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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent evidence suggests that oxygen free radicals generated during ischemia or reperfusion may contribute to myocardial dysfunction after brief coronary occlusion ("myocardial stunning"). Because neutrophil leukocytes represent a potential source of oxygen radicals, the concept of whether depletion of neutrophils could attenuate myocardial stunning after 10 min of ischemia was examined. In 16 anesthetized dogs, the left anterior descending coronary artery was perfused by an extracorporeal circuit, either with (n = 8) or without (n = 8) neutrophil filters in the perfusion line. The group with filters had near total absence of neutrophils in blood perfusing the left anterior descending coronary artery territory (16 +/- 8 versus 1,826 +/- 399/microliters in the control group). Systolic myocardial shortening and end-systolic pressure-segment length relations were recorded during rest conditions and during incremental intracoronary infusion of dobutamine (5 to 15 micrograms/min) before and after 10 min of coronary flow occlusion. Before coronary occlusion, systolic myocardial shortening at rest was similar in control (15.4 +/- 1.7%) and neutropenic (12.4 +/- 2.2%) groups. Dobutamine (15 micrograms/min) resulted in increased shortening in both control (18.2 +/- 1.4%, p less than 0.01) and neutropenic (15.8 +/- 1.5%, p less than 0.05) groups and in a leftward shift of the end-systolic pressure-length relation. During coronary occlusion, collateral coronary flow to the left anterior descending coronary artery territory was not significantly different in the control (0.10 +/- 0.03 ml/min per g) and neutropenic (0.18 +/- 0.06 ml/min per g) groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neutrophil depletion does not prevent myocardial dysfunction after brief coronary occlusion. 292 66

We determined the response of the reperfused myocardium to inotropic stimulation with dobutamine hydrochloride. The middle part of the left anterior descending coronary artery (LAD) was occluded in 15 greyhounds for 3 hours. Group 1 (N = 8) was reperfused for 3 hours in the beating, working heart. Group 2 (N = 7) was put on cardiopulmonary bypass (CPB) for 1 hour, received 500 ml of potassium cardioplegia in the aortic root and in the area of ischemia through an internal mammary-LAD graft, and the LAD was reperfused off CPB for 3 hours. After 3 hours of reperfusion, dobutamine was given at 10 micrograms/kg/min for 20 minutes. Regional myocardial function was determined with subendocardial ultrasonic crystals in the area of ischemia and in the base of the heart; segmental contractility was determined from the ratio of peak left ventricular pressure to end-systolic segment length; and global contractility was determined by the slope of the ventricular pressure wave at a developed pressure of 40 mm Hg. Measurements were made prior to LAD occlusion (control), at the end of 3 hours of reperfusion (6 hours from the beginning of occlusion), and after 20 minutes of dobutamine infusion. Dobutamine infusion improved segmental function in all animals compared with 3 hours of reperfusion. The study shows that the reperfused myocardium responds favorably to inotropic stimulation after 3 hours of occlusion and 3 hours of reperfusion, and that the contractile response both to reperfusion and to inotropic stimulation is greatly affected by the method of reperfusion.
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PMID:Inotropic response of the salvaged myocardium after acute coronary occlusion. 394 33

The effects of isoproterenol, norepinephrine, dobutamine, exercise, and nitroglycerin on left ventricular diameter, pressure, velocity of shortening, dP/dt, dP/dt/P, arterial pressure, left circumflex coronary blood flow, and coronary vascular resistance were examined in healthy conscious dogs with normal coronary perfusion and in the same animals after moderate global ischemia had been induced by partial occlusion of the left main coronary artery. In the normal nonischemic heart, all interventions improved left ventricular performance, as evidenced by increases in dP/dt/P and velocity at the same or lower left ventricular end-diastolic diameter. Interventions, which in the normal heart caused large increases in heart rate and myocardial contractility, e.g. isoproterenol and exercise, or which decreased coronary perfusion pressure, e.g. nitroglycerin or isoproterenol, elicited paradoxical responses in moderate global ischemia, i.e., left ventricular enddiastolic diameter and pressure rose, and dP/dt/P and velocity fell substantially. On the other hand, norepinephrine, which increased coronary perfusion pressure along with myocardial contractility but did not increase heart rate, improved left ventricular function. Dobutamine, which did not alter heart rate or arterial pressure substantially while improving myocardial contractility, produced an intermediate response between that of norepinephrine and isoproterenol in the presence of moderate global myocardial ischemia. Thus, interventions that increase myocardial O(2) requirements, by increasing heart rate and myocardial contractility without augmenting coronary perfusion pressure, can produce a paradoxical depression of ventricular function in the presence of global myocardial ischemia.
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PMID:Effects of catecholamines, exercise, and nitroglycerin on the normal and ischemic myocardium in conscious dogs. 415 59

The purpose of this study was to characterize left ventricular systolic elastances as derived from pressure-segment length and pressure-diameter relationships, and to compare the resulting regional and global elastances to known changes in inotropy. Left ventricular pressure-segment length and pressure-diameter were varied in a series of consecutive beats by means of a volume-loading technique, and both regional and global relationships at 20-msec intervals throughout systole were found to be nonlinear and to exhibit hysteresis. In eight animals, regional hysteresis was present after vagotomy, propranolol (1.0 mg/kg), and atropine (0.1 mg/kg), and was present no matter whether hearts were loaded by volume (45-60 ml/sec) or by pressure (partial aortic occlusion) over a similar range of left ventricular systolic pressures. Elastance was linearly approximated by the slope of the major axis of the hysteresis loops. In each instance, elastance increased to a maximum and then decreased, thus defining end-systole. In seven animals, maximum elastance-length and -diameter were compared before and after treatments with dobutamine (5-13 micrograms/kg per min) and propranolol (6-51 micrograms/kg per min), or after induction of global ischemia. Dobutamine increased maximum elastance-diameter by 37% (P less than 0.01) and maximum elastance-length by 159% (P less than 0.05). Propranolol decreased maximum elastance-diameter by 27% (P less than 0.05) and maximum elastance-length by 6% (P = NS). Global ischemia (50% reduction in coronary flow) did not significantly change either maximum elastance-diameter or -length. However, with ischemia, the diameter intercept of maximum elastance-diameter increased by 24% (P less than 0.025), and the time to maximum elastance-length decreased by 33% (P less than 0.01). Comparing all interventions, the percent changes in maximum elastance-length and -diameter related directly but with a low correlation coefficient (r = 0.49). These differences in regional and global elastance suggest a complex relationship between regional and global myocardial mechanics, and may not necessarily reflect specific changes in contractility.
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PMID:Regional end-systolic pressure-length relationships using a volume-loading technique in the intact pig heart. 646 26

The effect of dobutamine on exercise performance was assessed in 20 patients with ischemic heart disease (CAD) and a positive stress test. These patients had a wide range of resting left ventricular ejection fraction (range 22% to 69%, mean 42%). Each patient entered a double-blind crossover study in which two identical exercise radionuclide ventriculograms were performed in patients on dobutamine, 5 micrograms/kg/min intravenously, or placebo. Dobutamine increased resting left ventricular ejection fraction. Although ejection fraction fell with dobutamine during submaximal exercise, it remained higher than with placebo. At peak exercise, ejection fraction fell to the same level on dobutamine as with placebo. Dobutamine diminished exercise time and time to ischemia while peak pressure-rate product was unchanged. Four of 20 patients developed complex ventricular premature beats, all while on dobutamine. Although useful when administered to resting patients with acute left ventricular failure, dobutamine's effects may be deleterious in exercising patients with chronic ischemic heart disease.
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PMID:The effect of dobutamine on exercise performance in patients with symptomatic ischemic heart disease. 669 Dec 44

Coronary blood flow and myocardial energetics were assessed after the administration of a parenteral inotrope (dobutamine hydrochloride) and an oral vasodilator agent (hydralazine) in 10 patients with nonischemic congestive heart failure. Dobutamine (5 micrograms/kg per min) and hydralazine (1 mg/kg) when group-matched elicited an identical increase in cardiac index and stroke volume index. Both agents augmented coronary blood flow while reducing coronary vascular resistance. Both forms of therapy elicited a significant increase in myocardial oxygen consumption. Dobutamine, demonstrating a balanced effect on the coronary circulation, induced a proportional increase in coronary blood flow and myocardial oxygen consumption, with the arterial-venous oxygen difference across the coronary vascular bed remaining unchanged. Hydralazine enhanced the myocardial oxygen supply versus demand ratio; despite a significant increase in myocardial oxygen consumption, the arterial-venous oxygen difference and the myocardial extraction ratio diminished. Both forms of therapy enhanced cardiac performance without inducing any electrocardiographic or clinical evidence of ischemia. Dobutamine, a positive inotropic agent, elicited a balanced effect on the coronary circulation while hydralazine, a vasodilator agent, induced a greater increase in coronary flow than in myocardial oxygen demand.
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PMID:Dobutamine and hydralazine: comparative influences of positive inotropy and vasodilation on coronary blood flow and myocardial energetics in nonischemic congestive heart failure. 682 60

Cardiovascular effects of S-dobutamine were compared with effects of vehicle and other catecholamines in dogs during and after 3 days of approximately 90% ligation of the left anterior descending coronary artery (LAD). Twenty-four hours after LAD ligation, dogs infused with S-dobutamine (2.5 micrograms/kg/min intravenously, i.v.) maintained systolic blood pressure (SBP 149 +/- 6 mm Hg), diastolic blood pressure (DBP 100 +/- 6 mm Hg), and aortic dP/dt60 (2.8 +/- 0.2 s-1), with no significant changes from preligation values. In comparison, saline-treated dogs showed decreases in arterial BP and contractility: SBP 121 +/- 4 mm Hg; DBP 85 +/- 3 mm Hg; and aortic dP/dt60 was 1.9 +/- 0.1 s-1. S-Dobutamine-infused dogs had a heart rate (HR) of 148 +/- 5 beats/min with 44 +/- 14 beats/min premature ventricular contractions (PVCs), whereas dogs infused with saline, R-dobutamine, dopamine, norepinephrine (NE), or isoproterenol (ISO) all displayed a significantly greater number of PVCs at 24 h. Myocardial necrosis was limited by S-dobutamine treatment (2.5 micrograms/kg/min i.v. for 54 h). As demonstrated by histologic examination, S-dobutamine ameliorated the effects of ischemia as compared with vehicle, R-dobutamine, dopamine, hexamethonium, NE, or ISO. Myocardial tissue electrolytes, quantified 72 h after LAD ligation, were maintained by S-dobutamine-infused dogs in all sections of left ventricle (LV); but in saline-treated dogs, Ca2+ increased eightfold, Na+ increased twofold, and both K+ and Mg2+ decreased 50% in tissue "at risk" as compared with tissues "not at risk." Coronary nutrient blood flow (CNBF) to myocardial capillary vessels was calculated by radiolabeled microspheres 2 h after LAD ligation. As compared with CNBF in untreated hearts, endocardial CNBF in hearts receiving S-dobutamine (5 micrograms/kg/min i.v.) increased from 26 +/- 8 to 49 +/- 15 ml/min/100 g in tissue at risk, from 102 +/- 26 to 217 +/- 50 in "border zone," and from 133 +/- 13 to 215 +/- 41 in tissue not at risk. CNBF values in animals receiving vehicle infusion were not significantly different from CNBF values measured after ligation only. The S-enantiomer of dobutamine, infused in dogs for 54 h after coronary artery ligation, maintained cardiac performance, electrolyte balance, and myocardial cellular viability and reduced incidences of arrhythmias through its ability to increase CNBF without increasing HR.
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PMID:Effects of S-dobutamine on ischemic myocardium caused by coronary artery narrowing. 752 92

Our aim was to verify whether the sensitivity of pharmachological stress echocardiography for multivessel disease after acute myocardial infarction may be improved by a more aggressive protocol, i.e. not considering the appearance of the first wall motion abnormality as the absolute end-point if it occurs in the infarcted area without clinical or instrumental markers of extensive ischemia or left ventricular dysfunction. One-hundred twenty-one consecutive patients (age 32-71 years) prospectively underwent dobutamine-atropine stress echo (dobutamine infusion up to 40 micrograms/kg/min with additional atropine 1 mg) 11.8 +/- 4.8 days after uncomplicated myocardial infarction and coronary angiography within 6 weeks. Criteria for stopping the test were: significant ST depression or elevation, typical chest pain, major arrhythmias and left ventricular dysfunction. The test was considered as positive if a deterioration of basal wall motion pattern was observed: it was defined homozonally positive (the deterioration occurred in the myocardial area fed by the culprit vessel) or heterozonally positive (the deterioration occurred in a different vascular area). A coronary stenosis > 70% of vessel lumen was defined as critical. Thirty-four patients showed a negative test result. Among the 87 patients with positive test, 65 had no further wall motion deterioration from the first-induced wall motion abnormality (WMA) to peak test (Group A), whereas nine patients showed further homozonal (Group B) and 13 further heterozonal (Group C) asynergies. Sensitivity, specificity and accuracy of dobutamine stress echocardiography for multivessel disease were, respectively, 63%, 96% and 82% using the first-induced wall motion abnormality as test end-point, whilst they were 84% (P < 0.01), 93% and 89% according to the aggressive approach previously described. Dobutamine stress time of patients with multivessel disease was higher in Groups B and C (13.1 +/- 3.6 min) than in Group A (9.8 +/- 3.7 min, P < 0.01) and, finally, the mean obstruction of non-culprit vessel was higher in Group A (62.2%) than in Group C (47.4%, P < 0.05). No major complications were found. We conclude that the sensitivity of dobutamine stress echocardiography for multivessel disease following recent myocardial infarction is critically dependent on the test end-point. It may be improved by a more aggressive approach capable to identify less severe heterozonal coronary lesions.
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PMID:Dobutamine stress echocardiography for the identification of multivessel coronary artery disease after uncomplicated myocardial infarction: the importance of test end-point. 755 64

The ability of dobutamine to precondition the isolated rat heart against postischemic contractile dysfunction was assessed. Hearts were perfused with varying concentrations of dobutamine for 5 min followed by a 5 min "washout" period and 30 min of global ischemia. The hearts were reperfused for 30 min to assess postischemic function. Dobutamine improved postischemic developed pressure, +dp/dt, heart rate x developed pressure, end diastolic pressure, and coronary flow in a concentration-dependent manner. The concentration of dobutamine showing the maximum protective effect was 10(-6)M. Propranolol administered with dobutamine significantly attenuated the protective effect. The results indicate that transient treatment with dobutamine can precondition the rat heart against ischemia/reperfusion injury. The mechanism of protection appears to involve beta-adrenergic stimulation.
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PMID:Preconditioning with dobutamine in the isolated rat heart. 760 97

Dobutamine stress echocardiography (DSE) was performed after coronary angiography to evaluate the need to perform percutaneous transluminal coronary angioplasty (PTCA) for 46 stenoses of moderate severity (50% to 80%) in 46 patients. Patients were divided into 2 groups according to the DSE results in the distribution of the coronary artery with the lesion of moderate severity: group I (n = 32) were those without inducible myocardial ischemia; PTCA was not performed. Group II (n = 14) were those who exhibited myocardial ischemia; PTCA was performed in 12. The 2 groups were comparable in terms of clinical characteristics. Follow-up DSE was performed < or = 48 hours after PTCA, at 3 months, and 6 to 12 months after the first DSE. In group I at 3 months, DSE results were still negative in the distribution of the vessel with the moderately severe lesion in 24 patients; only 1 patient had a positive result, and 8 patients who refused DSE remained clinically stable. At 6 to 12 months (mean 7 +/- 2), 26 patients had negative study results; 3 patients who refused follow-up DSE remained clinically stable. In group II, 12 of 14 patients with inducible ischemia on the initial DSE underwent PTCA. Early follow-up DSE (< or = 48 hours) was negative in 7, and 4 had persistent inducible wall motion abnormalities in the myocardium subtended by the coronary artery in which the PTCA had been performed; 1 study was not performed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Usefulness of dobutamine stress echocardiography for the prospective identification of the physiologic significance of coronary narrowings of moderate severity in patients undergoing evaluation for percutaneous transluminal coronary angioplasty. 761 17


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