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

In the conclusion of this series of reports, the application of 31P/2H NMR to investigate the pathophysiology of sepsis in rat hindlimb muscle is demonstrated. Sepsis decreased muscle [PCr] by 18%, 18 +/- 4 SD vs 22 +/- 4 SD mmol/kg tissue wet wt (P = 0.01) in control rats but [ATP] was unchanged, 6 mmol/kg tissue wet wt (P = 0.2). The derived free cytosolic [ADP] in the two groups was similar, [ADP]septic = 0.023 +/- 0.004 SD and [ADP]control = 0.021 +/- 0.003 SD mmol/kg tissue wet wt, and not statistically different (P = 0.14). Likewise [Pi] in the septic and control groups was not statistically different, [Pi]septic = 1.1 +/- 0.5 SD and [Pi]control = 1.2 +/- 0.4 SD mmol/kg tissue wet wt (P = 0.2). Septic rats presented the symptom of respiratory alkalosis evidenced by elevated blood pH. Sepsis decreased muscle blood flow by 33%, P = 0.003, but examination of individual subjects did not demonstrate a correlation with the reduction in [PCr]. Thus, a metabolic energy deficit caused by cellular ischemia/hypoxia is not a likely cause of cellular abnormality in rat hindlimb muscle during sepsis.
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PMID:Concurrent quantification of tissue metabolism and blood flow via 2H/31P NMR in vivo. III. Alterations of muscle blood flow and metabolism during sepsis. 159 58

Intracellular pH was determined by neutral red color histophotometry in cerebral tissue from rats subjected to 10 minutes of cardiac arrest and from rats that had recovered for 1 and 6 hours following 8-10 minutes of total cerebral ischemia (TIA). Tissue concentrations of ATP, lactate and glucose were measured corresponding to the pH determinations. As expected, tissue ATP was depleted while tissue lactate was markedly elevated after 10 minutes of ischemia without reflow in the cerebral cortex, striatum and hippocampus. However, both metabolites were near control following 1 and 6 hours of recovery in all three regions. Tissue glucose was not significantly different from control following 1 and 6 hours of reperfusion. During ischemia, the intracellular pH dropped to 6.5-6.7 in all three regions (p less than 0.05). But, since the initial pH of the hippocampus was 7.79 while that of the cerebral cortex and striatum was approximately 7.02, the net drop in pHi the hippocampus was greater than in the other two regions. Following 1 hour of reperfusion, a trend towards tissue alkalosis was observed in the cerebral cortex and striatum.
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PMID:Regional changes in intracellular pH determined by neutral red histophotometry and high energy metabolites during cardiac arrest and following resuscitation in the rat. 177 24

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

The effects of metabolic acidosis and alkalosis in the initial reperfusate on post-ischemic stunned myocardium were investigated in isolated rat hearts. Metabolic acidosis and alkalosis were produced by altering the doses of artificial buffer (Tris) in place of sodium bicarbonate. All hearts were subjected to global ischemia for 15 min at 37 degrees C. The initial reperfusate under study was given during the subsequent 10 min of reperfusion, just prior to release of the aortic clamp. After that, reperfusion using normal Krebs-Henseleit buffer solution was carried out for 40 min. The acidotic initial reperfusate (pH 6.8) resulted in better protection than the alkalotic initial reperfusate (pH 7.8), as demonstrated by 1) a higher recovery of aortic flow (80.6% +/- 3.8% vs 32.7% +/- 4.8%, p less than 0.01), 2) a smaller leakage of creatine kinase during the initial reperfusion phase (6.0 +/- 0.7 vs 14.6 +/- 2.1 IU/10 min/g dry weight, p less than 0.05) and during the post-ischemic Langendorff perfusion phase (8.8 +/- 1.7 vs 37.3 +/- 5.2 IU/10 min/g dry weight, p less than 0.05), and 3) a lower myocardial water content at the end of reperfusion (84.8% +/- 0.2% vs 85.7% +/- 0.3%, p less than 0.05). Not only Tris buffer system, but also HEPES buffer system indicated that acidotic initial reperfusate was effective to protect against myocardial injury. These results suggest that 1) the extracellular pH during initial reperfusion profoundly influences the reversible myocardial dysfunction (stunned myocardium), and 2) the acidotic initial reperfusate improves post-ischemic myocardial performance.
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PMID:Beneficial actions of acidotic initial reperfusate in stunned myocardium of rat hearts. 195 71

This review has attempted to indicate areas of investigation that in vivo MRS methodology is particularly suited for and would answer important questions related to neonatal cerebral development or injury. There are several metabolites (PEth, PCr, NAA, taurine, glutamate) and lipids detectable by in vivo 31P or 1H MRS, which show substantial changes in concentration during ontogenesis. Do these biochemical markers correlate with major morphological changes, such as myelination? If they do, can this be used to quantitate abnormalities in brain development from congenital abnormalities or metabolic encephalopathies? In the neutral to mild acidic range (7.0 greater than pHi greater than 6.5) adult and neonatal brain appear to have similar intrinsic physicochemical buffering capacity. However, at the extremes of pHi induced by respiratory alkalosis or severe acidosis from partial ischemia, the possibility exists that the buffering capacities of adult and neonatal brain differ. Whether this is true requires further investigations using both neonates and adults, or perhaps more preferably, multiple measurements on a single species throughout its developmental period. Such studies are now feasible because multinuclear in vivo MRS can provide a large body of information from individual animals. A similar study design could prove useful for investigations of changes in cerebral resistance to hypoxia, ischemia, or asphyxia during development. The roles that blood pressure, glucose, temperature, or the administration of extrinsic buffers and drugs have on modulating the severity of and relationship between changes in blood flow, energy metabolites, or pHi, are all amenable to study using in vivo MRS. Furthermore, all of these variables can be measured simultaneously. The kinetics of brain acid and lactate homeostasis during chronic cerebral insults or following acute insults has not been thoroughly examined in either neonates or adult animals. There is evidence to suggest that following ischemia or seizures, brain acidosis resolves before brain lactosis. However, the clinical diagnostic significance of this post-insult uncoupling between pHi and lactate remains to be established. Finally, the application of in vivo MRS methodology to study the effects of trauma, drugs, environmental toxins, and other metabolic encephalopathies on neonatal cerebral perfusion and metabolism are virtually unexplored. Hopefully, the material presented here will prompt researchers to consider the application of in vivo MRS to new avenues of investigation.
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PMID:In vivo multinuclear magnetic resonance spectroscopy investigations of cerebral development and metabolic encephalopathy using neonatal animal models. 219 84

We investigated the long-term (up to 1 week) relationships between the duration of cerebral ischemia and postischemic energy metabolic profile, pH, and tissue edema in the rat. Ten rats each were subjected to 8 or 12 min of forebrain ischemia induced by bicarotid occlusion concurrent with systemic hypotension, and the results were compared with those of 10 sham-operated rat controls. In vivo 31P nuclear magnetic resonance spectroscopy was performed prior to ischemia and at intervals up to 168 h after ischemia. Cerebral edema (measured by specific gravity) was assessed prior to ischemia and at 24, 72, and 168 h after ischemia. The data revealed significant differences in the brain tissue pH profile over time between the ischemic groups (p less than 0.03). The 12-min ischemic animals exhibited brain tissue alkalosis (pH = 7.27 +/- 0.12) at 24 h compared with both sham (pH = 7.09 +/- 0.08) at 24 h and preischemic (pH = 7.06 +/- 0.04) pH values. The pH remained alkalotic (pH = 7.23 +/- 0.15) through the 48-h time period. In contrast, in the 8-min group, the onset of alkalosis was delayed until 48 h after ischemia (pH = 7.24 +/- 0.15), and pH remained alkalotic for only 24 h. No difference in high-energy phosphate metabolism was detected between groups. A different time dependence of tissue pH and specific gravity changes after 12 min of ischemia was detected. The present study suggests that the duration of an ischemic event marks the time of onset of brain tissue alkalosis and its duration and that cerebral edema alone cannot explain the pH changes.
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PMID:Time course of postischemic intracellular alkalosis reflects the duration of ischemia. 221 79

We measured cerebral intracellular pH using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy during 1 week after forebrain ischemia or sham operation in eight and seven rats, respectively. Mean maximum pH was significantly higher (p less than 0.003) in the ischemic group than in the sham-operated group (7.34 +/- 0.03 and 7.19 +/- 0.02, respectively). The difference between mean maximum pH and baseline pH (7.08 +/- 0.01 in each group) was significantly greater (p less than 0.02) in the ischemic group than in the sham-operated group. In the ischemic group, alkalosis occurred primarily after 48-72 hours of recirculation. We speculate that brain tissue alkalosis occurring chronically after ischemia is associated with delayed ischemic neuronal death.
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PMID:Chronic cerebral intracellular alkalosis following forebrain ischemic insult in rats. 230 71

The effect of pH of the reperfusion buffer on postischemic changes in tissue Ca and Na was examined in isolated Langendorff-perfused Sprague-Dawley rat hearts. Reperfusion began after 15-, 25-, or 60-min ischemia at 37 degrees C. After 60-min ischemia, reperfusion at pH 6.4 or 6.6 attenuated the reperfusion-induced Ca gain so long as the acidotic conditions were maintained (3.08 +/- 0.22, 1.37 +/- 0.41, and 16.96 +/- 1.18 mumol Ca gain/g dry wt for pH 6.4, 6.6, and 7.4, respectively after 15-min reperfusion). Conversely, reperfusion under alkalotic conditions (pH 7.9) after 60-min ischemia exacerbated the gain (27.45 +/- 4.75 and 8.92 +/- 1.53 mumol Ca gain/g dry wt during 5-min reperfusion at pH 7.9 and 7.4, respectively). Similar, but less pronounced Ca gains occurred during reperfusion after 15- or 25-min ischemia. Sodium content during reperfusion, but not during aerobic perfusion, was also found to be pH sensitive with acidosis causing a reduction and alkalosis an increase. These results could not be explained in terms of an effect of pH on recovery of high-energy phosphates, percentage "reflow" during reperfusion, or reperfusion-induced increases in tissue water or resting tension. The results are in agreement with the hypothesis that the "inhibitory" effect of acidosis on postischemic Ca overload could involve an effect of pH on the Na(+)-H+ exchanger and intracellular Ca storage.
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PMID:Effect of acidosis and alkalosis on postischemic Ca gain in isolated rat heart. 231 96

Opinions are still not unanimous about the mechanism behind circulation during external cardiac compression and this leads to uncertainty regarding the correct frequency, force of compression and its duration. Adrenaline and other alpha-stimulators increase blood flow during external cardiac compression and increase survival. Cardiac arrest results in anaerobic metabolism and combined metabolic and respiratory acidosis. On account of relatively low minute volume during external cardiac compression decrease in end-tidal carbon dioxide concentration is observed together with arterial alkalosis on account of hyperventilation and venous acidosis. No communications exist about the favourable effect of administration of bicarbonate during cardiac arrest. On the other hand, several conditions suggest that bicarbonate increases the intracellular acidosis with poorer possibilities for resuscitation with this form of treatment. Ischaemia results inter alia in intracellular accumulation of calcium which initiates potential cell destructive processes. No investigations are available which favour employment of calcium during cardiac arrest. Conversely animal experiments suggest the possibility of favourable effects from calcium-entry blockers. Ischaemia and, in particular, reperfusion release cell and vessel damaging free oxygen redicals. Intensive investigations are being conducted at present about the value of anti-oxidants for cerebral and myocardial protection.
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PMID:[Treatment of cardiac arrest. Recent aspects of cardiopulmonary resuscitation]. 267 53

Rats pretreated with sodium bicarbonate were functionally protected from the damage of bilateral renal artery occlusion. The rise in serum creatinine (day 1 minus day 0) during the first 24 h after ischemia was 2.88 +/- 0.28 mg% in the bicarbonate-loaded animals versus 3.90 +/- 0.26 mg% in their matched controls (p less than or equal to 0.01). Pretreatment with acetazolamide produced a similar alkaline urine as the bicarbonate loading (pH 8.3 vs. 7.0 in controls) and a similar degree of protection (delta creatinine 2.85 +/- 0.41 vs. 4.23 +/- 0.26 mg%; p less than or equal to 0.01). A direct effect of sodium loading was excluded by comparing NH4HCO3 with NaHCO3 loading and observing no difference in delta creatinine levels after ischemia (3.39 +/- 0.69 vs. 3.20 +/- 0.61 mg%). These data indicate that NaHCO3 protects in this model of acute renal failure and further suggest that the mechanism of protection is not related to either systemic alkalosis or sodium loading.
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PMID:Effect of sodium bicarbonate preloading on ischemic renal failure. 301


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