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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-six patients undergoing aortic valve replacement were investigated to ascertain whether the addition of glucose-insulin before and after ischaemic heart arrest could aid to the functional recovery of hearts following global ischaemia. One group of patients (n = 14) received glucose plus insulin from the onset of anaesthesia until crossclamping of the aorta (1 g + 1.5 U/kg bw X h). A second dose (0.5 g + 1.0 U/kg bw) was given at the end of ischaemia. 22 patients, serving as control received glucose in the same manner but without insulin. Needle biopsies from the left ventricular apex region were obtained: before starting cardiopulmonary bypass; at the end of ischaemia; and after 10 minutes of reperfusion and analyzed for its content of ATP, CP ADP and lactate. In both groups ATP and CP were significantly decreased after ischaemia and increased after reperfusion. ADP and lactate levels were elevated after ischaemia and decreased after reperfusion in the insulin-group but not in the control-group. During the total investigation period ATP- and CP-concentrations in the insulin-group were higher compared to the control-group, whereas ADP and lactate of the control-group were above the insulin-group.
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PMID:Enhancement of myocardial energy potentials in man by glucose-insulin treatment before and after ischaemic heart arrest. 388 27

Enflurane is a direct myocardial depressant and may act as a myocardial protective agent during ischemia. The authors studied the effects of enflurane on myocardial high-energy phosphates and tolerance to ischemia in the normothermic, isolated rat heart. After isolation and perfusion with Krebs-Henseleit buffer, the hearts were perfused with either buffer (control) or buffer gassed with 2% enflurane for 10 minutes. Thereafter, hearts were made globally ischemic and elapsed times to initiation of ischemic contracture (IC) were determined. ATP and creatine phosphate (CP) were measured at the conclusion of control and enflurane administration and at IC. Ten hearts per group were reperfused with buffer following IC for 20 min; peak pressure and ATP and CP were determined. Administration of 2% enflurane significantly decreased peak pressure by 20% but did not alter baseline high-energy phosphate levels nor did it prolong time to IC. However, enflurane-treated hearts exhibited significantly greater (P less than 0.01) recovery of function as defined by per cent return of peak pressure (67% +/- 3%) when compared with those hearts not treated with enflurane preischemically (44% +/- 5%). Also, enflurane-treated hearts had significantly higher (P less than 0.01) ATP levels at the conclusion of reperfusion than hearts not perfused with enflurane (12.2 +/- .8 mumol/g dry weight vs. 9.0 +/- 0.8 mumol/g dry weight). These findings suggest that enflurane administered prior to an ischemic interval enhances postischemic myocardial recovery.
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PMID:Enflurane enhances postischemic functional recovery in the isolated rat heart. 396 66

The protective effects of cardioplegic solutions (CS) containing creatine phosphate (CP) were studied in a rat heart model of cardiopulmonary bypass and ischemic cardiac arrest. Isolated rat hearts were subjected to a 3-minute coronary infusion with CS containing CP in normothermic (37 degrees C) and hypothermic (4-6 degrees C) regimes. In the normothermia group, the postischemic functional recovery was 70-75% of the preischemic control value, while the cellular ATP and CP content was reduced but insignificantly. By contrast, in the hypothermia group, the postischemic functional recovery was markedly depressed, with the tissue high-energy phosphate content being appreciably lowered. The data obtained confirm high efficacy of CP-containing cardioplegic solutions administered under normothermia conditions.
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PMID:[Effectiveness of protecting the myocardium against ischemia with a normothermic cardioplegic solution and creatine phosphate]. 396 61

The purpose of this study was (1) to monitor myocardial high-energy phosphate content and recovery of left ventricular (LV) contractile function following normothermic graded cardiac ischemia and single-dose hypothermic potassium cardioplegia, and (2) to assess the temporal limits of LV functional recovery during single-dose cardioplegia maintained at 17 degrees C. Rabbit hearts (30) were perfused, equipped with an LV balloon, paced at 240 beats/min, and placed in a nuclear magnetic resonance (NMR) magnet. Hearts underwent either graded, global normothermic ischemia or potassium cardioplegia arrest maintained at 17 degrees C for 1 hr. Myocardial high-energy phosphate level, LV contractility, and temperature were monitored continuously. Phosphocreatine (PCr) fell to 10 +/- 2, 2 +/- 1, and 0% of control and ATP to 70 +/- 3, 19 +/- 7, and 0% of control at 10, 40, and 60 min of 37 degrees C ischemia. After 1 hr of reperfusion, regression analysis of final developed pressure (DP) on end ischemic ATP (EIATP) content revealed: DP = 1.02 EIATP + 18 (r = 0.95). Following single-dose cardioplegia, maintained at 17 degrees C, PCr fell to 16 +/- 3% of control at 60 min while ATP fell only to 92 +/- 5% control. With reperfusion, recovery of DP was 100%. It was concluded that (1) PCr serves as an energy buffer for ATP, (2) EIATP predicts recovery of LV function, (3) single-dose cardioplegia maintained at 17 degrees C provides complete myocardial preservation for up to 60 min.
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PMID:Evaluation of myocardial preservation using 31P NMR. 396 74

Experiments were conducted on 18 dogs using an in situ blood-perfused canine heart model. Intracoronary infusion of AMP resulted in increased ATP and total adenine nucleotide levels. On reperfusion following a 15-min period of ischemia, ATP and total adenine nucleotide levels were significantly higher than control. Most important, contractile function recovered more rapidly in the AMP-treated dogs. It is therefore concluded that the delayed functional recovery noted after periods of ischemia is likely to be a direct result of delayed ATP resynthesis.
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PMID:Accelerated recovery of ischemic canine myocardium induced by AMP. Preliminary report. 399 46

The relationship between tissue levels of fatty acid metabolites in ischemic and reperfused hearts and recovery of mechanical function of these hearts on reperfusion was studied. Isolated rat hearts were exposed to global ischemia for periods up to 60 min under various conditions of coronary flow, O2 supply, and fatty acid concentrations and were then reperfused for either 15 or 30 min under aerobic conditions both with and without fatty acids present. Tissue levels of ATP, creatine phosphate, long-chain acyl CoA, and long-chain acyl carnitine were determined at the end of the ischemic and reperfusion periods. In some experiments K+ arrest during ischemia was used to prevent adenine nucleotide depletion both in the absence and presence of high fatty acids. Although the ability of these hearts to recover their preischemic mechanical function varied from 8 to 90% and tissue levels of acyl CoA and acyl carnitine during ischemia varied from 3- to 10-fold depending on the condition, no correlation was found between the recovery of function during reperfusion and either the presence of fatty acid or high levels of tissue long-chain acyl CoA and carnitine esters during ischemia.
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PMID:Recovery of ventricular function in reperfused ischemic rat hearts exposed to fatty acids. 403 99

The ability of nifedipine to enhance myocardial protection was assessed on isolated perfused rat hearts subjected to 180 min of hypothermic (20 degrees C), global ischemia, followed by 45 min of normothermic reperfusion. Intracellular pH, ATP, Pi and phosphocreatine content were serially measured at 4 min intervals by phosphorus-31 nuclear magnetic resonance spectroscopy and correlated with simultaneously recorded hemodynamic parameters. Addition of nifedipine (0.075 mumol/l and 0.5 mumol/l) to Saint Thomas' cardioplegic solution reduced Pi accumulation during ischemic arrest and increased phosphocreatine levels during reperfusion. Post-ischemic functional recovery was not improved at a drug concentration of 0.075 mumol/l and was depressed at 0.5 mumol/l. These results clearly show that the presence of nifedipine in Saint Thomas' cardioplegic solution does not provide significant additional myocardial protection under hypothermic conditions.
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PMID:Effect of nifedipine in hypothermic cardioplegia: a phosphorus-31 nuclear magnetic resonance study. 405 4

The concept of limiting irreversible damage due to ischemic arrest by inhibiting nucleoside breakdown was tested in the isolated perfused rat heart. Functional recovery measurements were combined with continuous high-energy phosphate measurements by means of 31P nuclear magnetic resonance (NMR) and with nucleoside release measurements in the reperfusion period. The adenosine deaminase inhibitors erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) and 2'-deoxycoformycin (DCF) were given 5 min before ischemia and for the first 5 min of reperfusion. These treated groups were compared with a control, untreated group. These were further compared with a group of hearts arrested with potassium and to a group combining potassium arrest and EHNA. It was found that all treated groups recovered mechanical function significantly better than the untreated group. DCF, K+, and K+ + EHNA slowed ATP decline and resulted in better ATP recovery than untreated or EHNA-treated, and all treatments decreased nucleoside base release. Intracellular pH fell equally in all groups and recovered to preischemic values. Thus, these adenosine deaminase inhibitors improve functional recovery following ischemia, although this improvement was not well correlated with purine losses observed during reperfusion.
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PMID:Effect of adenosine deaminase inhibitors on the heart's functional and biochemical recovery from ischemia: a study utilizing the isolated rat heart adapted to 31P nuclear magnetic resonance. 619 52

We studied the effect of selected metabolic substrates on recovery of myocardial function and ATP concentration when added to the reperfusate after normothermic ischemia. The hearts of 30 anesthetized, open-chest mongrel dogs were subjected to 45 min of global ischemia at 37 degrees C followed by 90 min of reperfusion. Left ventricular function curves were generated on right heart bypass before and at 30 min intervals after the ischemic period. ATP concentration was measured before, at the end of, and 90 min after the ischemic period. Experiments were randomized into five groups distinguished by the content of the myocardial reperfusate during the first 10 min of the reperfusion period. Hearts received either unmodified oxygenated pump blood (control; group I), normothermic oxygenated 28 mmol/liter potassium-blood cardioplegic solution (KBC; group II), 25 mmol/liter glutamate in KBC (group III), 250 mumol/liter adenosine with 1 mg erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (EHNA) and glutamate in KBC (group IV), or 2 mmol/liter ribose and glutamate (group V) in KBC. Hearts reperfused with KBC showed improvement early (group II vs group I; p less than .02) but not late recovery of left ventricular function over control. Glutamate, which replenishes Krebs cycle intermediates lost during ischemia, increased functional recovery (group III vs group II; p less than .002). Ribose, which is important in purine salvage and resynthesis, added to glutamate-KBC further improved functional recovery (group V vs group III; p less than .01). Adenosine, a precursor of ATP, with EHNA, an inhibitor of rapid adenosine catabolism, added to glutamate-KBC depressed early recovery (group IV vs group III; p less than .01); however, recovery improved with time. Both glutamate and ribose with glutamate in KBC improved ATP recovery (groups III and V vs group II; p less than .002). Thus selective substrate repletion during initial reperfusion after severe normothermic ischemia can improve recovery of myocardial function and ATP concentration.
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PMID:Reduction of postischemic myocardial dysfunction by substrate repletion during reperfusion. 643 May 93

The cardioprotective effects of mioflazine, a recently developed cardiovascular drug, were investigated in 41 anaesthetised open chest Beagle dogs subjected to 1 h normothermic global myocardial ischaemia. The severity of the model is evidenced by the finding that only one out of 20 control dogs could be weaned from extracorporeal bypass. Oral pretreatment with mioflazine (2.5 mg X kg-1) resulted in complete functional recovery in 17 out of 20 animals. Biochemical analysis of left ventricular biopsies taken before, during and after aortic cross clamping showed a preservation of purines and a better recovery of ATP, ATP/ADP X Pi ratio and energy charge (p less than 0.05) in the pretreated animals. Morphological and cytochemical assessment of the myocardium demonstrated that the ultrastructure of the sarcolemma and its calcium binding capacity is remarkably well preserved in the drug treated animals. These results indicate a strong cardioprotective effect of mioflazine. The biochemical, cytochemical and ultrastructural findings suggest an interaction of the drug with the sarcolemma.
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PMID:Cardioprotective effects of mioflazine during 1 h normothermic global ischaemia in the canine heart. 646 70


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