Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Midmyocardial and subendocardial pH monitoring was used as an indirect method for continuous evaluation of regional canine myocardial ischemia. Left ventricular midmyocardial pH (pHm) at 4 mm. depth was monitored in 10 dogs, under resting conditions, by means of a 5 mm. Beckman pH probe. pHm was 6.96 +/- 0.03, recorded at myocardial temperatures of 35 to 37 degrees C. Ischemia was then produced by snare occlusion of the proximal left main coronary artery for 2 minutes. pHm decreased to 6.87 +/- 0.03 (p less than 0.01) at 1 minute and 6.80 +/- 0.04 (p less than 0.005) in 2 minutes. When flow was restored, pHm returned toward normal within 2 minutes (pH 6.86 +/- 0.03) and at 5 minutes had returned to control values (pH 6.93 +/- 0.03). In another 5 dogs under similar conditions, pHm at 4 mm. and subendocardial pH (pHe at 8 mm.) were measured. Baseline pHm (6.97 +/- 0.01) and pHe (6.84 +/- 0.02) levels were significantly different (p less than 0.0005). After 2 minutes of ischemia, pHm was 6.82 +/- 0.03, whereas pHe decreased to 6.78 +/- 0.04 (p less than 0.1). Five minutes after snare release, pHe remained at 6.73 +/- 0.07; pHm (6.93 +/- 0.03) returned to control values. Both pHm (6.93 +/- 0.02) and pHe (6.84 +/- 0.09) levels were normal 15 minutes after release of the snare. The midmyocardium and subendocardium have different pH levels which can be monitored. Ischemia produces different pH patterns in these layers. pHm returns to control values within 5 minutes after 2 minutes of ischemia, whereas pHe remains depressed for at least 5 minutes. pH monitoring provides an accurate and simple method for on-line evaluation of endocardial ischemia.
J Thorac Cardiovasc Surg 1976 Jul
PMID:Monitoring of midmyocardial and subendocardial pH in normal and ischemic ventricles. 0 26

In studies in the isolated rat heart that were designed to optimize the composition of the infusion conditions for a cardioplegic protective solutuin, we have observed a complex relationship between the duration and volume of infusion and the extent of tissue protection. Our results would indicate that solutions, such as that formulated at St. Thomas' Hospital, which are based on extracellular electrolyte content, afford (after a brief equilibration period) a constant degree of protection, irrespective of infusion volume or duration. In contrast other solutions, such as the Bretschneider solution, which have extremes of electrolyre concentration, are associated with a complex dose-response relationship. In the latter instance, infusion of small volumes for short durations affords an increasing degree of protection against ischemia. Increasing the infusate volume may result in a progressive loss of protection. Excessive infusion may lead to an exacerbation of ischemia-induced damage. Our studies suggest that the relative patterns and rates of re-equilibration of various ions, especially sodium and calcium, during infusion may play a major role in determining the efficacy of the infusate.
J Thorac Cardiovasc Surg 1978 Nov
PMID:Protection of the ischemic myocardium. Volume-duration relationships and the efficacy of myocardial infusates. 2 95

Effects of methylprednisolone were studied on isolated, blood-perfused cat hearts subjected to 1 hr of normothermic ischemic arrest. Untreated hearts sustained decreases in peak ventricular pressure pulse, dP/dt, and ventricular compliance. Ischemic hearts also became edematous, gained sodium, and lost potassium and creatine kinase enzyme activity. Steroid treatment did not significantly alter any of these ischemia-induced changes. Methylprednisolone treatment did increase resting coronary flow and also increased the hyperemic response after reperfusion. These results, in isolated hearts, provide no evidence that steroid treatment exerts a direct protective effect on the globally ischemic myocardium.
J Cardiovasc Pharmacol
PMID:Methylprednisolone sodium succinate treatment in global ischemia of the cat isolated heart. 9 82

The hemodynamic effects of antimigraine drug ergotamine, which is considered contraindicated in patients with coronary artery disease, were studied in pigs with a normal myocardial circulation (doses of 8, 16, and 32 micrograms/kg, i.v.) or with acute coronary stenosis (8 micrograms/kg). In both groups of animals, ergotamine decreased heart rate, cardiac output, and arteriovenous anastomotic blood flow while increasing aortic blood pressure and systemic vascular resistance. No effects on total ventricular blood flow and its distribution within the myocardium were found in normal animals. In animals with a clamp on the left anterior descending coronary artery (LAD), the blood flow to the LAD-perfused area was reduced from 1.10 +/- 0.16 to 0.67 +/- 0.05 cm3/min/g. The endocardium was affected more than the epicardium and the endo/epi flow ratio decreased from 1.18 +/- 0.05 to 0.74 +/- 0.07. Ergotamine increased the blood flow to the ischemic zone towards normal values, and the endo/epi flow ratio to 1.05 +/- 0.21. However, myocardial wall thickness parameters, which showed functional deterioration during ischemia, did not change after ergotamine. The present study provides no clear support for cardiovascular contraindications to ergotamine administration.
J Cardiovasc Pharmacol
PMID:Regional myocardial perfusion and wall thickness and arteriovenous shunting after ergotamine administration to pigs with a fixed coronary stenosis. 9 33

Fifty-four patients with variant angina are described. They are divided into patients without hemodynamically (less than 50%) important coronary artery lesions (Group 1), patients with intermediate (greater than or equal to 50% and less than 90%) fixed obstruction (Group 2A), and patients with high grade (greater than or equal to 90%) fixed obstruction (Group 2B). Inferior ischemia occurred significantly more often in Group 1 (90% versus 33%. p less than 0.001), and exertional angina was more frequent in Group 2 (70% versus 36%, p less than 0.05). Maximum medical therapy with propranolol and nitrates failed to control angina in 55% of Group 1, 69% of Group 2A, and 63% of Group 2B. Twelve patients underwent intra-aortic balloon pumping (IABP), and in 10 there was complete control of variant angina. A total of 35 Group I patients underwent coronary artery bypass grafting (CABG), with a 2.9% mortality rate in patients without preoperative cardiogenic shock. Of these patients, 55% in Group 2A and 73% in Group 2B experienced marked improvement in their angina status. Therefore, we currently recommend bypass grafting for medically intractable variant angina in those patients with severely stenotic, fixed atherosclerotic lesions.
J Thorac Cardiovasc Surg 1979 Oct
PMID:Variant angina. Clinical spectrum and results of medical and surgical therapy. 11 30

Transmural left ventricular biopsies from 13 patients undergoing cardiopulmonary bypass were studied. The hypertrophic myocardium was protected by deep hypothermia (15 degrees C.) during ischemic arrest for a maximal period of 96 minutes. Biopsies were taken at the start of bypass, at the end of aortic cross-clamping, and after 20 minutes of reperfusion. The structure of the mitochondria remained normal, whereas cellular alterations in the form of widened intercalated discs, interstitial and intracellular edema, myelin figures, and slight myofibrillar lysis were observed in all stages. As no clear correlation between these structural injuries and aortic cross-clamping time was seen, they are a result of cardiac hypertrophy rather than intraoperative ischemia.
J Thorac Cardiovasc Surg 1978 Apr
PMID:Cardiac hypothermia evaluated by ultrastructural studies in man. 14 68

Although corticosteroids have been shown to stabilize lysosomal membranes and prevent release of hydrolytic enzymes, the mechanism of membrane stabilization remains obscure. The few reports regarding the use of steroids in myocardial ischemia have been conflicting. This study was undertaken to determine if a pharmacologic dose of the glucocorticoid methylprednisolone would protect the heart during ischemic cardiac arrest. A randomized double-blind study was performed in 25 dogs. Biochemical and hemodynamic parameters were assessed during and after cardiopulmonary bypass and after 30 minutes of ischemic cardiac arrest. Animals were divided into two groups. Group I served as controls and consisted of dogs injected intravenously with the vehicle of methylprednisolone 18 hours and 1 hour prior to experiment. Group II comprised dogs injected with methylprednisolone, 30 mg. per kilogram, IV, at the same time periods. Blood pH, gases, and electrolytes were measured; aortic, left atrial, and left ventricular pressures were monitored; the first derivative of the left ventricular pressure (dp/dt max.) was also determined. Arterial and coronary sinus blood samples were assayed for lactate levels and activity of the lysosomal enzyme, beta-glucuronidase. Left ventricular muscle was assayed for the nucleotides cyclic adenosine 3',5' monophosphate (AMP) and cyclic guanosine 3',5' monophosphate (GMP). Following restoration of coronary flow, mean aortic and left ventricular systolic pressures and left ventricular contractility as determined by dp/dt max. and dp/dt max./IP were depressed in both groups as expected but were significantly higher in Group II than in Group I (p less than 0.05). An increase in levels of both cyclic nucleotides occurred in each group during ischemia, but this increase in cyclic GMP was significantly greater in Group I (p less than 0.05). beta-glucuronidase activity and myocardial potassium loss as determined in coronary sinus blood were both significantly greater in Group I than in Group II (p less than 0.05). Results of this study demonstrate that pretreatment with a pharmacologic dose of methylprednisolone significantly enhances cardiac recovery after ischemia. Lysosomal membrane stability and modulation of cyclic GMP levels may be critical determinants in the mechanism of cardiac ischemia.
J Thorac Cardiovasc Surg 1975 Dec
PMID:Protective effect of methylprednisolone on the heart during ischemic arrest. 17 23

The resistance of the normal myocardium to ischemia can be determined by the metabolic and electric investigations, and particularly by the determination of the intra-myocardial potentials. The aspect of V.F. and the metabolic changes allow aetiologic deductions on the V.F. and are helpful for the treatment.
J Cardiovasc Surg (Torino)
PMID:Resistance and tolerance of myocardium in ischemia: experimental results. 23 1

This article is a short review of newer findings concerning the physiological and biochemical bases of the heart's tolerance to ischemia. The following themes are discussed. I. Energy-pool, energy-demand, and efficiency of anaerobic metabolism, the essential determinants of reanimation time and the heart's tolerance to ischemia. II. Experimental results of ischemic heart arrest and the heart arrest induced by a sodium-poor calcium-free, procaine-containing cardioplegic solution, developed by the author. III. Equivalents of function, metabolism and structure during the anaerobic period of the myocardium. IV. The myocardium's capability to recover in dependence on the metabolic state of ischemia and summary of the most important points of gaining a long time of tolerated ischemia. V. Survey and prospects.
J Cardiovasc Surg (Torino)
PMID:Myocardial resistance and tolerance to ischemia: physiological and biochemical basis. 23 2

To clarify the value of serum enzymes in the detection of intraoperative and postoperative myocardial injury associated with coronary artery bypass grafting, we evaluated 70 consecutive patients (151 grafts). We used electrocardiograms and serial determinations of serum levels: serum glutamic oxaloacetic transaminase (SGOT), creatinine phosphokinase (CPK), lactic dehydrogenase (LDH), and LDH isoenzymes on Days zero, 1, 3, 5, 7, and 10. Patency of all grafts 1 week postoperatively was 92 per cent. Fourteen patients (20 per cent) had ECG evidence of acute myocardial infarction (AMI) or ischemia lasting longer than 48 hours. This incidence of AMI was attendant with no deaths or discernible changes in postoperative ventriculography. LDH-1 (cardiac fraction) was elevated in all patients with myocardial injury. Late elevation of LDH-1 occurred in 2 patients at the time of postoperative catheterization, 1 of whom had negative findings on ECG. Diagnostic correlation was not observed with total LDH, CPK, or SGOT. Predisposing factors to AMI included preinfarction angina (4 of 14 patients), occluded grafts (4 of 14), and a bypass time greater than 120 minutes.
J Thorac Cardiovasc Surg 1975 Sep
PMID:Myocardial injury and bypass grafting. Value of serum enzymes in diagnosis. 24 Sep 85


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