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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The capability of cyclohexylphenol exaprolol of protecting the ischaemic myocardium during ischaemic cardiac arrest was assessed in the isolated working rat heart. Exaprolol added to the perfusion medium in a dose of 10(-7) mol.l-1 only minimally influenced the left ventricular function (reduced the stroke volume by 18.84% and cardiac output by 14.63%). The hearts were subjected to global ischaemia for 75 min at 26 degrees C and subsequently reperfused for 60 min at 37 degrees C. The recovery of left ventricular function following reperfusion, expressed as a percentage of preischaemic functional performance was used as an indicator of the ischaemic tolerance of the heart. The effect of exaprolol on sarcolemmal (Na+ + K+)-, Mg2+- and Ca2+-ATPase activities was also examined. Exaprolol-pretreated hearts revealed better postischaemic recovery of the left ventricular dP/dt max and stroke volume as well as improved efficiency in the transformation of chemical energy to mechanical work. Exaprolol in 10(-4) mol.l-1 concentration significantly stimulated the specific activity of sarcolemmal (Na+ + K+)-ATPase. Possible mechanisms of the salutary effect of exaprolol on the ischaemic heart are discussed.
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PMID:The influence of exaprolol upon the ischaemic rat heart and its interaction with sarcolemmal (Na+ + K+)-ATPase. 256 82

In Quin-2-loaded erythrocytes of two genetically hypertensive rat strains (spontaneously hypertensive rats, SHR, and the Milan hypertensive strain, MHS) intracellular Ca2+ (Ca2+i) concentration and 45Ca influx rate were increased by 25-30 and 15-20% respectively, in comparison with normotensive controls (Wistar-Kyoto rats, WKY, and rats of the Milan normotensive strain, MNS). After 4 h incubation in the presence of 5 mmol/l sodium vanadate (Na3VO4) as an inhibitor of Ca-ATPase, 45Ca content of intact erythrocytes of SHR was twofold higher while erythrocyte count of stroke-prone SHR (SHRSP) was threefold higher than in WKY. This increase was observed in SHR during the pre-hypertensive stage. Under the same conditions, no difference was noted between MHS and MNS rats. The rate of 32P influx, as well as the concentration of exchangeable chloride, was studied. We failed to detect any significant differences in either parameter between hypertensive and normotensive rats, suggesting that altered cell membrane potential was not responsible for allied Ca fluxes. Erythrocyte shrinking, however, resulted in a two to threefold increase in the rate of 45Ca influx. Neither the rate of 45Ca influx nor Ca2+i were modified by the inhibitor of calmodulin-dependent reactions, R24571 (10 mumol/l). It is suggested that the higher rate of Ca2+ influx in Quin-2-loaded erythrocytes of SHR, as well as the increment in 45Ca content in intact erythrocytes treated with orthovanadate, is due to a change in membrane skeleton organization and cell shrinkage.
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PMID:Calcium transport in erythrocytes of rats with spontaneous hypertension. 284 88

Development of heat stroke led to a decrease in main reactions of energy production and energy potential in erythrocytes, to a decrease in activity of Na+, K+-ATPase and in content of sodium and potassium as well as to alterations in forms and to decrease in volume of these cells.
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PMID:[Relation between energy metabolism, Na+ and K+ levels, and Na,K-ATPase activity in erythrocytes and their volume and shape during overheating]. 285 Dec 13

Membrane fractions enriched in sarcoplasmic reticulum (SR) were isolated from the cardiac ventricles of 10-month-old, stroke-prone spontaneously hypertensive rats (SHRSP) which had been maintained for nine months on one of four experimental diets: low protein (LP) (19% protein), standard (STD) (24% protein), high protein (HP) (32% protein), or high methionine (1.9% methionine) (MET). ATPase activities, as well as ATP-dependent Ca2+ binding and Ca2+-uptake activities, of the isolated SR were determined to examine the influence of diet on myocardial Ca2+-pump activity. SR from all four groups exhibited similar Mg2+-ATPase activity. However, the (Ca2+ + Mg2+)-ATPase activity was significantly elevated in SR from rats on the MET diet while the activity in the other groups showed no significant differences. After 15 sec of incubation, Ca2+-uptake (presence of oxalate) in SR from the LP group was significantly less than Ca2+-uptake in SR from each of the three other diet groups. Ca2+ binding (absence of oxalate) in the SR from the LP group was also significantly less than that from each of the three other diet groups. Kinetic analysis of SR Ca2+-uptake over 60 sec revealed that the Bmax of the MET group was significantly higher than Bmax of the STD diet group. In addition, the Bmax of the LP group was significantly lower than Bmax of the HP and MET groups. There was no significant difference in affinity of the SR Ca2+-uptake system among the four diet groups. These results indicate that modification of dietary protein can influence myocardial SR Ca2+-pump function.
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PMID:ATP-dependent calcium uptake in myocardial sarcoplasmic reticulum from spontaneously hypertensive rats: effect of modification of dietary protein. 293 82

These studies compared the importance of electrogenic Na+-K+ active (ATP driven) transport, changes in K+ conductance, and passive Ca2+-Na+ countertransport in the large relaxation that occurs in the rat caudal and basilar artery on return to K+ from K+-free solutions. Furthermore, we compared the importance of these three membrane electrical mechanisms in stroke-prone spontaneously hypertensive rats (SP-SHR) versus their normotensive Wistar-Kyoto control rats (WKY) in basilar (cerebral) and caudal arteries. We found that in both basilar and caudal arteries the hyperpolarization and relaxation that occurred on return to K+ after exposure to a 0 K+ (extracellular) solution was consistently greater in SP-SHR than in WKY. The change in membrane potential occurring on transition to 0 K+ in arteries maintained at low temperature (16 degrees C), used as an estimate of the change in K+ conductance during the K+ transition, was not different in either basilar or caudal arteries between SP-SHR and WKY. Thus the hyperpolarization on return to K+ at body temperature would depend primarily on the level of activity of the membrane ATPase, referred to as the Na+ pump. We also sought to compare the passive (but electrogenic) Ca2+-Na+ countertransport mechanism between strains for both arteries, but we were unable to detect any evidence of the predicted hyperpolarization-contraction on transition from 145 to 10 mM extracellular Na+. Furthermore, the return to extracellular Na+ solution failed to show the depolarization-relaxation predicted by the Ca2+-Na+ countertransport mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Membrane ATPase mechanism of K+-return relaxation in arterial muscles of stroke-prone SHR and WKY. 293 83

In this review we have attempted a synthesis of ideas from cross-bridge theories of muscle contraction with biochemical mechanisms of the actomyosin ATPase. This synthesis of ideas has been based on experimental approaches that permit mechanical and biochemical investigations on the same system. We have formulated an example of how biochemical processes may be influenced by strain in the cross-bridge and have highlighted how much has yet to be learned about the biochemistry (and protein structure) of the working stroke of the cross-bridge. Processes that do not appear to be related to the working stroke such as ATP-induced dissociation of actomyosin or protein-bound ATP hydrolysis appear to be similar kinetically in fibers and isolated actomyosin. But, as might be expected, this is not the case in those processes that involve force production and the performance of mechanical work. There appears to be a sound base from which the mechanochemistry of individual processes within the cross-bridge cycle can be analyzed in detail. There is a need for the development of spectroscopic techniques, particularly those that might detect the rate of Pi and ADP dissociation from cross-bridges into the medium. The combination of pulse photolysis of caged ATP and time-resolved structure analysis by use of synchrotron radiation (53) should lead to better understanding of the structure of cross-bridge states in relation to the chemistry and mechanics of transient intermediates.
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PMID:Relationships between chemical and mechanical events during muscular contraction. 294 Oct 26

A therapeutic role for naloxone during stroke has been suggested, but a neurochemical site of action remains to be determined. Previous work with the gerbil cerebral cortex has shown that either bilateral secondary ischemia (60-min occlusion of the carotid arteries followed by 40-min reflow) or unilateral primary ischemia (permanent ligation of one carotid artery for 6 hr in symptomatic animals) produced deficits in both Na+, K+-ATPase (EC 3.6.1.3) activity and various parameters of activation of adenylate cyclase (EC 4.6.1.1). Pretreatment of gerbils with either naloxone or morphine failed to ameliorate or exacerbate, respectively, the neurological signs of ischemia; however, morphine did reduce mortality. Infusion of naloxone prior to ischemia afforded varying degrees of protection to forskolin, GTP analogs, and NE (norepinephrine) activation of adenylate cyclase, as well as to Na+, K+-ATPase (bilateral ischemia only). Similarly, morphine inhibited damage to basal activity of adenylate cyclase and to stimulation by NE, forskolin, and Gpp (NH)p (5'-guanylyl imidodiphosphate). Under in vitro conditions morphine increased the basal activity of adenylate cyclase but reduced responses to NE and forskolin. Furthermore, morphine injected into control gerbils elevated basal- and forskolin-elicited activities but reduced the activation of adenylate cyclase by NE.
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PMID:Effects of naloxone and morphine on cerebral ischemia in gerbils. 294 23

Many characteristics expected from the cyclic ATPase mechanism of Scheme 1 are apparent in reactions measured directly in muscle fibers. ATP detaches rigor cross-bridges rapidly. Reattachment and force generation are also rapid compared to the overall cycling rate, but reversibility of many of the reactions allows significant population of detached states during contraction. ATP hydrolysis shows rapid, "burst" kinetics and is also readily reversible. Pi is released before ADP in the cycle. Pi release is slow in relaxed fibers but is promoted by the interaction between myosin and actin during contraction. Actomyosin kinetics differ in fibers from the ATPase reaction in solution in that Pi binds more readily to AM' X ADP in fibers, and complex, Ca2+-dependent kinetics are evident for ADP release. These properties suggest that the mechanical driving stroke of the cross-bridge cycle and events during physiological relaxation are closely linked to the product release steps. All of the reactions, except step 7a, in the main pathway for ATP hydrolysis, indicated in Scheme 1 by heavy arrows, are fast compared to the overall cycling rate in isometric contractions. Based on this finding, we expect step 7a (or isomerizations of the flanking states) to be relatively slow (approximately 3 s-1). But neither the rate-limiting reaction, nor the expected major dependence on mechanical load or shortening that would explain the Fenn effect, have actually been detected. Use of the pulse photolysis and oxygen exchange methods with structural and spectroscopic techniques and with perturbations of mechanical strain promise to reveal these aspects of the mechanism.
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PMID:Kinetics of the actomyosin ATPase in muscle fibers. 295 53

The activity of three forms of ATPase were examined in fractions of the brain of the gerbil treated with ethylene glycol-N-N-tetra-acetic acid (EGTA) under a variety of conditions of primary and secondary (reflow) ischemia. In animals which were unilateral ischemic (ligation of the right common carotid), damage to Na+, K+-ATPase alone was observed only after at least 6 hr of ischemia had elapsed. The phenomenon occurred in only symptomatic gerbils and was absent in animals which were either asymptomatic or only displayed partial neurological symptoms. Under conditions of bilateral cerebral ischemia, in which both carotid arteries were clamped, only irreversible ischemia (60 min) followed by reflow, was associated with highly significant damage to cerebral Na+, K+-ATPase. In regional studies of the forebrain involving ischemia for 60 min plus 30 min reflow, damage to Na+, K+-ATPase was evident in the cerebrum, hippocampus, striatum and thalamus, while the hypothalamus and olfactory bulb were spared. Pretreatment of gerbils with allopurinol, clonazepam or combinations of thiopental plus either indomethacin or methylprednisolone offered protection to cerebral Na+, K+-ATPase subsequent to secondary ischemia. With only minor exceptions (striatum) neither Ca2+, Mg2+- nor Mn2+-ATPase were altered by stroke or treatment with drugs.
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PMID:Classification of ischemic-induced damage to Na+, K+-ATPase in gerbil forebrain. Modification by therapeutic agents. 299 3

The present study has examined early cellular effects of chronic adriamycin administration to dogs using a protocol (1 mg/kg/week to a total cumulative dose of 240 mg/m2) producing significant but small reductions in ejection fraction and stroke volume as determined echocardiographically prior to the development of clinical or radiological manifestations of heart failure. At this early phase of cardiomyopathy, significant reduction (P less than 0.05) in sarcoplasmic reticulum Ca2+, K+-ATPase was observed without any change in mitochondrial, lysosomal or sarcolemmal marker enzymes. Myocardial calcium (P less than 0.01) and glutathione (P less than 0.001) levels were increased significantly. Detailed analysis of myocardial phospholipid profiles failed to show any significant differences between control and treated dogs. In contrast, red cell membranes showed increased phosphatidylcholine (PC) and decreased phosphatidylserine (PS) contents, resulting in a significant increase in PC/PS ratio (P less than 0.05). No significant changes were detected in activities of catalase, superoxide dismutase or glutathione peroxidase in erythrocytes or myocardial tissue from control and adriamycin-treated animals. A significant (P less than 0.05) elevation in plasma sialic acid was observed following adriamycin treatment. Our results suggest that early adriamycin-induced damage is unlikely to result from alterations in cellular processes protecting tissues against oxidant injury. Regression analysis indicated that, of the various abnormalities observed, only the elevated myocardial calcium levels and the increases in plasma sialic acid correlated with the degree of myocardial functional impairment. Our findings suggest the presence of sarcolemmal alterations in Ca2+ handling in early adriamycin-induced myocardial injury and indicate that measurement of plasma sialic acid should be further investigated as a possible noninvasive indicator of impending adriamycin cardiotoxicity.
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PMID:Adriamycin cardiomyopathy: implications of cellular changes in a canine model with mild impairment of left ventricular function. 299 97


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