UMLS:C0022116 - FACTA Search

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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of moderate post-ischemic hypothermia on neuropathological outcome and cerebral high energy phosphate metabolism, intracellular pH and Mg2+ concentration in the rat. Three groups of animals were investigated: (1) Wistar rats subjected to 12 min of forebrain ischemia under normothermic conditions (n = 17), (2) rats subjected to the identical procedure of ischemia, except that 30 degrees C hypothermia was induced post-ischemia and maintained for 2 h of reperfusion (n = 6), and (3) control hypothermic rats not subjected to ischemia (n = 4). In vivo 31P NMR spectroscopy was performed prior to ischemia, and at intervals up to 168 h after ischemia. Histological analysis of brain tissues was performed 7 days after ischemia. No significant differences in cortical and hippocampal neuronal damage was detected between the two experimental groups. Significantly lower pH values were detected in the hypothermic ischemic animals at 24 h (P = 0.0001) and 48 h (P = 0.018) post-ischemia compared to the normothermic ischemic animals. Normothermic ischemic animals exhibited significantly lower [Mg2+] at 72 h (P less than 0.006) compared to the pre-ischemia level. Our data indicate that post-ischemic hypothermia modifies the profiles of post-ischemic brain tissue pH and Mg2+ concentration, and this modification is not associated with histopathological outcome 7 days after ischemia.
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PMID:The effects of post-ischemic hypothermia on the neuronal injury and brain metabolism after forebrain ischemia in the rat. 156 17

The present study tested the hypothesis that a reduction in calcium flux across the sarcolemma or the sarcoplasmic reticulum at the onset of reperfusion could attenuate subsequent mechanical "stunning" (postischemic myocardial dysfunction). The isolated working rat heart was subjected to 20 minutes of total global ischemia, reperfused in the Langendorff mode for 5 minutes, and then made to work again for 10 minutes. During the early reperfusion period (first 2 minutes), the effects of agents thought to increase cytosolic calcium (high external calcium [modified Tyrode's solution replaced Krebs-Henseleit buffer as the perfusate], isoproterenol, forskolin, and Bay K 8644) were tested. All these interventions worsened stunning. The cardiac output (CO) of control hearts recovered to 74.7 +/- 3.4%, whereas recovery was 56.3 +/- 3.7% (p less than 0.05) for high calcium (10 mM), 53.4 +/- 3.6% (p less than 0.05) for isoproterenol, 43.4 +/- 4.1% (p less than 0.05) for Bay K 8644, and 62.7 +/- 2.4% (p less than 0.002) for forskolin. Interventions aimed at limiting calcium flux during early reperfusion, such as reperfusion with a low extracellular calcium or the addition of ryanodine (3 x 10(-9) M), nisoldipine (10(-8) M), or the inorganic blockers Mn2+ (2 mM) or Mg2+ (16 mM), were also tested. Low extracellular calcium (0.75 mM) improved CO to 91.8 +/- 0.8% (p less than 0.05). Reperfusion with ryanodine and nisoldipine gave CO recoveries of 103.6 +/- 1.8% (p less than 0.002) and 99.0 +/- 2.8% (p less than 0.002), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of severity of reperfusion stunning in the isolated rat heart by agents altering calcium flux at onset of reperfusion. 156 4

The aim of this study was to determine whether acute changes in [Mg2+]free occur during increased hydrolysis of cytosolic ATP, and whether these changes were of sufficient magnitude to be involved in the modulation of myocardial metabolism. 31P-NMR was used to estimate free cytosolic Mg2+ levels ([Mg2+]free) during hypoxia, isoproterenol stimulation, and graded low-flow ischemia in crystalloid perfused, isovolumic rat hearts. Cytosolic [Mg2+]free was calculated to be 0.73 +/- 0.12 mM in control hearts (100 mmHg hydrostatic pressure, 95% O2, n = 18). Cytosolic [Mg2+]free increased gradually during 10 min periods of hypoxia (65%, 50%, 35%, 5% O2), and 20 min infusions of isoproterenol (0.4, 3.0, 75 nM), to maximum values greater than 250% of control (P less than 0.05). During 8 min periods of graded low-flow ischemia (12.0, 7.2, 5.3, 3.4, and 1.6 ml/min/g), [Mg2+]free did not change significantly. [Mg2+]free displayed an inverse linear correlation with total cytosolic [ATP] during isoproterenol infusion (r = 0.87), and an exponential correlation during hypoxia (r = 0.82). The data indicate that acute changes in cytosolic [Mg2+]free can occur during conditions of net ATP hydrolysis although changes in ATP alone do not appear to be solely responsible for the changes in [Mg2+]free. Since the magnitude of the changes in [Mg2+]free are sufficient to alter equilibria of enzymes such as creatine kinase and myokinase, it is possible that these changes are involved in the acute modulation of myocardial metabolism.
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PMID:Cytosolic free magnesium in stimulated, hypoxic, and underperfused rat heart. 165 49

During cardiac surgery, the heart is infused with cold crystalloid cardioplegic solutions such as St. Thomas' Hospital (StT) solution, which contains high concentrations of K+ and Mg2+. The high K+ and Mg2+ block impulse conduction and inhibit Ca2+ influx, thereby arresting the heart and reducing cardiac oxygen consumption. Nevertheless, myocardial edema and post-operative abnormalities have been noted after cardioplegia and attributed to ischemia and reflow or to hypothermia. We found, however, that cold StT (9 degrees C) was hypotonic and induced cell swelling in the absence of ischemic injury. Cell swelling in cold StT was not due to hypothermia alone, but rather was caused by KCl influx and was prevented by partially replacing Cl- with an impermeant anion. After exposure to cold StT, cells transiently shrank to less than control volume on rewarming in physiological saline (Tyrode's solution, 37 degrees C). The transient shrinkage was blocked by ouabain suggesting that Na+ loading of depolarized hypothermic cells and Na(+)-K+ pump activation on rewarming were responsible. Hypothermic ventricular cells seem to follow Donnan equilibrium, and the product of [K+] x [Cl-] in cardioplegic solutions affects cell volume in the absence of ischemic injury.
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PMID:Prevention of myocardial intracellular edema induced by St. Thomas' Hospital cardioplegic solution. 166 12

Isolated hearts from normotensive (NT) and spontaneously hypertensive (SH) rats, subjected to normothermic global ischemia, were used to study whether cicletanine (a new antihypertensive drug) treatment exerts an antiarrhythmic effect against reperfusion-induced arrhythmias. The effect of the drug on myocardial ion contents (Na+, K+, Ca2+, and Mg2+) during ischemia and reperfusion was also determined. Using the optimal doses of cicletanine (30 and 100 mg/kg orally for 14 days), the incidence of reperfusion-induced ventricular fibrillation (VF) and ventricular tachycardia (VT) was reduced from their control values of 91 and 100% (after 30 min of ischemia) to 41 (p less than 0.05), 50 (p less than 0.05) and 41 (p less than 0.05), 58% in the NT group, while the corresponding value in the SH group for VF and VT were 17 (p less than 0.001), 33 (p less than 0.01) and 17 (p less than 0.001), 25% (p less than 0.001), respectively. The results obtained indicate that the cardioprotective effect of cicletanine was greater in the SH group than in the NT group. Cicletanine significantly reduced the ischemia- and reperfusion-induced myocardial Na+ and Ca2+ gains and inhibited the loss of myocardial K+ and Mg2+ in both NT and SH groups. The antiarrhythmic effect of cicletanine appears to be correlated with the preservation of myocardial Na+, K+, Ca2+, and Mg2+ contents via an ion transport modulation.
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PMID:Effect of cicletanine on reperfusion-induced arrhythmias and ion shifts in isolated rat hearts. 168 16

Isolated hearts excised from normotensive (NT) and spontaneously hypertensive (SH) rats subjected to transient normothermic global ischemia were used to study the effect of chronic treatment with iloprost on reperfusion-induced arrhythmias and myocardial ion shifts. After 30 min of ischemia, iloprost given s.c. in doses of 10, 50, 100 and 200 micrograms/kg per day for 14 days reduced the incidence of reperfusion-induced ventricular fibrillation (VF) in isolated hearts from the control value of 91 to 83, 75, 50 (P less than 0.05) and 25% (P less than 0.01) respectively, in NT rats. In the SH groups, the incidence of VF was also reduced from 100 to 75, 58, 33 (P less than 0.01) and 17% (P less than 0.001), respectively, with 10, 50, 100 and 200 micrograms/kg per day of iloprost. A similar reduction was observed in the incidence of reperfusion-induced ventricular tachycardia (VT). Ischemia and reperfusion caused significant changes in myocardial ion contents, i.e. an increase in Na+ and Ca2+ and a decrease in K+ and Mg2+ concentrations. The myocardial water content was also increased in parallel to the Na+ gain. The effect of iloprost given s.c. in doses of 50 and 200 micrograms/kg per day for 14 days was also measured on myocardial ion contents after 15- or 30-min ischemia and 30-min ischemia plus 10-min reperfusion. The higher iloprost dose significantly reduced the myocardial Na+, Ca2+ and water gains and the loss of K+ induced by ischemia and reperfusion in the NT and SH groups, while the decrease in Mg2+ content was alleviated only in SH rats. The results suggest that long-term iloprost treatment reduces the incidence of reperfusion-induced VF and VT by preventing Na+, Ca2+ and water accumulation as well as K+ and Mg2+ loss from myocardial tissue.
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PMID:Effect of iloprost on reperfusion-induced arrhythmias and myocardial ion shifts in isolated rat hearts. 170 6

We studied the effects of cicletanine, an anti-hypertensive drug, on reperfusion arrhythmias in relation to 6-keto-PGF1 alpha, thromboxane B2 (TXB2), and ion shifts (Na+, K+, Ca2+, and Mg2+) induced by ischemia and reperfusion in hearts isolated from spontaneously hypertensive rats. Hearts were subjected to 30-min global ischemia followed by 10-min reperfusion. 6-keto-PGF1 alpha and TXB2 concentrations were determined by radioimmunoassay (RIA) from coronary effluents, and myocardial Na+, K+, Ca2+, and Mg2+ contents were measured by atomic absorption spectrophotometry from myocardial tissue. Two basic protocols were used: (a) acute administration when 3, 10, 30, or 100 mg/L cicletanine was included in the perfusion buffer; and (b) chronic application, in which rats received cicletanine 3, 10, 30, or 100 mg/kg/day orally for 14 days. Acute administration of the drug in low concentrations (3 or 10 mg/L), significantly increased endogenous 6-keto-PGF1 alpha production before ischemia and during reperfusion, whereas higher doses of cicletanine (30 or 100 mg/L) as well as chronic application of the drug failed to increase production of 6-keto-PGF1 alpha in the myocardium. TXB2 production was not influenced by either acute or chronic treatment with the drug. Neither treatment changed myocardial ion contents in comparison with control values (Na+ = 45 +/- 4, K+ = 252 +/- 7, Ca2+ = 1.4 +/- 0.1, and Mg2+ = 12.5 +/- 0.3 mmol/kg dry weight) in nonischemic hearts. Thirty-minute ischemia resulted in a two- and fourfold accumulation of myocardial Na+ and Ca2+ and a 50% decrease in both K+ and Mg2+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cicletanine and reperfusion injury: is there any correlation between arrhythmias, 6-keto-PGF1 alpha, thromboxane B2, and myocardial ion shifts (Na+, K+, Ca2+, and Mg2+) induced by ischemia/reperfusion in isolated rat heart. 171 20

We have investigated hypertension-associated alterations in intracellular cations in the kidney by measuring intracellular pH, free Mg2+, free Ca2+, and Na+ concentrations in perfused normotensive and hypertensive rat (8-14 weeks old) kidneys using 31P, 19F, and double quantum-filtered (DQ) 23Na NMR. The effects of both anoxia and ischemia on the 23Na DQ signal confirmed its ability to detect changes in intracellular Na+. However, there was a sizable contribution of the extracellular Na+ to the 23Na DQ signal of the kidney. The intracellular free Ca2+ concentration, measured using 19F NMR and 5,5'difluoro-1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid, also increased dramatically during ischemia; the increase could be partly reversed by reperfusion. No significant differences were found between normotensive and hypertensive kidneys in the ATP level, intracellular pH, intracellular free Mg2+, and the 23Na DQ signal or in the extent of the extracellular contribution to the 23Na DQ signal. Oxygen consumption rates were also similar for the normotensive (5.02 +/- 0.46 mumol of O2/min/g) and hypertensive (5.47 +/- 0.42 mumol O2/min/g) rat kidneys. The absence of a significant difference in intracellular pH, Na+ concentration, and oxygen consumption between normotensive and hypertensive rat kidneys suggests that an alteration in the luminal Na+/H+ antiport activity in hypertension is unlikely. However, a highly significant increase (64%, p less than 0.01) in free Ca2+ concentration was found in perfused kidneys from hypertensive rats (557 +/- 48 nM, blood pressure = 199 +/- 5 mmHg, n = 6) compared with normotensive rats (339 +/- 21 nM, blood pressure = 134 +/- 6, n = 4) indicating altered renal calcium homeostasis in essential hypertension. An increase in intracellular free Ca2+ concentration without an accompanying change in the intracellular Na+ suggests, among many possibilities, that the Ca2+/Mg(2+)-ATPase may be inhibited in the hypertensive renal tissue.
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PMID:Multinuclear NMR studies of intracellular cations in perfused hypertensive rat kidney. 174 Apr 16

Several studies suggest that the protection exerted by Mg2+ on the reperfused myocardium may be mostly due to its competitive effect with respect to Ca2+. The aim of this research was to evaluate the inhibitory action of Mg2+ on mitochondrial Ca2+ uptake in the reperfused myocardium. Hearts of male Wistar rats (250-300 g) were isolated and perfused by the Langendorff technique. Aerobic control hearts (n = 6) were perfused with a constant flow of 10 ml/min/g for 65 min. In a second group (n = 6) the hearts were aerobically equilibrated for 20 min, then subjected to 30 min of ischemia (98% reduction of coronary flow) and subsequently reperfused for 15 min at the same preischemic flow. The hearts of both groups were electrically stimulated at 300 b/min. Then, the hearts were pooled in groups of 2 each and homogenized for the isolation of mitochondria. One part of mitochondrial suspension was used to evaluate the respiratory function by a polarographic technique. The remaining part was incubated with fura-2/AM for 10 min at 30 degrees C in order to determine the kinetics of Ca2+ transport within mitochondria in the presence of succinate as substrate. Ca2+ uptake was reduced in the mitochondria of reperfused hearts with respect to control, particularly in the presence of elevated extramitochondrial Ca2+ concentrations (greater than 10 nM). On the contrary the initial rate of Ca2+ uptake was increased in the reperfused mitochondria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The inhibitory effect of magnesium on mitochondrial calcium uptake in ischemic and reperfused rat hearts]. 179 May 35

Brain Mg2+ ion concentrations, [Mg2+], were evaluated in three groups of animals subjected to either 8 minutes (n = 10), or 12 minutes (n = 10) of near-complete forebrain ischemia, or sham operation (n = 10), from their 31P NMR spectra. No significant differences were observed in [Mg2+] among sham operated animals prior to or at any time point after surgery. In the 8-min ischemia group, mean [Mg2+] were significantly lower at 48 (0.28 +/- 0.06 mM, p = 0.014) and 72 (0.29 +/- 0.07 mM, p = 0.005) hours post-ischemia when compared to their mean pre-ischemia levels (0.39 +/- 0.08 mM). [Mg2+] was restored to pre-ischemia values at 96 hours after induction of ischemia. In the 12 min ischemia group, [Mg2+] were lower at all time points post-ischemia when compared to their pre-ischemia levels. Our data shows that forebrain ischemia causes a chronic decline of cerebral Mg2+ concentration, and the observed reduction of this cation can be partially attributed to concurrent brain tissue alkalosis.
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PMID:Chronic changes in the brain Mg2+ concentration after forebrain ischemia in the rat. 181 93

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