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At least 199 records · Page 11Linked to original sources
PubMed1987

Haemodynamic dose-response actions of cicloprolol in left ventricular dysfunction due to ischaemic heart disease.

Cicloprolol is a cardioselective beta-1 partial agonist; its haemodynamic and radionuclide (nuclear stethoscope) effects were determined in 22 patients with impaired left ventricular function due to coronary artery disease. Following a 20 min stable control period, the effects of four doses of cicloprolol (0.025, 0.025, 0.05 and 0.1 mg/kg at 10 min intervals) were measured at rest 5-10 min after each intravenous injection. The effects of the cumulative 0.2 mg/kg dosage were assessed during supine bicycle exercise and compared with a control exercise period. At rest there were significant increases in systolic arterial without change in mean blood pressure. The heart rate and cardiac index were unchanged. There was a significant increase in left ventricular ejection fraction with a reduction in filling pressure and volume. Patients with resting heart rate below 75 beats/min and with ejection fraction greater than 35% showed the greatest improvement. During supine bicycle exercise, ejection fraction was increased compared to control (31 +/- 2 to 36 +/- 2; P less than 0.01), cardiac volume reduced and exercise tachycardia attenuated. These data suggest that cicloprolol may be of value where beta-blockade is considered in the presence of underlying left ventricular dysfunction due to ischaemic heart disease.

Adrenergic beta-Antagonists↗
PubMed1989

Hemodynamic effects of intravenous pimobendan in patients with left ventricular dysfunction.

Sequential hemodynamic effects of intravenous pimobendan (UD-CG 115 BS), a novel compound with positive inotropic and vasodilating properties, were investigated during left heart catheterization in nine patients with left ventricular dysfunction (ejection fraction less than or equal to 40%) and moderate congestive heart failure (NYHA classes II and III). Studies were carried out before (C) and for 60 min after intravenous administration of 5 mg of pimobendan over 1 min. Pimobendan immediately and progressively reduced systemic resistance [16 and 28% at 10 and 60 min postdrug, respectively (p less than 0.05 vs. C)] and left ventricular end diastolic pressure [from 24 +/- 3 (C) to 12 +/- 3 mm Hg at 60 min, p less than 0.001)]. Cardiac output gradually increased by 24%, but stroke volume did not, due to an equally progressive 14% rise in heart rate, whereas stroke work increased by 21% (all p less than 0.05 vs. C). Both contractility and relaxation, measured at fixed heart rates, significantly improved by 30 and 20%, respectively, at 50 min postdrug. Thus, pimobendan has immediate and prolonged arterial vasodilating effects, together with positive inotropic and lusitropic properties, resulting in an early but sustained improvement of left ventricular pump function and filling pressures.

Aged↗
PubMed1988

Hemodynamic comparison of dopexamine hydrochloride and dopamine in ischemic left ventricular dysfunction.

The hemodynamic dose-response effects of intravenous dopexamine hydrochloride (0.5 to 2.0 micrograms/kg/min) have been compared with dopamine (2.5 to 10 micrograms/kg/min) in 12 patients with ischemic left ventricular dysfunction in an open randomized crossover study. Both drugs increased cardiac output and decreased systemic vascular resistance. Dopexamine hydrochloride appeared to increase heart rate more than dopamine although this did not reach statistical significance. Dopexamine hydrochloride produced small increases in systolic and decreases in diastolic blood pressure, whereas dopamine had a biphasic effect resulting in a decrease in mean blood pressure at low doses and an increase at the highest dose studied. With increasing dosage, there was a trend toward more vasodilator activity with dopexamine hydrochloride than with dopamine. Dopexamine hydrochloride produced fewer adverse effects than dopamine.

Adult↗
PubMed1984

Vasodilator therapy in children: acute and chronic effects in children with left ventricular dysfunction or mitral regurgitation.

To determine the acute and chronic effects of vasodilator therapy in children, vasodilator therapy was evaluated in 13 children (aged 0.2 to 14.5 years) with severe left ventricular dysfunction or mitral regurgitation. In seven children, nitroprusside increased cardiac index by an average of 33% (P less than .01) and increased stroke index by 29% (P less than .01). In eight children, hydralazine caused a 31% increase in cardiac index (P less than .01) and a 27% increase in stroke index (P less than .02). Ten children received chronic oral vasodilator therapy and were followed for 5.7 +/- 1.4 (SEM) months. Early clinical improvement was observed in every child. Symptoms of heart failure diminished in all, and five children became entirely asymptomatic. A significant (P less than .05) improvement was noted in growth velocity, respiratory rate, heart size, and incidence of gallop rhythm after 1 month of therapy. The duration of the beneficial response to vasodilator therapy varied considerably, however, and significant improvement for the group was not found after 1 month. Four children had sustained clinical improvement for 6 months or longer, but the others experienced recurrent heart failure within 1 to 4 months.

Adolescent↗
PubMed1992

Effect of diltiazem on norepinephrine-induced acute left ventricular dysfunction.

The present study has examined the role of diltiazem as a protective agent in a canine model of norepinephrine cardiotoxicity. Effects of diltiazem, 20 micrograms/kg/min x 5 min pretreatment followed by 10 micrograms/kg/min x 90 min, or saline infusion were examined at baseline and 1 h after infusion of norepinephrine, 4 micrograms/kg/min for 90 min, in closed-chest anesthetized dogs. Left ventricular function was assessed by equilibrium radionuclide angiogram and two-dimensional echocardiogram. In 7 saline experiments, hypotension and increased heart rate were observed at 1 h post infusion. In the diltiazem-treated group (n = 7), mean arterial pressure and heart rate were unchanged. In the saline group, left ventricular ejection fraction fell from 0.50 +/- 0.04 to 0.28 +/- 0.04. Left ventricular ejection fraction was unchanged in the diltiazem-treated group: 0.52 +/- 0.03 to 0.55 +/- 0.07. Left ventricular end-diastolic volume was increased at 1 h post infusion in saline controls but not in the diltiazem-treated group. Measurement of fractional shortening from two-dimensional echocardiograms also indicated left ventricular dysfunction in the saline but not diltiazem-treated groups. Left ventricular end-systolic wall stress following norepinephrine infusion was significantly increased in the saline but not diltiazem-treated groups: 122.7 +/- 18.7 vs 67.6 +/- 19.7 g/cm2, respectively. In dogs receiving saline without norepinephrine infusion, no significant changes occurred over the course of the experiment. Histologic examination showed mild contraction band necrosis in saline controls but not in sham saline dogs. Diltiazem showed intermediate histologic evidence of injury, which was not further quantified. This study suggests that effects of norepinephrine on left ventricular function in the canine model of norepinephrine cardiotoxicity may be largely due to increased wall stress following a prolonged increase in afterload. Diltiazem pretreatment afforded significant protection of left ventricular function.

Animals↗
PubMed1987

Conventional and high frequency controlled mechanical ventilation in patients with left ventricular dysfunction and pulmonary edema.

The cardiopulmonary effects of conventional controlled mechanical ventilation (CMV), high frequency controlled mechanical ventilation (HFV), and intermittent mandatory ventilation (IMV) were compared in nine patients with ischemic left ventricular dysfunction and pulmonary edema. Ventilatory support during IMV and CMV was adjusted by changing the ventilator rate while tidal volume was maintained at 12 ml/kg. HFV was produced at a frequency of 100 cycles/min and an I/E ratio of 1:2. End-expiratory airway pressure and inspired oxygen concentration were maintained constant. The three ventilatory modes produced similar mean airway, transpulmonary, and intra-thoracic pressures. Mechanical control of respiration required hyperventilation during both CMV and HFV. Arterial blood oxygenation, heart rate, vascular pressures, cardiac output, and myocardial ischemia were unaffected by the changes in ventilation. Decreased arteriovenous oxygen content difference (p less than 0.05) and increased mixed venous oxygen content (p less than 0.05) suggested improved systemic blood flow during IMV. Controlled ventilation by conventional means or with a high frequency technique had no detectable advantage over partial ventilatory support with IMV during cardiopulmonary failure stabilized with vasoactive therapy and continuous positive airway pressure.

Aged↗
PubMed1991

Electrophysiologic mechanisms for ventricular arrhythmias in left ventricular dysfunction: electrolytes, catecholamines and drugs.

Cardiac arrhythmias are generated as the result of disorders of automaticity or of impulse conduction. Regardless of the mechanism, calcium is likely to be involved, although calcium antagonists are rarely useful antiarrhythmics in ventricular arrhythmias. Myocardial cells that do not ordinarily initiate action potentials may do so when they are partially depolarized, giving rise to an ectopic focus. Early afterdepolarizations (EADs) are also induced in cardiac cells by partial depolarization, whereas delayed afterdepolarizations (DADs) are induced by Ca++ overloading. EADs may be the initiating mechanism of torsade de pointes, a complication of QT prolongation associated with quinidine therapy. Both in the animal model and in humans, treatment with magnesium, isoproterenol, or pacing, all of which suppress EADs, will also suppress torsade de pointes. Ventricular tachycardia is a manifestation of ordered re-entry, and may be exacerbated by antiarrhythmics, especially class 1c drugs. In the individual patient, prediction of proarrhythmia is not possible. The risk of proarrhythmia is increased in patients with episodes of sustained ventricular tachycardia or with significant left ventricular dysfunction.

Anti-Arrhythmia Agents↗
PubMed1992

Reversible and irreversible left ventricular dysfunction after acute myocardial infarction.

Left ventricular function after acute myocardial infarction depends on several mechanisms leading to left ventricular remodeling: (a) infarct size and healing and (b) adaptive changes involving both the dysfunctioning but viable myocardium (hibernating and stunned myocardium) and the nonischemic myocardium. The prognosis after acute myocardial infarction is strongly related to regional and global left ventricular function and the loss of dysfunctioning viable myocardium is a main factor in the worsening in left ventricular function in survivors of the acute phase. Thus, medical strategies should exert their beneficial effect on the "mechanical instability" of ventricular myocardium by saving the viable myocardium. beta-Blocker therapy has been shown to be effective in improving the prognosis via anti-ischemic and antiarrhythmic actions. The combination of metoprolol and nisoldipine seems to be able to preserve the contractile function of viable myocardium in the first 6 months after acute myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1991

Coronary sinus occlusion: effect on ischemic left ventricular dysfunction and reactive hyperemia.

Pressure-controlled intermittent coronary sinus occlusion (PICSO) has been shown to reduce experimental infarct size. To examine the role of PICSO in limiting the consequences of brief ischemia on left ventricular function, we studied the effect of PICSO in nine open-chest anesthetized dogs. PICSO was performed using a pump-inflated, balloon-tipped catheter in the coronary sinus until coronary sinus occlusion pressure reached a plateau (10 +/- 3 seconds). The balloon was then rapidly deflated (2 seconds) and the cycle was repeated. Regional left ventricular function in the ischemic zone was assessed by sonomicrometry. Coronary blood flow was measured with a flow probe around the left anterior descending artery (LAD) proximal to an occluding suture. Measurements were obtained at baseline, during a 3-minute LAD occlusion, and for 10 minutes of reperfusion. In an additional five dogs, this sequence was repeated during an infusion of adenosine at a dose that abolished reactive hyperemia following LAD occlusion. The addition of PICSO beginning 15 minutes prior to ischemia and continuing throughout LAD occlusion and reperfusion did not prevent, reduce, or shorten ischemic left ventricular dysfunction. PICSO uniformly blunted reactive hyperemia during reperfusion. However, PICSO also reduced coronary blood flow during maximal vasodilatation achieved by adenosine infusion prior to LAD occlusion. Therefore, it is likely that PICSO decreases reactive hyperemia due to mechanical factors arising from venous engorgement rather than by reducing the ischemic stimulus causing vasodilation.

Animals↗
PubMed1989

Nursing implication for pulmonary artery balloon counterpulsation: a treatment for right ventricular dysfunction after cardiac surgery.

PPRVD is a phenomenon frequently observed in the operating room. Its development can be attributed to a single or many factors associated with cardiac operation. Namely, its presence is precipated by injury to the RV myocardium or changes in the normal hemodynamic functions of the RV. While PPRVD occurs in isolation, it is usually seen with concomitant LV dysfunction. When conventional medical management of LV dysfunction does not improve yet unmasks RV dysfunction, some type of ventricular assist device to support RV dysfunction may be needed to wean patients from cardiopulmonary bypass such as PABC. PABC has been demonstrated to be useful in the management of mild to moderate PPRVD and weaning from CPB. Severe PPRVD has not been demonstrated to benefit from PABC. The major concern in managing PPRVD is the lack of quantifiable criteria for determining levels of RV injury. Research is continuing in this area. Likewise, investigations are under way to develop a transvenous PABC catheter. This catheter would allow for increased PABC use as it would not require surgical placement or removal. The present PABC model could potentially be used in any hospital that uses conventional intra-aortic balloon counterpulsation. The patient presented in this case was cared for in a 350-bed community hospital in the Northeast section of the United States. A PABC patient can present a unique nursing challenge. It is hoped that this article will assist nurses in the future management of these patients.

Aged↗
PubMed1989

Emergency coronary angioplasty in patients with severe left ventricular dysfunction or cardiogenic shock after acute myocardial infarction.

Emergency percutaneous transluminal coronary angioplasty (PTCA) was performed during an acute myocardial infarction (AMI) after either systemic or intracoronary thrombolytic therapy in six patients with severe ischaemic left ventricular dysfunction or cardiogenic shock, among 37 patients (17%) who were treated with PTCA during AMI over a 13-month period. Thrombolytic therapy with streptokinase (1.5 x 10 Units) was initiated after a mean (+/- SD) time delay of 5.5 +/- 1.3 h from the onset of symptoms. The infarct-related artery was found to be occluded (TIMI grade 0-1) in three patients and partially reperfused (TIMI grade 2) in the remaining patients at baseline coronary angiography. Intracoronary administration of urokinase (100-200,000 Units) was ineffective in those patients failing systemic thrombolysis and resulted in only a slight increase of residual lumen in three patients. The coronary artery could be opened by a guidewire mechanical technique in patients with persistent coronary artery occlusion and coronary dilation could be done in all patients. The mean percentage diameter stenosis of the infarct-related vessel was reduced from 98.8 +/- 2% to 27 +/- 11% (P less than 0.005). After the procedure, left ventricular ejection fraction increased from 27 +/- 8% to 41 +/- 7% (P less than 0.02), systemic blood pressure and cardiac index increased respectively from 86 +/- 10 to 126 +/- 14 mmHg (P less than 0.005) and from 2.2 +/- 0.6 to 3.3 +/- 0.6 (P less than 0.01). Left ventricular end-diastolic pressure decreased from 26 +/- 8 to 18 +/- 3 mmHg (P less than 0.05). Severe mitral regurgitation was relieved in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Value of the handgrip apex cardiography test for detection of early diastolic ventricular dysfunction in patients with angina pectoris].

Left ventricular (LV) diastolic dysfunction is the earliest manifestation of myocardial ischemia. There are no simple stress tests for detecting ischemia by assessing abnormal changes of early (relaxation) and late (end-diastolic compliance) LV diastolic function. This study attempts to establish the diagnostic accuracy of the handgrip-apexcardiographic test (HAT) for detecting exercise-ischemia-induced diastolic dysfunction. Apex- and phonocardiogram were obtained during a 2-min handgrip (40% of maximal voluntary contraction using a balloon dynamometer). Indices of LV diastolic function were provided by relative A-wave to total height (A/H) of ACG, total apexcardiographic relaxation time (TART), TART corrected for heart rate (TARTI), and diastolic amplitude time index (DATI). HAT was performed in 63 patients with typical stable angina pectoris and 202 healthy volunteers. Positivity of HAT is defined by the presence of at least one of the following new criteria: 1) A/H during or after handgrip greater than 21% (= largest individual value in controls), 2) TART during greater than TART before handgrip greater than 143 ms or TARTI during handgrip less than 0.14 (= lowest individual value in controls), and 3) DATI during handgrip less than 0.27. According to this definition, all controls showed a negative HAT (specificity: 100%). By contrast, HAT was positive in 54 out of the 63 angina patients (sensitivity: 86%). These results demonstrate that HAT is a highly sensitive stress test for identifying patients with angina pectoris by assessing LV diastolic abnormalities. Thus, this quick and simple exercise method represents a new aspect in the clinical evaluation of angina patients for the practicing physician.

Adolescent↗
PubMed1987

Sex differences in exercise induced left ventricular dysfunction in patients with syndrome X.

Clinical, electrocardiographic, and scintigraphic data were reviewed from 32 patients (18 men and 14 women) who had syndrome X (chest pain, evidence of ischaemia, and normal coronary arteries without coronary vasospasm). The mean (SD) resting left ventricular ejection fraction, determined by first pass radionuclide angiography was 62.6 (9.2)% and was greater than 50% in all subjects. There was no significant difference between men and women. On exercise, left ventricular ejection fraction decreased significantly to 57.4 (13.0)%. In 17 of 32 subjects there was a fall in left ventricular ejection fraction of greater than 5%, and regional wall motion abnormalities developed in 12 subjects. The fall in left ventricular ejection fraction on exercise was significant in women (from 61.9 (8.5)% at rest to 54.0 (9.8)% on exercise) but not in men (from 63.2 (9.8)% at rest to 60.0 (14.8)% on exercise). Exercise left ventricular ejection fraction fell by greater than 5% in 10 (71%) of 14 women and in seven (39%) of 18 men. Dyskinetic segments developed in eight (57%) of 14 women and only four (22%) of men. Exercise duration in women was significantly shorter than in men (4.1 (1.5) vs 6.6 (2.1) minutes) and was the only one of several clinical and scintigraphic variables that correlated with the change in left ventricular ejection fraction on exercise. In this selected group of subjects with chest pain and angiographically normal coronary arteries, exercise induced left ventricular dysfunction, as shown by a fall in ejection fraction or the development of regional abnormalities, is a common finding. These are more likely to occur in women than men and are associated with a lower exercise capacity. The data suggest that the sex of the patient is important in the interpretation of the non-invasive evaluation of subjects suspected of having syndrome X.

Adult↗
PubMed1984

Left ventricular dysfunction discriminated noninvasively beat by beat.

To discriminate left ventricular (LV) dysfunctional beats noninvasively, simultaneous systolic time intervals (STI), acceleration ballistocardiograms (BCG) and respiratory cycle were recorded in 102 men with no history of cardiac disease and in 20 men with proved myocardial infarction or systemic hypertension. Thirty-six measurements were made on each heartbeat on a maximum of 20 beats per patient. The ratio of preejection period to LV ejection time (ET) varied significantly with the respiratory cycle in normal men, but not in men with proved myocardial infarctions or systemic hypertension. The BCG I-wave amplitude varied significantly with respiration in all 3 groups. Various statistical methods identified 9 primary variables of the 36, which differed significantly in a training group of 275 heartbeats in 19 normal, vs 46 beats in 5 coronary patients. A nonlinear quadratic discriminant function based on these primary variables identified 87% of the heartbeats as "normal" in the normal men and 98% as "coronary" in the coronary men. A test group of normal men older than 40 years showed 89% of 97 heartbeats "normal" and in hypertensive men 67% of 85 beats "normal." Comparison by patients showed a range of "coronary" beats in the training normal group from 0 to 50%, the older normal group 0 to 33%, and in the hypertensive patients 0 to 88%. The appropriate use of quadratic discriminant analysis to multivariable data may yield information not otherwise seen. A beat-by-beat identification of dysfunctional beats at rest may lead to a sensitive index that is prognostically useful.

Adult↗
PubMedDate not supplied

Hemodynamic and myocardial metabolic effects of the beta-agonist prenalterol in ischemic left ventricular dysfunction.

Hemodynamic and myocardial metabolic parameters in ischemic left ventricular (LV) dysfunction were evaluated in response to the beta-agonist prenalterol. Twenty micrograms/kg intravenous prenalterol increased resting heart rate and cardiac output and decreased LV filling pressure, systemic vascular resistance, and pulmonary artery pressure. Resting coronary blood flow and myocardial oxygen consumption increased but net myocardial lactate and oxygen extraction did not change significantly. During pacing induced tachycardia (121 +/- 4 beats/min), prenalterol improved cardiac index and stroke work index; whereas, LV filling pressure, systemic vascular resistance, and pulmonary artery pressure decreased. Coronary blood flow and myocardial oxygen extraction did not change significantly. Net myocardial lactate extraction during pacing decreased insignificantly; one patient developed overt lactate production. Thus, prenalterol improves cardiovascular function at rest and during pacing-induced tachycardia in ischemic LV failure, but at the cost of higher resting myocardial oxygen consumption. The majority of subjects had no adverse metabolic response.

Adrenergic beta-Agonists↗
PubMed1991

Effects of chronic administration of a vasopressin antagonist with combined antivasopressor and antiantidiuretic activities in rats with left ventricular dysfunction.

The present experiments were designed to study the long-term aquaretic effect of [d(CH2)5-D-Tyr(Et)VAVP], an antagonist to arginine vasopressin (AVP) with combined vascular (V1) and renal (V2) receptor inhibiting properties, in rats with left ventricular dysfunction resulting from myocardial infarction (MI). The continuous intravenous infusion of the AVP antagonist (36 micrograms/12 microliters/day) via osmotic minipumps over 11 days resulted in an increase in urine volume and a decrease in urinary osmolality by approximately 10-fold on the first day, but in subsequent days this response decreased in both the post-MI (n = 7) and normal (n = 6) rats. Nevertheless, the daily urine volume remained significantly higher and the urinary osmolality lower in the post-MI rats than in the normal ones throughout the study (p less than 0.05). In two other groups of post-MI (n = 5) and normal (n = 6) rats, intermittent intraperitoneal injections of the AVP antagonist (100 micrograms/kg) every third day resulted in a profound diuresis that was reproducible by each injection and was again significantly greater in the post-MI rats than in the normal rats (p less than 0.05). The cumulative urinary output over the first 10-day period of each treatment was greater with intermittent injections than with continuous infusion in both the post-MI and normal rats, but the difference was significant only in the post-MI rats (398.82 +/- 12.87 ml vs 309.07 +/- 32.44 ml, intermittent vs continuous, respectively, p less than 0.05), even though the cumulative dose of AVP antagonist given intermittently was only about one third of that given continuously.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator.

To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1992

Salicylate reduces ventricular dysfunction and arrhythmias during reperfusion in isolated rat hearts.

Recent studies have shown the ability of salicylic acid (SA) to trap hydroxyl radicals (OH.) generated during reperfusion in ischemic myocardium. Since OH. is implicated in the pathogenesis of reperfusion injury, we examined the effect of SA on reperfusion-induced arrhythmias and postischemic ventricular dysfunction. Isolated rat hearts perfused by the Langendorff technique were preperfused with Krebs-Henseleit buffer containing SA for 10 min. Hearts were then made ischemic for 30 min, followed by 30 min of reperfusion. In a separate group, SA was administered only at the onset of reperfusion. The left ventricular contractile functions, left ventricular developed pressure (LVDP) and its first derivative (LV dP/dt), coronary flow (CF), and creatine kinase (CK) release were determined before and after ischemia. Epicardial electrocardiogram (ECG) was also recorded to analyze the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF). SA improved LVDP, LV dp/dt, and CF recovery and reduced CK release compared to the control group. The incidence of VT and VF during reperfusion was also significantly reduced by SA. Analysis of tissue thiobarbituric acid-reactive products indicates that SA decreased oxidative stress during reperfusion. In conclusion, these results suggest that SA reduces myocardial reperfusion injury and attenuates ventricular arrhythmias by trapping OH. radicals upon reperfusion in isolated rat hearts.

Animals↗