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

Changes in energy metabolism induced by norepinephrine were observed in liver perfused immediately after dissection and in liver stored in Euro-Collins solution at 0 degrees C for 24 hr. Oxygen consumption, glucose output, ATP content, and tissue pH were measured in isolated perfused rat liver at 37 degrees C. In fresh liver, a two-fold increase in glucose output and oxygen consumption was induced by norepinephrine (1 microM), while changes in ATP content and tissue pH were minimal. In stored liver, the cumulative increments in glucose output and oxygen consumption induced by norepinephrine were 30 and 27% those of fresh liver, respectively. ATP content of the unstimulated liver was 76% that of the fresh liver, then decreased to 50% during stimulation. A transient decrease in tissue pH (0.14 pH unit) was significant compared with that of fresh liver. These results suggest that norepinephrine stimulation is useful for assessing energetic and functional recovery of reperfused liver following hypothermic storage.
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PMID:Energetic recovery from hypothermic preservation in the rat liver. 229 80

Alterations in energy substrate utilization during reperfusion of ischemic hearts can influence the functional recovery of the myocardium. Energy substrate preference by the reperfused myocardium, however, has received limited attention. Therefore, we measured oxidation rates of glucose and palmitate during reperfusion of ischemic hearts. Isolated working rat hearts were perfused with 1.2 mM palmitate and 11 mM [14C]glucose, 1.2 mM [14C]palmitate and 11 mM glucose, or 11 mM [14C]glucose alone, at an 11.5 mm Hg preload and 80 mm Hg afterload. Hearts were subjected to 60-minute aerobic perfusion or 25-minute global ischemia followed by 60-minute aerobic reperfusion. Steady-state oxidative rates of glucose or palmitate were determined by measuring 14CO2 production. In hearts perfused with glucose alone, oxidative rates during reperfusion were not significantly different than nonischemic hearts (1,008 +/- 335 vs. 1,372 +/- 117 nmol [14C]glucose oxidized/min/g dry wt, respectively). In the presence of palmitate, glucose oxidation was markedly reduced in reperfused and nonischemic hearts (81 +/- 11 and 101 +/- 15 nmol [14C]glucose oxidized/min/g dry wt, respectively). Palmitate oxidation rates were not significantly different in reperfused compared with nonischemic hearts (369 +/- 55 and 455 +/- 50 nmol [14C]palmitate oxidized/min/g dry wt, respectively). [14C]Palmitate was incorporated into myocardial triglycerides to a greater extent in reperfused ischemic hearts than in nonischemic hearts (26.0 and 13.8 mumol/g dry wt, respectively). Under the perfusion conditions used, palmitate provided over 90% of the ATP produced from exogenous substrates. Addition of the carnitine palmitoyltransferase I inhibitor, ethyl 2-[6-(4-chlorophenoxy)hexyl]oxirane-2-carboxylate (Etomoxir, 10(-6) M), during reperfusion stimulated glucose oxidation and improved mechanical recovery of ischemic hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose and palmitate oxidation in isolated working rat hearts reperfused after a period of transient global ischemia. 229 17

Intermittent restoration of coronary flow during ischemia reduced myocardial damage and improved recovery of function. The mechanisms of the protective effects of intermittent perfusion were investigated in isolated rat hearts. Ventricular function was assessed as the product of developed pressure (left ventricular systolic pressure minus end-diastolic pressure) and heart rate. Recovery of function was calculated by division of the product at the end of reperfusion by that before ischemia. After 40 minutes of sustained global ischemia, intracellular Na+ (Nai) increased from 11 to 74 mumol/g dry wt. During 30 minutes of reperfusion, these hearts took up a large amount of 45Ca2+ (10 mumol/g dry wt), recovered only 24% of preischemic function, and had an increased left ventricular end-diastolic pressure (48 mm Hg). When the 40-minute period of ischemia was interrupted at 10-minute intervals by intermittent perfusion (three periods of 3 minutes) with either oxygenated or hypoxemic buffer, Nai increased to only 12 or 17 mumol/g dry wt, and reperfusion resulted in much lower 45Ca2+ uptake (0.5 and 0.5 mumol/g dry wt, respectively). Recovery of function was 100% of the preischemic value. When hypoxemic buffer without glucose was used for intermittent perfusion, Nai increased to 50 mumol/g dry wt, ATP was depleted, and reperfusion resulted in reduced recovery of function (76%) and moderately increased 45Ca2+ uptake (2.1 mumol/g dry wt). The role of Na(+)-K+ pump activity in maintaining low Nai was assessed by removing K+ from oxygenated or hypoxemic buffers used during intermittent perfusion. Under these conditions, Nai rose to 64 or 102 mumol/g dry wt, 45Ca2+ uptake increased to 4.4 or 9.4 mumol/g dry wt, and recovery of function was poor. There was a highly significant correlation between Nai during ischemia and reperfusion Ca2+ overload (r = 0.87) or impaired recovery of function (r = 0.96). These results indicate that prevention of an increase in Nai by maintenance of Na(+)-K+ pump activity is associated with a reduction of Ca2+ overload through Na+/Ca2+ exchange.
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PMID:Intermittent perfusion of ischemic myocardium. Possible mechanisms of protective effects on mechanical function in isolated rat heart. 237

The purpose of the present study was to determine whether the combined administration of superoxide dismutase (SOD) and catalase (CAT) or efforts to maintain the glutathione redox pathways with sulfhydryl agents could improve Na+ imbalance, reduce Ca2+ overload, and enhance recovery of function and metabolites upon reperfusion in isolated ischemic rat hearts, presumably by scavenging oxygen free radicals. After a 30-min exposure to zero-flow ischemia, left ventricular developed pressure (LVDP) and heart rate recovered to 31 and 81% of the preischemic value, respectively, ATP fell by approximately 40%, and 45Ca2+ uptake rose from 0.8 to 10.4 mumol/g dry tissue. A combination of SOD and CAT at low concentrations (5 X 10(4) and 7.5 X 10(4) U/l, respectively) had a beneficial effect on recovery of LVDP (to 59%), reperfusion 45Ca2+ uptake (to 7.9 mumol/g dry tissue), and recovery of Na+ imbalance. When sulfhydryl donors, such as glutathione, cysteine, N-acetyl-L-cysteine, or dithiothreitol, were administered 20 min before induction of ischemia, no significant protective effects were observed. These results indicated that the extracellular free radical scavengers, SOD and CAT, could attenuate partially the ionic imbalance in ischemic-reperfused myocardium and result in improved recovery of contractile function. Attempts to enhance the intrinsic scavenging system were not successful, suggesting that this system may not play an important role in disposing of free radicals.
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PMID:Effects of anti-free radical agents on Na+, Ca2+, and function in reperfused rat hearts. 237 99

Multidose potassium cardioplegia is known to result in greater preservation of myocardial ATP content and better recovery of function as compared to cardiac arrest induced by aortic clamping. The present study was undertaken to assess the effects of this procedure on biochemical markers of tissue damage. Rat hearts undergoing either multidose cardioplegia or ischemic cardiac arrest were maintained at 18 degrees C for 1 or 2 hr and processed without reperfusion. Control hearts were processed at time zero. The activity of two lysosomal enzymes (beta-glucuronidase and acid phosphatase), as well as membrane phospholipid content, was measured in cardiac homogenates. One hour of arrest by either technique did not induce significant changes in these parameters. Two hours of arrest affected lysosomal integrity, as indicated by release of lysosomal enzymes into the cytosol. Soluble acid phosphatase activity averaged 44.7 +/- 1.3 mU/mg of protein in the hearts processed after 2 hr of cardioplegic arrest, and was significantly higher than that of control hearts (12.3 +/- 3.8 mU/mg of protein; P less than 0.01) and that of hearts subjected to 2 hr of ischemic arrest (29.2 +/- 4.5 mU/mg of protein; P less than 0.01 vs cardioplegic arrest; P less than 0.01 vs controls). Phospholipid content in hearts subjected to 2 hr of cardioplegic arrest was lower than in controls (0.49 +/- 0.06 micrograms Pi/mg of protein vs 0.76 +/- 0.03 micrograms Pi/mg of protein; P less than 0.01). In conclusion, 2 hr of hypothermic cardiac arrest was associated with biochemical indices of tissue damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Paradoxical effects of cardiac arrest by multidose potassium cardioplegia on myocardial lysosome integrity and phospholipid content. 238 Dec 2

The influence of pressure-controlled postischemic reperfusion (Rp) on functional and metabolic parameters in hearts of sham-operated rats and hypertrophied hearts of rats with aortic constriction were studied. Hypertrophied hearts are considered to be more susceptible to ischemia. The hearts were perfused in the Langendorff-technique for thirty minutes at 35 degrees C with Krebs-Henseleit bicarbonate buffer at a perfusion pressure (PP) of 75 mmHg and for five minutes at 15 degrees C with St. Thomas' Hospital cardioplegic solution at a PP of 60 mmHg. After a period of global ischemia of forty minutes' duration at 15 degrees C, reperfusion was started either abruptly (aRp: PP 75 mmHg immediately) or gently (gRp: PP 75 mmHg within thirty minutes); it lasted for forty-five minutes. Intraventricular peak systolic pressure (ISP) was monitored and energy-rich compounds (ATP, ADP, AMP, CrP, free Cr) were analyzed. In normal hearts, metabolic recovery was not affected by the mode of reperfusion, but functional recovery (ISP) averaged 88% of the preischemic control value after gRp as compared with 73% after aRp. In hypertrophied hearts, gentle reperfusion ameliorated both metabolic and functional recovery. At forty-five minute recovery, CrP averaged 5.1 mumol/g ww after aRp and 6.6 mumol/g ww after gRp (p less than 0.01), and ISP amounted to 73% of the preischemic control after aRp and to 85% after gRp.
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PMID:Pressure-controlled reperfusion improves postischemic recovery of LV-hypertrophied rat hearts. 252 79

We have evaluated the impact of inhibiting adenine nucleotide dephosphorylation on the metabolic and functional consequences of renal ischemia. Intramuscular injection of the ADP-analogue adenosine alpha, beta-methylene diphosphate (AMP-CP) achieved a 70% reduction in 5'-nucleotidase activity, as measured in crude extracts of rat kidney. AMPCP-treated animals had an increased residual nucleotide pool at the end of 45 min of ischemia compared with untreated rats. Assessment of renal ATP by 31P-nuclear magnetic resonance (31P-NMR) in vivo during reflow demonstrates the following: 1) higher rapid initial recovery of ATP (69.3 +/- 1.2 vs. 50.0 +/- 0.5% control value, P less than 0.005), 2) accelerated rate of ATP restoration (0.20 +/- 0.02 vs. 0.11 +/- 0.01% control/min, P less than 0.005), and 3) significantly enhanced renal ATP content after 120 min (93.6 +/- 2.0 vs. 63.1 +/- 0.7% control, P less than 0.005). Kidney function, as measured by the rate of inulin clearance 24 h after the insult, was also significantly improved in AMPCP-treated rats (725 +/- 50 vs. 313 +/- 28 microliters.min-1.100 g body wt-1). Thus inhibition of 5'-nucleotidase results in enhanced metabolic and functional recovery from a renal ischemic insult.
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PMID:Protection of the kidney against ischemic injury by inhibition of 5'-nucleotidase. 253 26

Actually the maximum preservation time for donor hearts is limited to 4 hours. The aim of this experimental study in dogs was to develop techniques allowing an extension of this period up to 24 hours. In the first part of the study the influence of diastolic arrest on the preservation of high energy phosphates was studied: The following methods of cardioplegic arrest were used: 1. hyperkalemic arrest 2. hyperkalemic arrest plus high magnesium 3. low sodium and calcium-free cardioplegia. In all experiments cardioplegic arrest was followed by cold storage (0.5 degrees C). Single dose K+ plus Mg2+ cardioplegia offered the least protection. The other two types of cardioplegia were better but the ATP content was still below 50% after 24 hrs preservation. Reperfusion after cardiac transplantation induced irreversible injury and function did not recover after transplantation. In the second part of the study continuous hypothermic perfusion with low sodium and calcium-free cardioplegia was studied. With this technique HEP content, myocardial structure and functional recovery were 100% after transplantation.
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PMID:[Long-term preservation of the heart in view of its transplantation. An experimental study]. 263 87

The objective of this study was to characterize the effect of prostacyclin (PGI2) on ventricular function following total global ischemia in isolated working rat hearts and to investigate the mechanism of its action. Ischemia was initiated for 10, 15, 20 or 25 min with or without treatment with PGI2. Increasing durations of ischemia resulted in a progressive decline in high energy phosphate (HEP) stores, an elevation in tissue lactate, and incomplete recovery of function with reperfusion. Prostacyclin at either 1 or 10 ng/ml had no effect on HEP levels or total adenine nucleotides, and tissue lactate was not significantly affected by PGI2 in hearts made ischemic for 10 to 20 min, but both PGI2 concentrations significantly elevated lactate levels after 25 min ischemia. Reperfusion recovery of left ventricular function was complete following 10 and 15 min ischemia, but incomplete recovery was evident following 20 min ischemia (77% of pre-ischemic function); and although PGI2 had no direct effect on the function of aerobically perfused hearts, recovery of aortic flow with 1 ng/ml PGI2 after 20 min of ischemia was reduced to approximately 20% (P less than 0.01). This depression in recovery was associated with significantly increased lactate levels during reperfusion. At a concentration of 10 ng/ml PGI2 did not depress ventricular recovery or elevate lactate content after 20 min ischemia. When hearts made ischemic for 20 min were analyzed, a significant negative correlation was found between ventricular recovery (aortic flow rate) and lactate concentration; however, no correlation existed between recovery and ATP levels. After 25 min of ischemia, five of eight (62.5%) untreated hearts demonstrated some degree of ventricular recovery, however, only two of ten hearts studied demonstrated any measurable functional recovery with either PGI2 concentration. This effect of PGI2 to reduce or prevent recovery of ventricular function following either 20 or 25 min of ischemia as well as the corresponding elevation in lactate levels was prevented by treatment with the calcium channel blocker verapamil. This study therefore shows that PGI2 at critical low concentrations can depress left ventricular recovery following total ischemia. This effect of PGI2 becomes more pronounced as ischemia duration is prolonged and is associated with elevated tissue lactate levels. The studies with verapamil suggest that PGI2 may be acting via the slow calcium channel to increase lactate levels and depress ventricular recovery following prolonged periods of ischemia.
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PMID:Inhibition of post-ischemic ventricular recovery by low concentrations of prostacyclin in isolated working rat hearts: dependency on concentration, ischemia duration, calcium and relationship to myocardial energy metabolism. 266 90

The purpose of this study is to evaluate the myocardial protective effects of two types of solution during heart transplantation procedure following cold storage in Collins' solution. Based on the concept whether the ischemic time during the procedure is an extension of heart storage or is an usual aortic cross-clamped ischemic time, we compared the effects of our cardioplegic solution (Group I) and Collins' solution (Group II) using isolated working rat heart model. After 30 minutes of global ischemia at 25 degrees C following 2 hours of cold storage, the hearts in Group I exhibited better functional recovery than those in Group II (% recovery of cardiac output was 61.1 +/- 5.4% in Group I and 42.4 +/- 7.4% in Group II, p less than 0.01). In Group II, marked elevation of coronary vascular resistance occurred on reperfusion. CPK release during reperfusion period was greater in Group II (0.41 +/- 0.24 IU/15 min/heart in Group I, 1.92 +/- 1.25 IU/15 min/heart in Group II, p less than 0.01). Myocardial metabolites contents (ATP, TAN, creatine phosphate and lactate) and energy charge were not significantly different between two groups. We conclude that it is harmful to ischemic myocardium to use Collins' solution as myocardial protection during transplantation procedure even if following cold storage in Collins' solution.
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PMID:[Myocardial protection during transplantation procedure following cold storage in Collins' solution]. 267 Nov 86


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