused at a rate of 1 ml/min. Myocardial blood flow was measured with tracer-labeled microspheres (15 ±m diameter) before occlusion, after 5 to 10 min of occlusion, after 150 min of occlusion, and 5 to 10 min after reperfusion. Size of infarction was measured 24 hr later by dual-perfusion staining with Evans blue and triphenyl tetrazolium. Size of infarction (expressed as a percentage of area at risk) did not differ significantly among the three groups: control, 32 ± 17% (mean ± SD); SOD, 38 ± 17%; CAT, 27± 17%. Hemodynamic parameters and myocardial blood flows (measured before infusion of any agents) were not significantly different among the three groups. Serum SOD levels in SOD-treated dogs were 19 ± 2 μg/ml at the onset of reperfusion and 29 ± 3 μg/ml at the end of the infusion. Blood assays collected after infusion showed a monoexponential decay of SOD levels with a half-life of 22 ± 6 min. We conclude that myocardial protection by SOD or CAT is model dependent. In conscious dogs subjected to 3 hr of coronary occlusion followed by reperfusion, SOD and CAT failed to alter size of infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

ABSTRACTReperfusion of the previously ischemic myocardium is associated with the production of oxygen free radicals and their metabolites, which contribute to the ultimate extent of irreversible myocardial injury. The relative importance of polymorphonuclear leukocytes vs intracellular-derived oxygen metabolites has remained uncertain. We evaluated the effectiveness of a free-radical scavenger, N-2-mercaptopropionyl glycine (MPG), in limiting infarct size after ischemia/reperfusion in dogs that were depleted of neutrophils with specific antisera. Twenty-four urethane-anesthetized open-chest dogs were subjected to 90 min of ischemia by occlusion of the left circumflex coronary artery followed by 6 hr of reperfusion. Dogs were randomly assigned to receive nonimmune serum, neutrophil antiserum, or neutrophil antiserum plus MPG (20 mg/kg intra-atrially 15 min before reperfusion was initiated and for 45 min after reperfusion). Infarct size, as a percent of the area at risk, was reduced by 33% in the neutrophil antiserum group as compared with the nonimmune group (30.7 ± 2.7% vs 45.6 ± 3.7%, p < .01). The combined administration of neutrophil antiserum plus MPG reduced the size of infarction by 63% of the area at risk compared with that in the nonimmune group (17.0 ± 2.7% vs 45.6 ± 3.7%, p < .01). The reduction in infarct size with neutrophil antiserum plus MPG was significantly greater than that with the neutrophil antiserum alone (p < .01). The areas at risk did not differ among the groups. Myocardial protection could not be explained on the basis of hemodynamic differences. The observation that MPG enhances the protective effects of neutrophil depletion suggests that both extramyocardial- and intramyocardial-derived oxygen free radicals contribute significantly to reperfusion- induced myocardial injury.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID