Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We wished to determine whether histidine scavenges hydroxyl radical, H2O2, and superoxide anion in vitro and to investigate the protective effect of histidine on isolated perfused rat hearts after global ischemia (40 min) and reperfusion (30 min) (I/R). Left ventricular (LV) function was recorded and coronary effluent was collected for measurement of lactate dehydrogenase (LDH) before ischemia and at 5, 10, 15, and 30 min of reperfusion. At the end of the experiment, a portion of the LV wall was fixed with 2% glutaraldehyde for morphological analysis; the remaining heart was immediately frozen in liquid nitrogen for determination of adenine nucleotides. Histidine effectively quenched hydroxyl radicals and H2O2, but not superoxide anions, in in vitro and in vivo conditions. Hearts treated with histidine exhibited significantly greater functional recovery during reperfusion as compared with nontreated hearts (p < 0.05). Cell morphology was well preserved, and enzyme release was significantly attenuated by histidine treatment (p < 0.05). Histidine raised the ATP level to 73% and the creatine phosphate level to 68% of normal control during reperfusion. Total adenine nucleotide pool and energy charge rate in histidine-treated hearts significantly increased as compared with those in nontreated hearts (p < 0.05), but no effect on ATP and creatine phosphate was noted during ischemia, Histidine prevents postischemic reperfusion injury in isolated heart by inhibiting reactive O2 species and preserving high-energy phosphates (HEP).
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PMID:Antioxidative properties of histidine and its effect on myocardial injury during ischemia/reperfusion in isolated rat heart. 772 45

Aspartate and glutamate each have been shown to improve cardiac recovery after hypoxia or ischemia under normothermic conditions, but whether their effects are additive and to what extent they are modified by hypothermia has not been studied systematically. We set out to compare the individual and combined protective effects of aspartate and glutamate during cardioplegic arrest under normothermic and hypothermic conditions in the rat. Using isolated working rat hearts, functional and metabolic recovery was assessed after 0.5 hours of potassium arrest at 37 degrees C or 5 hours at 2 degrees C in control hearts (C) and in hearts in which 20 mmol/L glutamate (G), 20 mmol/L aspartate (A), or both (A + G) was added to the cardioplegic solution. Under normothermic conditions, percentage recovery of prearrest work (mean +/- standard error of the mean) was as follows: C = 31.7 +/- 2.8, G = 34.8 +/- 0.2, A = 49.6 +/- 2.8*, A + G = 53.7 +/- 2.3*. Under hypothermic conditions, the values were as follows: C = 40.4 +/- 4.0, G = 45.2 +/- 2.3, A = 59.4 +/- 1.8*, A + G = 54.1 +/- 1.2* (*p < 0.01 versus C and G). Recovery of postischemic high-energy phosphate content followed the same pattern: A = A + G > G or C. Measurement of postischemic myocardial content of amino acids showed that recovery of function and energy status correlated with maintenance of myocardial levels of aspartate (r = 0.9; p < 0.01) but not glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differing protection with aspartate and glutamate cardioplegia in the isolated rat heart. 777 37

Isolated rat hearts can be protected by preconditioning, although this has not been found when they are perfused with pyruvate. We addressed the question of whether pyruvate could increase the threshold for preconditioning in isolated rat hearts and whether this could be overcome with increased durations of ischemia. A protocol of four periods of 5 min of ischemic preconditioning (4 x 5 min) protected hearts (improved recovery of function, reduced lactate dehydrogenase release) not perfused with pyruvate from a subsequent 30-min period of global ischemia, but did not protect pyruvate-perfused hearts. Pilot studies indicated that hearts perfused in the presence of pyruvate must be ischemic for approximately 40% longer to produce equivalent ischemic damage in nonpyruvate-treated hearts. Thus the preconditioning period of 5 min was increased by approximately 40% to 7 min to produce equivalent degrees of preconditioning. Hearts preconditioned with the 4 x 7 min protocol with pyruvate were significantly protected against a subsequent severe global ischemia (enhanced recovery of function, reduced lactate dehydrogenase release). High-energy phosphates were measured at the end of the preconditioning protocol (before final global ischemia) to determine whether there was a correlation between cardioprotection and high-energy phosphate levels. There was no correlation between ATP, ADP, or AMP levels and the efficacy of preconditioning. However, an increase in creatine phosphate was associated with cardioprotection, although the importance of this in mediating preconditioning is doubtful. Thus the ability to precondition rat hearts is somewhat dependent on their energy source, but this appears to be due to changes in the severity of the ischemic preconditioning event.
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PMID:Pyruvate increases threshold for preconditioning in globally ischemic rat hearts. 794 85

Amino acid enrichment of cardioplegic solutions has been shown to improve both the metabolic and functional recovery of ischemic myocardium. However, because of the marked systemic vasodilatation involved, use of amino acid enrichment is limited to the periods of induction and reperfusion. Fumarate is a Krebs' cycle intermediate whose conversion to succinate is responsible for the generation of adenosone triphosphate and the oxidation of the reduced form of nicotinamide-adenine nucleotide which is the pathway by which aspartate exerts its effect. Fumarate may also function as a free-radical scavenger and is involved in calcium transport. To determine if fumarate-enriched blood cardioplegia would improve the functional recovery of the neonatal heart, 14 neonatal piglet hearts were isolated and placed on a blood-perfused working heart circuit. After the baseline functional and metabolic assessment was done, cold ischemic arrest was initiated with either standard blood cardioplegic solution (group I; N = 7) or fumarate-enriched (13 mmol/L) blood cardioplegic solution (group II; N = 7). Cardioplegic solution was given at a pressure of 40 mm Hg every 20 minutes for 2 hours, and topical hypothermia was used. Sixty minutes after warm whole blood reperfusion, the functional recovery at left atrial pressures of 3, 6, 9, and 12 mm Hg was 70%, 66%, 66%, and 65%, respectively, in group I, versus 102%, 106%, 105%, and 109%, respectively, in group II (p < 0.05). The tissue creatinine phosphate levels after reperfusion were significantly higher in group II hearts (15.0 +/- 1.2 mumol/g dry heart tissue) than in group I hearts (9.2 +/- 1.9 mumol/g dry heart tissue), although the adenosine triphosphate levels were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fumarate-enriched blood cardioplegia results in complete functional recovery of immature myocardium. 801 Aug 14

The effects of coenzyme Q10 (CoQ) were studied in isolated, isovolumic rat hearts during a 30-min period of global ischemia followed by 40 min of reperfusion. After reperfusion 1) the relative recovery of developed pressure (DP) was increased by CoQ (75 vs. 40% of the preischemic value for 20 microM CoQ and control hearts, respectively, P < 0.001); 2) diastolic pressure elevation was decreased by CoQ (20 vs. 50 mmHg in CoQ vs. control hearts, respectively, P < 0.001); and 3) recovery of high-energy phosphates and reduction of inorganic phosphate were approximately twofold greater in CoQ vs. control hearts (P < 0.001 for each parameter). The beneficial effects of CoQ were not observed when CoQ was added at the onset of reperfusion. The total free generation during reperfusion was not affected by CoQ. In unpaced hearts, in the presence of verapamil to prevent spontaneous beating, spontaneous Ca2+ oscillations were measured as scattered laser light intensity fluctuations (SLIF). The transient rise in SLIF in the postischemic reperfused myocardium, which previously has been shown to predict the extent of Ca2+ overload, was suppressed by CoQ (P < 0.001). These results suggest that while early CoQ treatment does not scavenge the primary burst of superoxide or hydroxy radical generation, which occurs on reperfusion, it markedly improves the functional recovery during reperfusion by enhancing the recovery of high-energy phosphates and preventing Ca2+ overload.
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PMID:Coenzyme Q10 enhances cardiac functional and metabolic recovery and reduces Ca2+ overload during postischemic reperfusion. 802 79

Functional recovery following ischemia and reperfusion in the isolated working rat heart perfused with glucose (11 mM) was examined in relation to pre- and postischemic levels of ATP, glycogen, glucose 6-phosphate, and the lactate-to-pyruvate ratio. The following variables were studied: feeding and fasting in vivo, addition of L-lactate (10 mM), dl-beta-hydroxybutyrate (10 mM), glucagon (0.01 and 1 micrograms/ml), and a 15-min anoxic perfusion before ischemia in vitro. Recovery was assessed as the percentage of preischemic power. Good correlation was found between functional recovery and the postischemic content of glycogen. Glycogen depletion by anoxia or glucagon before ischemia impaired recovery. There was no relationship among lactate produced, or the lactate-to-pyruvate ratio, and recovery. The addition of lactate or beta-hydroxybutyrate to hearts from fed rats increased the content of glycogen and glucose 6-phosphate, whereas addition of lactate, but not beta-hydroxybutyrate, improved recovery. There was a linear relationship between glycogen content and glucose 6-phosphate levels. In conclusion, the degree of return of oxidative metabolism and of net glycogen resynthesis reflects postischemic recovery of function. The results also suggest a role for anaplerosis of the citric acid cycle as an additional determinant of postischemic recovery.
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PMID:Metabolic recovery of isolated working rat heart after brief global ischemia. 806 97

Phosphorus-31 nuclear magnetic resonance and left ventricular pressure development (dP/dt) were used to test the hypothesis that age-related differences in myocardial functional recovery after ischemia and cold crystalloid cardioplegia (CCC) are the result of an inverse relationship between recovery and the decrease in intracellular pH (pHi) during ischemia. Neonatal (3-8 days) and adult rabbit hearts were Langendorff perfused using two protocols: (1) control--30 min perfusion, 30 min global ischemia, 2 h reperfusion; (2) CCC--the same except ischemia was initiated after a 4-min infusion of cold hyperkalemic solution. Analysis of variance and the Tukey test showed the following significant differences between the protocols (p < 0.05). CCC decreased inorganic phosphate (Pi) during ischemia in both age groups, but more in adult hearts, and decreased Pi during reperfusion in adult hearts. CCC increased pHi during ischemia and ATP during ischemia and reperfusion in both age groups but more in adult hearts. CCC increased dP/dt during reperfusion only in adult hearts. The results are consistent with the hypothesis.
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PMID:Are age-related differences in response to myocardial ischemia and cardioplegia pH dependent? 811 42

The rate of recovery of rat myocardial alpha 1-adrenoceptor density and responsiveness after in vivo block with phenoxybenzamine (1 mg/kg, i.p.) have been investigated by measuring [3H]prazosin binding, and noradrenaline-stimulated [3H]inositol phosphate production. Repopulation of alpha 1-adrenoceptors was monoexponential, with a t1/2 of 33 h; functional recovery was also monoexponential, with t1/2 of 28 h. Furthermore, our results clearly demonstrate the absence of a receptor reserve for alpha 1-adrenoceptors mediating noradrenaline-stimulated phosphoinositide breakdown in rat myocardial tissue. These observations indicate a close relationship between the density of [3H]prazosin binding sites and the ability of alpha 1-adrenoceptors to respond to noradrenaline. Moreover, based on competition curves for inhibition of specific [3H]prazosin by WB-4101 to rat myocardial membranes 48 h and 7 days after the administration of phenoxybenzamine, the results suggest that rat myocardial membranes contain both alpha 1-adrenoceptors subtypes, i.e., alpha 1A and alpha 1B, in an approximate ratio of 20:80, and this relative ratio does not seem to be altered during the recovery process.
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PMID:In vivo recovery of alpha 1-adrenoceptors in rat myocardial tissue after alkylation with phenoxybenzamine. 813 81

Isolated working guinea pig hearts were subjected to 30-min total normothermic ischemia and 30-min reperfusion with modified Krebs solution to which various agents were added. The presence of glutamate in the solution resulted in better recovery of cardiac pump function and higher myocardial energy phosphate levels. Addition of phrelone, a calmodulin inhibitor, or adenosine and ribose did not improve pump function. The similar functional recovery was observed after addition of taurine instead of glutamate and their combination exerted even higher functional recovery while further addition of phosphocreatine was not so effective.
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PMID:[Modifications to the solution for reperfusion of the ischemic heart]. 813 78

The present study determined whether the administration of cyclocreatine phosphate (CCrP) prior to ischemia can enhance the recovery of rat hearts hypothermically preserved for a prolonged period. Rats (n = 6 per group) were injected intravenously with 1 ml saline or CCrP (500 mg/kg). After 2 hr, hearts were excised and arrested by an infusion of University of Wisconsin solution. Saline hearts were then incubated in 40 ml UW, while CCrP hearts were incubated in 40 ml UW containing 100 mg CCrP; a mixture that is now referred to as Hartford Hospital (HH) solution. After 6 hr of storage at 4 degrees C, hearts were reperfused in the Langendorff mode for 15 min and then in the working heart mode for 30 min. Results indicated that the recovery of cardiac function--measured as aortic flow, coronary flow, cardiac output, stroke volume, and stroke work--was significantly better in CCrP group (50-55% baseline) compared with that of saline hearts (20-25%). Although no difference in enzyme leakage (i.e., creatine kinase) or lactate was detected between the two groups, the increase in heart weight after the initial 6-hr storage was significantly higher in saline hearts compared with that of CCrP hearts. Results of this study support the conclusion that CCrP treatment provides improved functional recovery after prolonged hypothermic preservation.
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PMID:Enhancement of the recovery of rat hearts after prolonged cold storage by cyclocreatine phosphate. 815 24


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