Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0022116 (
ischemia
)
91,303
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Heart muscle mitochondria with satisfactory functional parameters of oxidative phosphorylation and with morphologically intact structure were isolated from canine myocardium employing a modified KEA-medium (0.18 M KCl, 10 mM EDTA, 0.5% bovine serum albumin, pH 7.1) according to Sordahl and Schwartz (1). The functional behaviour of mitochondria was investigated after different durations of in situ
ischemia
(cardioplegia, 15 degrees C) and correlated with metabolic findings. During
ischemia
the following changes were seen: 1. Successive reduction of electron flow. 2. Relatively small impairment of phosphorylation efficiency. 3. Less damage of FAD- than NAD-catalyzed oxidative phosphorylation. 4. A marked increase of electron flow and thus recovery of phosphorylation rate even after longer ischemic periods by addition of cytochrome c. As important factors of accelerating mitochondrial impairment during
ischemia
the myocardial ATP decrease, the lactate and H+-activity increase are discussed.
Basic Res
Cardiol
PMID:Functional behaviour of isolated heart muscle mitochondria after in situ ischemia. Polarographic analysis of mitochondrial oxidative phosphorylation. 20 84
The pretreatment of rats with amiodarone for 2 minutes to 3 weeks before the excision of their hearts caused a dose-related decrease in heart rate and an increase in the ventricular fibrillation threshold both before and after coronary arterial ligation. Similarly, amiodarone decreased the incidence of ventricular premature extrasystoles, ventricular tachycardia and fibrillation during the period of regional
ischemia
after coronary arterial ligation and also after reperfusion of the ischemic myocardium. There was no evidence of a metabolic protective effect on ischemic myocardium because tissue high energy phosphate content decreased to a similar extent in ischemic myocardium from control and amiodarone-treated rats. Instead, the protective effect of amiodarone against fibrillation was accompanied by attenuation of the increase in tissue cyclic adenosine monophosphate in ischemic myocardium after coronary arterial ligation. It is proposed that amiodarone exerts a potent antifibrillatory effect by decreasing tissue cyclic adenosine monophosphate in ischemic myocardium.
Am J
Cardiol
1979 Mar
PMID:Protective action of amiodarone against ventricular fibrillation in the isolated perfused rat heart. 21 61
In isolated rabbit hearts with an experimental coronary arterial occlusion, epicardial
ischemia
was identified by reduced nicotinamide adenine dinucleotide (NADH) fluorescence photography, a technique that detects areas of myocardial anoxia. Epicardial S-T segment mapping was performed to evaluate the S-T segment changes across an ischemic border defined by NADH fluorescence. After S-T segment mapping and perfusion with a fluorescein dye, serial selections of the hearts revealed that the ischemic area was transmural and and the border was nearly perpendicular to the epicardial surface. As the epicardial ischemic border was approached, S-T segment elevation was first detected 3.3 mm outside the ischemic border, and increased over a transition zone 7 mm wide. S-T segment negativity was not detected immediately outside the ischemic border. It is concluded from these studies that S-T segment changes give relatively imprecise definition of an ischemic border, and that S-T segment changes across an ischemic border are not consistent with those predicted by solid angle analysis.
Am J
Cardiol
1979 Aug
PMID:Epicardial ischemia as delineated with epicardial S-T segment mapping andnicotinamide adenine dinucleotide (NADH) fluorescence photography. 22 28
Contractile dysfunction is characteristic of the acutely ischemic myocardium. This study was undertaken to assess the temporal relations between the onset of cell anoxia and ischemic contractile failure in isolated, isovolumetric contracting rabbit hearts. High speed epicardial fluorescence photography using reduced nicotinamide adenosine nucleotide (NADH) was used to identify areas of cell anoxia. The onset of
ischemia
was correlated with deterioration of pressure generation over the course of sequential 60 second coronary arterial occlusions. In the isovolumetric contracting rabbit heart, areas of
ischemia
were detected 2 seconds after coronary occlusion. Significant reduction in peak systolic pressure occurred at 6 seconds of ischemic time and pressure continued to decrease throughout the 60 second period of coronary occlusion. NADH accumulation indicates imbalance of myocardial oxygen supply and demand and the cessation of oxygen utilization by the mitochondria. The results of this study indicate that
ischemia
is detectable within 1 to 2 seconds after coronary occlusion and that ischemic ventricular dysfunction occurs several seconds thereafter. Myocardial oxygen reserve is negligible.
Am J
Cardiol
1979 Oct
PMID:Temporal relation between onset of cell anoxia and ischemic contractile failure. Myocardial ischemia and left ventricular failure in the isolated, perfused rabbit heart. 22 47
In order to determine the natural evolution of different clinical types of "unstable angina", 167 patients were included in a prospective study. After angiography, 11 (6.5%) were excluded because they had no significant coronary lesions. The remaining 156 were sorted into different groups according to their clinical characteristics and were followed up for a period of 24 months at least. After that follow-up period, mortality and incidence of acute myocardial infarction (AMI) were as follows: angina of recent onset (Class III--IV NYHA): 8.5% (3/35) and 34.2% (12/35). Progressive angina: 7.4% (2/27) and 7.4% (2/27). Intermediate syndrome: 41.6% (10/24) and 37.5% (9/24). Prinzmetal's angina: 10% (1/10) and 10% (1/10). Post acute myocardial infarction angina: 35% (7/20) and 10% (2/20). Acute persistent
ischemia
: 2.5% (1/40) and 20% (8/40). Comparison of these figures pointed out significant differences (p less than 0.001 for mortality and p less than 0.03 for AMI incidence respectively). We conclude that it is clinically possible to identify different groups within the so-called unstable angina. Such a division not only allows for the creation of more homogeneous groups, but it contributes to a more rational therapeutic approach and also permits identification of high risk prodromes of greater complications, such as myocardial infarction or sudden death.
Clin
Cardiol
1979 Apr
PMID:Clinical spectrum of "unstable angina". 26 65
Various pharmacologic interventions that suppressed chemotactic factor activity in the coronary sinus after acute
ischemia
were analyzed for protective effects on myocardium. Ischemic injury was determined by comparing the slopes of the regression lines derived from 24 hour myocardial creatine kinase content versus S-T segment elevation 15 minutes after coronary ligation. Dogs treated 30 minutes after ligation with cobra venom factor, hydrocortisone or Trasylol showed a marked decrease in chemotactic activity in the coronary sinus. These agents also showed a protective effect on ischemic injury when compared to control. Myocardial biopsy specimens from areas of significant
ischemia
defined by S-T segment elevations in dogs treated with cobra venom factor were essentially devoid of an inflammatory response whereas those from dogs treated with Trasylol or hydrocortisone showed moderate neutrophil infiltration and minimal tissue exudate.
Am J
Cardiol
1977 Oct
PMID:Chemotactic activity in the coronary sinus after experimental myocardial infarction: effects of pharmacologic interventions on ischemic injury. 30 50
Hypertension during pregnancy and its complications are the most important cause of maternal and foetal death and morbidity. The chronic primary hypertension can be differentiated from the dysgravidia by anamnestic, biological, clinical and technical investigations. However the diagnosis remains difficult and the renal needle biopsy can help to ascertain it. The pathogenesis of dysgravidia is still obscure: the placental
ischemia
leads to a slow disseminated intravascular coagulation state with renal injury, while a vascular hyperreactivity leads to an increase of the resistance, a relative hypovolemia and lowering of cardiac output. The treatment and remote prognosis of the hypertensive disease associated with the pregnancy are summarized. The antihypertensive drugs improve the maternal prognosis while jeopardize the foetal outcome.
Acta
Cardiol
1977
PMID:[Hypertension and pregnancy]. 30 56
A 65 years old woman with an acute myocardial infarction, as it was judged by serial enzyme changes, developed transitory Q waves in V2-V4 and II, III and AVF during the attack of chest pain. These Q waves were not present 12 hours later. It is suggested that these changes represent a focal block in the septal fibers of the left bundle system. This defect could explain the transient right precordial Q waves seen in myocardial infarction or
ischemia
, as well as the fixed Q waves of many patients without septal infarction at autopsy.
Acta
Cardiol
1978
PMID:Transient abnormal Q waves during acute myocardial infarction. 31 75
A decrease in systolic blood pressure that occurs with treadmill exercise testing may be a sign of reversible ischemic left ventricular dysfunction. To test this hypothesis, we examined retrospectively the postoperative treadmill responses of 37 patients who had exertional hypotension (end exercise systolic blood pressure less than or equal to initial preexercise levels) before coronary arterial bypass grafting. This group of 37 patients was characterized preoperatively by an abnormal exercise electrocardiogram (36 patients), multiple vessel occlusive disease (36 patients) and a normal ejection fraction at rest (32 patients). Postoperative exercise tests showed improvement in hemodynamic and electrocardiographic changes with reversal of exertional hypotension (33 patients), and conversion to a normal exercise electrocardiogram (29 patients). Coronary bypass surgery can be expected to reverse exertional hypotension in patients with symptomatic angina pectoris and evidence of
ischemia
in the exercise electrocardiogram.
Am J
Cardiol
1979 Oct
PMID:Reversal of exertional hypotension after coronary bypass grafting. 31 49
The effect of coronary arterial bypass surgery on exercise-induced ventricular arrhythmias and their relation to sudden death was examined in 102 patients with stable angina pectoris randomly assigned to medical and surgical therapy (54 and 48 patients, respectively). Symptom-limited treadmill tests were performed at entry and at 1 and 5 years. The surgical group demonstrated significant improvement in exercise performance at 1 year compared with the medical group, and at 5 years exercise-induced
ischemia
as evidenced by S-T depression and exertional angina remained substantially decreased in the surgical group with little change in the medical group. However, the frequency and severity of exercise-induced ventricular arrhythmias in each group remained unchanged at 1 and 5 years from those at entry. Similar results were obtained from an evaluation of ventricular arrhythmias in the electrocardiogram at rest. With the exception of exercise-induced ventricular tachycardia and fibrillation, no relation was found between ventricular arrhythmias and sudden death. Coronary bypass grafting does not decrease the frequency or severity of exercise-induced or resting ventricular arrhythmias. In patients with stable angina pectoris, with the exception of ventricular tachycardia and fibrillation, exercise-induced ventricular arrhythmias are poor predictors of sudden death. The data suggest that exercise-induced ventricular arrhythmias may not be related to
ischemia
but to other effects of exercise such as cardiac stimulation by catecholamines or other factors.
Am J
Cardiol
1979 Nov
PMID:Effect of coronary arterial bypass surgery on exercise-induced ventricular arrhythmias. Long-term follow-up of a prospective randomized study. 31 62
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>