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

The antianginal effect of three drugs (isosorbide dinitrate-nifedipine-oxprenolol) and of two drug associations (isosorbide dinitrate-oxprenolol; nifedipine-oxprenolol) was studied in six patients, by means of a bicycle ergometer exercise test. The study was double blind; placebo was also included in the test. Treatments were administered according to the sequence of a 6 X 6 "balanced" latin-square design. After treatment with isosorbide dinitrate and nifedipine a significant delay in the appearance of angina and of signs of electrocardiographic positivity was observed while after treatment with oxprenolol a significant delay was noticed only in the time of appearance of electrocardiographic positivity. On the contrary, placebo did not determine significant changes in the studied parameters. The best results were achieved with the associations oxprenolol-isosorbide dinitrate and oxprenolol-nifedipine. With these treatments, angina appeared during the exercise test in only two patients while the others had to stop the test because of muscular exhaustion; electrocardiographic signs of ischemia did not appear in one patient. The favourable results of the associations oxprenolol-isosorbide dinitrate and oxprenolol-nifedipine can be explained by the pharmacologic effect of these drugs and by their complementary action.
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PMID:[Evaluation and comparison of five antianginal treatments by means of a bicycle ergometer exercise test (author's transl)]. 79 9

Evaluation of the concentration of atrial natriuretic peptide, angiotensin P, renin activity in the blood of the coronary sinus and aorta in 18 patients with IHD and hypertrophy of the left ventricle during development of induced ischemia revealed that in left ventricular hypertrophy secretion of atrial natriuretic peptide by the myocardium is reduced. The level of this reduction depends on the kind of hypertrophy. Dilatation of the left ventricle cavity furthers exhaustion of the secretory function of the ischemic myocardium.
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PMID:[The interrelation of the secretory activity of the myocardium with its hypertrophic characteristics in patients with ischemic heart disease]. 129 16

After 30 s ischemia induced by decapitation, the contents of ATP and phosphocreatine (PC) in mouse brain reduced, while that of lactic acid (LA) increased. When mexiletine (3.1-50 mg.kg-1) was injected ip 30 min before decapitation, the brain ATP and PC reduction, and LA accumulation were both alleviated in a dose-dependent manner. These findings suggested that mexiletine was effective in ameliorating the energy exhaustion in the ischemic brain.
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PMID:[Effect of mexiletine on energy metabolism of ischemic brain in mice]. 145 59

Oxygenated cardioplegic solutions can deliver sufficient oxygen to support aerobic metabolism of heart tissue during cardiac arrest, but little is known about oxygen use after cardioplegic solution infusion. Exhaustion of myocardial oxygen stores after infusion of oxygenated crystalloid cardioplegic solution or Krebs-Henseleit buffer was measured in rat hearts. Since nicotinamide adenine dinucleotide accumulates when mitochondria become anaerobic, the epicardium was monitored during perfusion and ischemia. As ischemia progressed, nicotinamide adenine dinucleotide fluorescence increased, indicating exhaustion of oxygen. After buffer perfusion, at 37 degrees C, 50% of peak fluorescence was seen at 13 +/- 1 seconds and 90% at 37 +/- 3 seconds. Oxygenated cardioplegic solution increased these intervals to 57 +/- 6 and 114 +/- 9 seconds, respectively. Oxygenated cardioplegic solution at 10 degrees C increased the time to 50% fluorescence to 238 +/- 12 seconds and to 90% to 320 +/- 14 seconds. Differences between buffer and cardioplegic solution were less at 10 degrees C. Aerobic metabolism was completely abolished 6 minutes after infusion of 10 degrees C oxygenated cardioplegic solution. Maintenance of continuous aerobic metabolism during surgical cardiac arrest would require frequent administration of oxygenated crystalloid cardioplegic solution.
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PMID:Effects of oxygenated cardioplegic solutions on myocardial aerobic metabolism. 151 53

Clinical heart preservation is currently limited to only 4-6 hr, while the kidney, liver, and pancreas can tolerate 24-48 hr of cold ischemia. A fundamental difference between these organs is that the heart is contractile, containing large quantities of actin and myosin, and is susceptible to contracture-induced injury caused by energy deprivation. We have quantified and correlated the onset of contracture with levels of ATP and glycogen during cold storage in rabbit hearts flushed with UW solution, with and without 1 mM calcium (Ca), or 3 mM iodoacetate (IAA). A fluid-filled left ventricular balloon was used to generate pressure-volume curves (compliance) at 1, 6, 12, 18, and 24 hr of cold storage. Onset of contracture occurred in UW stored hearts at 18 hr, contracture in hearts exposed to Ca occurred between 6 and 12 hr. Compliance was significantly less in hearts exposed to Ca at 12, 18, and 24 hr (P less than .01) than in hearts without Ca. ATP levels were well maintained for up to 18 hr in the hearts preserved in UW solution (78%), but fell more rapidly in the presence of Ca at 12 hr (P less than .005), 18 hr (P less than .005), and 24 hr (P less than .05). In comparison, the ATP supply of the liver and kidney was exhausted by only 4 hr of cold storage. Onset of myocardial contracture correlated with a decrease in ATP to less than 80% of control, and contracture accelerated ATP decline 3-6-fold. IAA caused nearly complete myocardial contracture and ATP depletion within 2 hr. Isolated heart function was 77% and 73% at 6 and 12 hr of storage, but fell to 54% and 42% at 18 and 24 hr, respectively, coinciding with development of contracture. We conclude that ischemic contracture in this model is a major cause of myocardial damage during cold storage, and is accelerated by the presence of Ca. Other organs can be successfully stored despite exhaustion of ATP reserves. Thus successful cold-storage of the heart is highly ATP-dependent. Since cold storage inevitably leads to ATP depletion, extension of myocardial ischemic tolerance will depend on either reversible inhibition of ATP hydrolysis during storage, reversible uncoupling of contracture development from ATP depletion, or maintaining ATP production by continuous hypothermic perfusion.
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PMID:Limitations of heart preservation by cold storage. 173 22

Changes of brain tissue calcium in the focal ischemia model of Wistar rat were investigated by three different methods; atomic absorption spectrophotometer, calcium stain with alizarin red S, and new histochemical method using aequorin, a calcium ion sensitive photoprotein. Tissue pH and tissue ATP were concomitantly investigated by histochemical method. Rat brain was frozen in situ at 15, 60 or 240 minutes after left middle cerebral artery was occluded. Coronal brain sections of 16 microns thickness was made and the brain slices applied for calcium stain and histochemical studies. The residual brain block was applied for atomic absorption spectrophotometric study. Tissue calcium content of left hemisphere increased from 1.34 +/- 0.09 (mean +/- SEM) (n = 7) to 1. 54 +/- 0.16 (n = 12), 2.07 +/- 0.12 (n = 9). 1.69 +/- 0.11 (n = 10) mumol/g wet weight after 15, 60 and 240 minutes respectively. Calcium stain with alizarin red S showed that the increase of calcium was observed in the peripheral part of the ischemic lesion where ATP was left in a spotty fashion, and calcium deposits disappeared with correspondence to exhaustion of ATP. Tissue calcium ion content studied by newly histochemical method, showed heterogeneous change. At an early stage of the ischemia, the increase of tissue calcium ion was shown only in the peripheral part of the ischemic lesion, and it gradually extended to the central part. Calcium ion increased in density in an area corresponding to that of the ATP decrease. Within the area of calcium ion increase, regional differences were noted; a greater increase at the border with the intact area and in the parts where ATP was heterogeneously preserved. In the non-ischemic area close to the ischemic area, where ATP was preserved with mild acidosis, calcium ion decreased more than in the surrounding area where ATP was preserved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in cerebral energy and calcium metabolisms on focal cerebral ischemia]. 179 92

Two hundred and eighteen patients (209 males and 9 females, mean age 57.1 +/- 0.6 years) with I class coronary ischemia were subdivided into two groups of 109 subjects each. Group I received NaCl baths, group II underwater massage-showers. On days 2-3 and 23-24 of treatment all underwent incremental stress testing until exhaustion. In group I, only subjects with moderate maximal muscular power improved their stress endurance. In group II, stress endurance significantly improved in all subjects: all hemodynamic indices (cardiac, output, stroke volume, systemic vascular resistances) showed variations indicative of improved cardiorespiratory function and peripheral blood supply.
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PMID:[Cardiovascular effects of sodium chloride bath and underwater shower in coronary ischemia]. 183 51

The association between pressure overload, left ventricular (LV) hypertrophy and failure, and abnormalities in diastolic function has been described both clinically and experimentally. The mechanisms underlying this association, however, are complex and controversial. Factors that have been implicated include mechanical alterations due to hypertrophy alone, changes in collagen type and content, alterations in beta-adrenergic responsiveness, and chronic myocardial ischemia. Studies in our laboratory have identified limitations in subendocardial flow reserve in compensated LV hypertrophy and near exhaustion in subendocardial reserve in animals with decompensated LV hypertrophy and failure. These abnormalities in coronary reserve are associated with impaired diastolic function, particularly during periods of physiological stress. For example, with pacing-induced stress, impairment in diastolic function was observed in conscious dogs with compensated LV hypertrophy. In conscious dogs with LV hypertrophy and failure, isoproterenol also resulted in altered diastolic function. Thus, in the model of severe pressure-overload hypertrophy, which is characterized by limitations in coronary reserve, the mechanism of subendocardial ischemia might be responsible in part for the impairment in diastolic function observed in response to superimposed stress.
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PMID:Reduced subendocardial coronary reserve. A potential mechanism for impaired diastolic function in the hypertrophied and failing heart. 213 53

Recent data strongly suggest that repetitive ischemic episodes have an adverse cumulative effect on development of edema and tissue damage. We wanted to assess further whether special risks such as exacerbation of extracellular acidification reflecting progressive exhaustion of the capacity to buffer H+ in the extracellular space are associated with repeated short ischemic insults. We monitored spontaneous electrical activity, extracellular direct-current potential, extracellular H+ activity, and tissue PCO2 in the cerebral cortex of rats subjected to four cycles of 3-minute ischemia produced by four-vessel occlusion with 27-minute reperfusion after each insult. Except for electrical activity, which failed to recover fully from the first ischemic insult, all parameters returned to a level close to normal after each reperfusion. Changes during ischemia did not evolve with repetition of the insult. Electrical silence occurred within approximately 20 seconds after the onset of each ischemic episode and always preceded the steep drop of direct-current potential, indicating ischemic depolarization. Each four-vessel occlusion immediately initiated a steep rise of tissue PCO2 and extracellular H+ activity, with extracellular H+ activity reaching a maximum within approximately 145 seconds. Changes in extracellular H+ activity during each recirculation period consistently included an additional and short-lasting increase associated with repolarization, a rapid decrease closely related to that of tissue PCO2, and a slow progressive return to normal. These results suggest that short, repetitive ischemic episodes severe enough to produce cell membrane depolarization and maximum acidosis of the neuronal microenvironment do not have a deleterious cumulative effect on the studied parameters, in particular, on interstitial acidosis.
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PMID:Cortical activity, ionic homeostasis, and acidosis during rat brain repetitive ischemia. 238

Exogenous fructose 1,6-diphosphate (FDP), a glycolytic intermediate, has recently been demonstrated to accelerate ATP production, prevent glycogen breakdown, stimulate glycogen synthesis, and synthesize free fatty acids in animals and humans. To assess the effects of FDP on the hormonal and metabolic response to exercise, ten trained males (34 +/- 7 yr) underwent 1 h of continuous exercise at 70% VO2max followed by 20 W.min-1 increments to exhaustion. Two hundred fifty mg.kg-1 body weight FDP or placebo was infused in randomized, double-blind, crossover fashion. No differences were observed in heart rate, blood pressure, gas exchange data, perceived effort, or glucose, insulin, free fatty acid, lactate, beta-hydroxybutyrate, glycerol, and glucagon concentration at rest, during exercise, or upon exhaustion. In contrast to the previously reported bioenergetic effects of FDP under conditions in which glycolysis is impeded (acidosis, hypoxia, and ischemia), FDP did not affect the gas exchange, hormonal, or substrate response to moderately high intensity exercise in healthy normals.
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PMID:Effect of fructose 1,6-diphosphate infusion on the hormonal response to exercise. 240 38


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