摘要:

To determine the relative contributions of milrinone's positive inotropic and vasodilator actions in patients with severe congestive heart failure, the drug was administered by constant infusion directly into the left main coronary artery of 11 patients with New York Heart Association functional class III or IV heart failure. Intracoronary infusion of milrinone at rates up to 50 μg/min had no effect on mean arterial pressure or systemic vascular resistance but resulted in dose-related increases in peak positive dP/dt (+ 21%), stroke volume index (+ 18%), and stroke work index (+ 21%) and decreases in heart rate (−33%), mean right atrial pressure (− 25%), and left ventricular end-diastolic pressure (− 17%). In eight patients, intravenous administration (75 jig/kg) after the intracoronary infusion resulted in significant decreases in mean arterial pressure (− 14%) and systemic vascular resistance (40%), further increase in stroke volume index compared with intracoronary administration, further decreases in mean right atrial and left ventricular end-diastolic pressures compared intracoronary administration. These data indicate that milrinone exerts both positive inotropic vasodilator actions that contribute significantly to the drug's overall hemodynamic effect.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Previous studies have suggested that (1) nitroglycerin causes vasodilatation by interacting with sulfhydryl groups in vascular smooth muscle, thereby activating guanylate cyclase and increasing the intracellular concentration of cyclic GMP, and (2) N-acetylcysteine, a source of sulfhydryl groups, potentiates the peripheral vasodilatory effect of nitroglycerin. This study was performed to explore the influence of N-acetylcysteine on nitroglycerin-induced coronary dilatation. In 18 patients (13 men and five women, 30 to 76 years old), coronary sinus blood flow (by thermodilution) was measured before and during intracoronary administration of nitroglycerin, 25 μg, both before and 5 min after a 15 min intravenous infusion of (1) 5% dextrose in water (n = 8, control) or (2) 100 mg/kg N-acetylcysteine (n = 10). Nitroglycerin caused no change in heart rate or systemic arterial pressure. In the control patients, coronary sinus blood flow behaved similarly during the two injections: it was 134 36 ml/min (mean ± SD) before and 183 + 50 ml/min during injection No. 1 (average increase, 49 25 ml/min; average percent increase, 38 + 21%); and it was 131 ± 34 ml/min before and 178 + 45 ml/min during injection No. 2 (average increase, 47 + 23 ml/min; average percent increase, 37 + 20%) (NS compared with injection 1). In the patients who received N-acetylcysteine, coronary sinus blood flow was 149 + 48 ml/min before and 191 + 54 ml/min during injection 1 (average increase, 42 + 15 ml/min; average percent increase, 30 + 12%) (NS compared with eight control values). After Nacetylcysteine, coronary sinus blood flow was similar before nitroglycerin (145 ± 44 ml/min), but it rose markedly with nitroglycerin (218 + 68 ml/min) (average increase, 73 + 35 ml/min; average percent increase, 50 20%) (p < .01 compared with the values obtained in the same patients during injection 1). Thus, N-acetylcysteine, a source of sulfhydryl groups, potentiates the coronary vasodilative effect of nitroglycerin.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Tocainide was administered to 228 patients referred for treatment of recurrent ventricular tachyarrhythmias that were refractory to therapy with conventional antiarrhythmic drugs. After baseline studies, 1200 to 2400 mg tocainide/day was given for 4 days. Tocainide was effective in 49% of 180 patients evaluated with monitoring and exercise testing and in 35% of 48 patients undergoing electrophysiologic testing. No clinical parameter predicted the response to tocainide, although there was a correlation with the effect of lidocaine. Tocainide was selected for long-term treatment in 73 patients who were followed for an average of 26.4 months (range 1 to 92 months). The incidence of sudden death was 4.3% per year and two patients had nonfatal recurrence of arrhythmia. It is concluded that tocainide is effective and well tolerated during long-term use if therapy is evaluated carefully and is individualized.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Thallium-201 (201T1) uptake and redistribution kinetics were examined in an open-chest canine preparation of occlusion and reperfusion. Seven dogs (group I) underwent 3 hr of sustained occlusion and received 1.5 mCi of 201TI after 40 min of occlusion of the left anterior descending coronary artery (LAD). Group II (n = 18) underwent 60 min of LAD occlusion followed by sudden and total release of the ligature. Group lla (n = 8) received intravenous 201T1 during occlusion of the LAD, whereas group JIb (n 10) received intravenous 201T1 at the time of peak reflow. Group III dogs (n = 26) also underwent 60 min of LAD occlusion that was followed by gradual reflow through a residual critical stenosis. Animals in this group also received 20MT1 either before (Illa; n = 16) or after reflow was established (IlIb; n = 10). In group I, the relative 201T1 gradient (nonischemic minus ischemic activity) decreased from 88 + 8% (mean + SEM) to 59 + 6% during 3 hr of coronary occlusion (p = .034). After rapid and total reperfusion (group lla), this gradient decreased from 71 + 6% during occlusion to 26 + 5% after reflow (p < .001). After slow reperfusion through a residual stenosis (group Illa), the gradient decreased from 81 ± 5% to 31 ± 5% (p < .001) (p = .56 compared with group Ha). In rapidly reperfused dogs receiving intravenous thallium during peak reflow (Ilb), initial 201T1 activity in the ischemic zone was 155 ± 20% of initial normal activity and fell to 93 ± 13% of normal after 2 hr of reperfusion. Similarly, in dogs reperfused slowly through a critical stenosis (IlIb), which received 201T1 during reflow, 201T1 activity soon after reflow was 94 ± 4% of initial normal and decreased to 80 + 6% at 2 hr of reperfusion (p = .10). Histochemical evidence of necrosis was present in the biopsy region in 80% of the 20 dogs subjected to triphenyl tetrazolium chloride (TTC) staining. Microsphere-determined transmural blood flow was similar in all groups during LAD occlusion and final flows after 2 hr were comparable in all subgroups undergoing reflow. Ischemic zone flow (% normal) was significantly higher at the time of 201TI administration in groups Ilb (192 ± 25%) and IfIb (1 10 + 5%), which received 201T1 during reflow, than in groups lla (31 ± 9%) and Illa (22 + 5%), which received 201T1 during occlusion. These differences in flow at the time of administration of 20MT1 explain the different thallium uptake patterns observed. These data suggest that after 1 hr of LAD occlusion there is no difference between rapid reperfusion through a totally patent vessel and slow reperfusion through a critical stenosis with regard to ultimate degree of flow restoration or magnitude of 201T1 redistribution in instances in which 201T1 is given before reflow. With both methods of reperfusion a residual 201T1 gradient is seen. Administration of 201T1 during reflow, however, probably overestimates the degree of myocardial salvage as reflected by final 201T1 uptake values. In dogs rapidly reperfused, a relative "hot spot"' of 201T1 activity was observed in the ischemic zone when 201T1 was administered at peak reflow, despite histochemical evidence of necrosis. These results have clinical implications with respect to the timing of 201T1 administration and interpretation of serial 201T1 scintigrams in patients with acute myocardial infarction undergoing thrombolysis.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We define matching between ventricle and afterload to imply that the ventricle is adapted to its afterload to yield maximum external work output. For the ventricle, this optimal adaption will depend on end-diastolic dimension, heart rate, and contractility. Because contractility is impaired during ventricular failure, we propose that the adaption between ventricle and load is not as good during failure as during normal conditions. According to our definition, this implies that during failure external work output is less than maximum. Ventricle-load matching is then not present, i.e., a mismatch exists between ventricle and load. This hypothesis was tested in a canine preparation in which arterial load of the left ventricle was varied from one beat to the next. Left ventricular depression was induced by injections of 50 gm microspheres into the left coronary bed. We observed left ventricular stroke volume and external work during afterload variations at three different preload levels before and after microembolization. Before embolization the control observations of work and stroke volume were positioned at the apex of parabolas relating work to stroke volume. After embolization, however, control observations fell down along the left limb of the parabolas. These observations were independent of preload. Thus this study, carried out in a preparation with the heart in situ, supports the idea that the normal left ventricle is matched to its load and demonstrates ventricle-load mismatch when the left ventricle is failing.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Recent studies suggest that intracellular Trypanosoma cruzi invasion with release of intracellular myocardial antigens during T. cruzi infection is crucial to the pathogenesis of chronic chagasic myocarditis. However, in areas endemic for Chagas' disease, the incidence of clinical acute chagasic myocarditis has been reported to be low among infected individuals, while the incidence of chronic chagasic myocarditis is relatively high. Thus, either acute chagasic myocarditis rarely complicates T cruzi infection and is not important to the pathogenesis of chronic chagasic myocarditis, or acute chagasic myocarditis rarely impairs left ventricular function and therefore causes no symptoms. To investigate this question we innoculated T. cruzi from a human patient with Chagas' disease into the subconjuntivae of six rhesus monkeys (7.5 x 103 parasites each). Parasitemia was monitored and weekly two-dimensional echocardiograms (for determination of end-diastolic and fractional change in area, EDA and FCA) were obtained to quantify global left ventricular function for 10 weeks. Regional left ventricular function was assessed by visual analysis of two-dimensional echocardiograms. Extent of acute myocarditis was established at autopsy. All monkeys had the Romafna sign and detectable parasitemia in the second week. Parasitemia rose in all by the ninth week (mean = 1.8 x 105 parasites/ml); four monkeys lost weight (mean = − 12%), three died, and three were killed. Twodimensional echocardiographic EDA and FCA remained unchanged from control to the last study within 12 hr of death (EDA = 2.6 + 0.9 to 2.7 + 1.0 Cm2, FCA = 80 + 6.8 to 74 + 7.6%, NS). Furthermore, regional left ventricular function remained unchanged throughout the period of study. At autopsy two monkeys had severe acute myocarditis (one had been killed with no weight loss) with abundant intracellular T. cruzi (one nest of T. cruzi/cm2 of myocardium sectioned). Two had moderate and two mild acute myocarditis. In conclusion, acute chagasic myocarditis may be severe after T. cruzi infection, yet cause no impairment in resting left ventricular function despite intense intracellular T. cruzi invasion.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

A period of drive in the presence of norepinephrine (NE) may be followed by the induction or acceleration of spontaneous activity. Experiments were carried out in sheep cardiac Purkinje fibers to determine whether the effects of NE on automaticity were modified during superfusion with hypoxic glucose-free Tyrode's solution and to assess the possible contribution of a-adrenergic influences on automaticity under these conditions. The following results were obtained: (1) Low concentrations of NE (10 ` and 3 X 10 7M) were able to induce automaticity after a period of drive in normal oxygenated (97% 02, 3% CO2) Tyrode's solution. (2) Superfusion with hypoxic (97% N2, 3% CO2) glucose-free Tyrode's solution enhanced NE-induced automaticity. (3) Practolol, in concentrations able to block the effects of NE in normal oxygenated solution, did not counteract the effects of NE in hypoxic glucose-free solution. (4) Yohimbine, but not prazosin, antagonized the effects of NE in hypoxic glucose-free solution. At the same concentration, yohimbine did not affect transmembrane potentials or automaticity induced by isoproterenol. It is concluded that a-adrenergic responsiveness appears to be enhanced during superfusion in vitro with hypoxic glucose-free solution, and that aadrenoceptors belonging to the a2-subtype in sheep cardiac Purkinje fibers might influence abnormal automaticity, possibly through an effect on oscillatory potentials.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Conduction velocities along longitudinal (vL) and transverse (VT) fiber axes were determined in isolated porcine hearts from subepicardial activation patterns that were produced by local stimulation and measured with a multiterminal electrode. In some of the experiments extracellular [K'] ([K'].) and transmembrane potentials were recorded. During normal perfusion VL and VT were (cm/sec) 50.08 + 2.13, (SE) and 21.08 0.97. After 3 to 5 min of global ischemia, VL and VT decreased to approximately 30 and 13 cm/sec. Before the occurrence of total inexcitability propagation became time dependent (1) 2: 1 block developed and (2) centrifugal spread from the stimulus site was partially blocked at short intervals and was normal at long intervals. This suggested that slowed conduction was dependent on spatial nonuniformities of recovery from excitability. Slowing of conduction during ischemia was not explained by accumulation of [K+], alone, because VL and VT at a given [K+], were lower during ischemia than during perfusion with elevated K'. In hearts perfused at 20 mM [K+]. "'slow responses" were produced by addition of epinephrine (2.5 x 10-5M). Resting membrane potentials of slow responses were significantly lower than of depressed action potentials during ischemia. The values vL and vT of slow responses (10 and 5 cm/sec) were much lower than the lowest values during ischemia (20 and 10 cm/sec). This indicates that slow conduction in ischemia is associated with depressed action potentials initiated by a partially inactivated rapid Na+ inward current. The time dependence of nonuniform propagation and the relatively high conduction velocities explain two major characteristics of reentrant tachycardias in acute ischemia: (l) the large diameters ofreentrant circuits and (2) the beat-to-beat changes in localization of conduction block.

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:1986

数据来源: OVID