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

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severity of renal injury and recovery of function in acute renal failure (ARF) are strongly related not only to the magnitude and nature of ARF insult but also to numerous factors in the host which govern renal susceptibility to the insult and repair of renal lesion. Prior ARF affords resistance to a rechallenge with the same or different ARF insult. The mechanisms for this acquired resistance to ARF have not been well established, but suggested mechanisms include (a) increased resistance of regenerated tubular epithelial cells to a rechallenge, (b) glomerular refractoriness to vasoactive substances, (c) failure of damaged kidney to concentrate the toxic substance, (d) enhanced antioxidant enzyme activity in glomeruli, and (e) increased Na(+)-K(+)-ATPase activity in regenerated tubular epithelial cells. Controversy still exists regarding roles of these factors in the resistance to renal failure. Functional and morphologic recovery of postischemic kidney is enhanced by antecedent unilateral nephrectomy but delayed in the presence of the contralateral kidney. The mechanisms for the effect of uninephrectomy remain unsettled. Recent studies suggest contributions of changes in preglomerular vascular resistance; alterations in the environment which follow ischemia to all functioning excretory renal tissues; and altered production and release of vasoactive substances such as angiotensin, endothelin, thromboxane, and atrial natriuretic peptide.
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PMID:Factors affecting severity of renal injury and recovery of function in acute renal failure. 132 11

The success of heart transplantation is limited by the negative correlation between the length of the cold ischemic storage period and the quality of functional recovery. We use 23Na, 31P NMR spectroscopy, and hemodynamic parameters to describe temperature-dependent changes in sodium influx and the concentration of phosphorus high-energy compounds during different storage periods. Perfusion with Krebs-Henseleit solutions containing Dy(TTHA)3- permitted discrimination of intra- and extracellular sodium during cold ischemic storage. The 23Na NMR visibilities under the acquisition and processing parameters used in our experiments were 40 +/- 4% for the intracellular compartment and 97 +/- 11% for the extracellular compartment. At 4 degrees C, the intracellular Na+ accumulation exceeded that observed at 15 and 22 degrees C. The ATP and PCr depletion rates were much lower at 4 degrees C and the left ventricular contractility was higher after longer periods of storage, as the storage temperature decreased. The intracellular Na+ concentration cannot serve as a marker for the postischemic recovery probability. The relative activity of the Na/K ATPase pumps is not correlated with the preservation success. However, intracellular sodium ion accumulation is a major factor in the time lag of the reperfusion recovery.
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PMID:Sodium ion transport in rat hearts during cold ischemic storage: 23Na and 31P NMR study. 146 Nov 25

The characterization of unique responses of immature hearts to ischemic injury is important in devising better methods of myocardial protection for neonatal cardiac operations. Two end-points used to assess the vulnerability of immature myocardium to ischemic injury, namely, the time between onset of ischemia to the beginning of contracture and the functional recovery after reperfusion, had yielded results that appeared to be contradictory. In this study both the immature and adult rabbit hearts were used to study these two end-points in the same model, to assess their relationships and physiologic implications. Our data confirmed that, although immature hearts have greater capacity than adult hearts for functional recovery after identical periods of ischemic insult, their times to ischemic contracture are not prolonged, as could have been expected. A negative correlation between the rise in resting myocardial tension (i.e., contracture) and the recovery of ventricular function after reperfusion was noted both in the neonatal and in the adult hearts. However, reperfusion undertaken after "the onset of contracture" showed that the ventricle could still regain a measure of its function, which indicates that the "irreversibility" in global ventricular function is a gradual and progressive phenomenon. Biochemical studies of sarcoplasmic reticular calcium-adenosinetriphosphatase activity indicated that the immature myocardium has a significantly lower activity of this enzyme. Further depression of this enzyme activity after ischemia is seen in the immature hearts and may in part explain the earlier onset of contracture reported. A unifying concept to explain these unique responses of neonatal hearts to ischemia is proposed, based on the immaturities of certain key enzymes. The implications of these findings in the development of better protective techniques are also discussed.
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PMID:Unique responses of immature hearts to ischemia. Functional recovery versus initiation of contracture. 153 57

Isolated working rat hearts were exposed to 25 min ischemia, and functional recovery was assessed by aortic flow (AoF) and rate-pressure product (RPP) to evaluate the beneficial effects of potassium (20 mM) induced arrest (K-arrest) prior to ischemia. K-arrest improved the recovery of function after 30 min of reperfusion compared with the control group (%AoF: 68 +/- 6 vs 0%, %RPP: 90 +/- 3% vs 60 +/- 3%, p less than 0.01). The accumulation of Ca++ at the end of reperfusion was less in hearts with K-arrest (2.2 +/- 0.1 vs 4.5 +/- 0.3 mumol/g dry, p less than 0.01). There was no difference between the two groups in high energy phosphate content at the end of ischemia. The increase in intracellular Na+ (Nai) during ischemia was reduced in hearts with K-arrest (delta: 19 vs 46 mumol/g dry), and the level of intracellular K+ (Ki) was higher at the end of ischemia in hearts with K-arrest (341 +/- 4 vs 318 +/- 2 mumol/g dry, p less than 0.01). During the first 5 min of reperfusion, the level of Ki in K-arrested hearts jumped to a higher level than in the control group (delta: 15 vs 2 mumol/g dry, p less than 0.01). The level of Nai was lower in hearts with K-arrest after 5 min of reperfusion. These data suggested that K-arrest might preserve the activity of Na+/K+ ATPase during ischemia and early reperfusion, and that it attenuated the increase in Nai during ischemia and reperfusion, which resulted in less Ca++ overload during reperfusion via the Na+/Ca++ exchange mechanism and led to improved recovery.
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PMID:[Mechanism of myocardial protection with potassium arrest in isolated ischemic rat hearts]. 166 47

The effectiveness of diltiazem on the functional recovery of the heart, calcium (Ca++) uptake and binding, Ca++ ATPase of cardiac sarcoplasmic reticulum (SR), and MB fraction of creatine kinase (MBCK) of coronary sinus blood was investigated after one and a half hours of reperfusion following three hours of ischemic cardiac arrest. The dogs were divided into three groups: group I, sham bypass; group II, cold crystalloid cardioplegia; and group III, cold crystalloid cardioplegia with diltiazem. There was a decrease in aortic pressures left ventricular pressure development (dp/dt), left ventricular work index (LVWI), total systemic vascular resistance (TSVR), and left ventricular systolic pressure (LVSP) in the sham bypass group. There was a decrease in cardiac index (CI), LVWI, and mean right atrial pressure (mRAP) and an increase in TSVR and pulmonary vascular resistance (PVR) in group II as compared with group I. Although there was a tendency for a decrease in the indices of myocardial contractility in group II, they were not significantly different from those in group I. The indices of myocardial contractility, CI, and LVWI in group III were slightly higher than in group II, but they were not significantly different from each other. The values for calcium uptake by SR in groups II and III were similar but significantly lower than those in group I. Calcium binding in group III was significantly lower than that in group I. Calcium ATPase of SR in the three groups were similar. Although MBCK increased in all the groups, the increases were not significantly different among the three groups. The results of this study indicate that cold crystalloid cardioplegia with diltiazem was not better than cold crystalloid alone in preserving the cardiac contractility and cellular function during prolonged ischemic cardiac arrest. However, the cardiac function in terms of cardiac index was better preserved with diltiazem.
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PMID:Effects of diltiazem on the functional recovery of the myocardium at organ and cellular level during prolonged hypothermic ischemic cardiac arrest. 214 87

The purpose of this study was to explore the relationship between the extent of sarcolemmal damage observed 2 h after reperfusion of myocardium which had been ischemic for either 0.5 or 1 h and the long-term recovery of function of that same myocardium. For this purpose we studied the Ca2+ pumping ATPase activity and protein phosphorylation of sarcolemmal vesicles isolated after 2 h reperfusion. Both activities declined depending on the duration of ischemia, which suggests the development of sarcolemmal Ca2+ pump failure. Morphological examination of the sarcolemma by thin-section and freeze-fracture electronmicroscopy, in biopsies obtained after 2 h of reperfusion, showed severe clustering of intramembranous particles and formation and extrusion of lipidic liposomal structures which also depended on the duration of ischemia. Except for the occurrence of minor particle aggregation in the samples which had been ischemic for 0.5 h, sarcolemmal disruption was only seen in those myocardial segments which had been subjected to 1 h of coronary artery ligation. Recovery of regional myocardial function, assessed by 2-D-echocardiography after 2 weeks of reperfusion, was closely related to the degree to which sarcolemmal integrity was maintained after 2 h reperfusion.
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PMID:Loss of functional and structural integrity of the sarcolemma: an early indicator of irreversible injury of myocardium? 244 91

Ischemic injury results in proximal tubule (PT) dysfunction and loss of surface membrane (SM) polarity. Since epithelial vectorial transport requires SM polarity, we set out to determine if correction of renal cortical PT dysfunction following ischemia was dependent on the reestablishment of SM polarity. Acute renal failure was induced using a bilateral 50-min pedicle clamp. Serum creatinine and fractional sodium excretion were maximal on day 1, remained elevated on day 3, and returned toward base line by day 8. PT cellular ultrastructure was normal by day 3. Despite rapid morphological recovery, ischemia resulted in a prolonged defect in glucose reabsorption. The delayed recovery of normal glucose handling closely paralleled the slow normalization of apical membrane lipid polarity. Na+-K+-ATPase polarity was also lost secondary to ischemia as demonstrated cytochemically and biochemically by the redistribution of Na+-K+-ATPase to the apical membrane. The time required to reestablish normal Na+-K+-ATPase polarity (8 days) paralleled the recovery of normal PT Na+ reabsorption (8 days), as assessed by fractional lithium clearances. This finding supports the hypothesis that apical Na+-K+-ATPase is in part responsible for reduced Na+ reabsorption following ischemic injury. In summary, these data suggest that functional recovery of PT glucose and Na+ reabsorption following a reversible ischemic insult requires not only morphological recovery, but also the reestablishment of surface membrane lipid and protein polarity.
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PMID:Epithelial polarity following ischemia: a requirement for normal cell function. 253 79

The present investigation was undertaken to compare the effects of cold crystalloid and blood cardioplegia on the functional recovery of the heart; on Ca++ binding and uptake, Ca++-ATPase of the sarcoplasmic reticulum (SR), and sarcolemmal (SL) ATPase; and on serum MB fraction of creatine kinase (MBCK) after one and half hours of reperfusion following one hour of ischemic cardiac arrest in dog. This study was made also to determine if the functional changes are related to the changes in biochemistry at the molecular level. The dogs were divided into three groups: sham bypass (SB), cold crystalloid cardioplegia (CC), and pump blood cardioplegia (PB). There was a decrease in the cardiac index (CI), left ventricular work index (LVWI), and mean aortic pressure (MAP) in all three groups. The index of myocardial contractility [dp/dt)/IIP) and CI were lower in the CC group as compared with the SB and PB groups. All the hemodynamic values for the PB group were similar to those of the SB group except total systemic vascular resistance (TSVR) and left ventricular end-diastolic pressure (LVEDP) which were lower in the PB group. The index of myocardial contractility and cardiac index appeared to be greater in the PB group than in the CC group. There was a decrease in the Ca++ uptake by SR from both the CC and PB groups. Ca++ binding and Ca++,-ATPase of SR from the PB group were depressed. The sarcolemmal ATPase was unaffected in both groups. The serum MBCK increased in both PB and CC groups, though the increase was smaller in the PB group. These results indicate that the functional recovery of the heart was slightly better with pump blood cardioplegia than with cold crystalloid cardioplegia. The depressed myocardial contractility and cardiac function in the CC group were associated with a decrease in the Ca++ uptake by SR. However, the decreases in the Ca++ binding, Ca++ uptake, and Ca++ ATPase by SR from the pump blood cardioplegic group were not accompanied by decreases in the cardiac contractility and cardiac function. Myocardial damage as assessed by serum MBCK was smaller in the PB group than in the CC group.
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PMID:Effects of blood and crystalloid cardioplegia on cardiac function at organ and cellular levels during hypothermic cardiac arrest. 282 61

A study was undertaken to assess the effectiveness of cold crystalloid cardioplegia with or without verapamil on the functional recovery of the heart, Ca++ binding and uptake, Ca++ ATPase of sarcoplasmic reticulum, sarcolemmal ATPase and the MB fraction of creatine kinase (MBCK) after 1.5 h of reperfusion following 1 h of ischemic cardiac arrest. The dogs were divided into three groups: group I, sham bypass; group II, cold crystalloid cardioplegia; group III, cold crystalloid cardioplegia with verapamil. There was a decrease in the cardiac index (CI), left ventricular work index (LVWI) and mean aortic pressure (MAP) in the sham bypass group at the end of the protocol (time period corresponding to 60 mins off bypass). There was a decrease in the Cl and index of myocardial contractility in the cold crystalloid cardioplegic group compared to sham bypass group. The decrease in the cardiac function in cold crystalloid group was associated with a decrease in Ca++ uptake by sarcoplasmic reticulum and a tendency for an increase in the sarcolemmal Na+-K+ ATPase. The Ca++ binding and the Ca++ ATPase of sarcoplasmic reticulum were not affected. The index of myocardial contractility and cardiac function were better with cold crystalloid containing verapamil than with cold crystalloid alone. This improvement, although partial, in cardiac contractility and function with cold crystalloid cardioplegia containing verapamil was associated with an improvement in the Ca++ uptake by the sarcoplasmic reticulum. The Ca++ ATPase and Ca++ binding were depressed in group III. The MBCK in systemic and coronary sinus blood increased progressively in groups II and III. Although there was an increase in MBCK in group I the increase was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of crystalloid cardioplegia and verapamil on cardiac function and cellular biochemistry during hypothermic cardiac arrest. 296 3

Contact hypersensitivity (CH) responsiveness to 2-4-dinitro-1-fluorobenzene (DNFB) is depressed in mice that are sensitized through skin sites exposed to ultraviolet radiation (UVR). This is partially due to a reduction in antigen-presenting cell (APC) activity within UVR-exposed skin, a condition marked by a decrease in the density of ATPase/Ia-positive epidermal cells. The purpose of this study was to correlate the histological and functional recovery of APC activity in the skin of C3H mice exposed to low-dose (4 X 450 J/m2) or high-dose (1 X 15 kJ/m2) UVR with the normalization of CH responsiveness. Skin biopsy specimens taken at various intervals after UVR exposure revealed a rapid recovery in the density of ATPase/Ia positive cells: about 70% of normal by 3 days, and normal after 5 days. Functional analyses showed that lymph node cells obtained from donors that were sensitized with DNFB 3 days after UVR treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus indicating that APC activity in UVR-exposed skin paralleled the recovery of ATPase/Ia-positive epidermal cells. This suggested that an alternative mechanism causes the persistent depression of CH in mice exposed to UVR. Mice pretreated with indomethacin prior to UVR exposure demonstrated a capacity to elicit CH responses to DNFB, which paralleled the histological and functional recovery of APC in the skin (i.e., normal CH responses were elicited 3 days after exposure to UVR). We conclude from this study that APC activity in the skin recovers rapidly after exposure to UVR, and that a PG-dependent mechanism is responsible for many of the persistent and systemic effects that cause a depression in the CH responsiveness of mice treated with UVR.
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PMID:Parallel recovery of epidermal antigen-presenting cell activity and contact hypersensitivity responses in mice exposed to ultraviolet irradiation: the role of a prostaglandin-dependent mechanism. 296 91


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