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

Simultaneous measurements of tissue PCO2 (PtCO2), interstitial H+ concentration ([H+]o), and tissue lactate content were used to examine changes in interstitial HCO3- concentration ([HCO3-]o) during complete ischemia. In normoglycemic rats (blood glucose of 6-8 mM; neocortical ischemic-induced lactate content 8-12 mmol/kg) [H+]o increased from 7.22 +/- 0.02 to 6.79 +/- 0.02 pH (n = 3). By contrast, in hyperglycemic rats (blood glucose 18-75 mM; ischemic-induced lactate content 19-31 mmol/kg) [H+]o rose by a significantly larger amount to 6.19 +/- 0.02 pH (n = 7). Given that HCO3- is the predominant interstitial H+ buffer, changes in peak PtCO2 show why peak [H+]o were bimodally distributed compared with lactate content. Between 8 and 12 mmol/kg lactate, when peak PtCO2 rose from 99 to 186 Torr but [H+]o was constant at 6.79 pH, calculated [HCO3-]o increased from 11.9 to 21.9 mM. Then after transitional changes, peak PtCO2 and [H+]o remained constant at 389 +/- 9 Torr (n = 7) and 6.19 pH despite the fact that tissue lactate ranged from 19 to 31 mmol/kg lactate, respectively; [HCO3-]o must have remained constant at 12.3 +/- 0.7 mM (n = 7). Since ischemic brain continued to produce another 12 more mmol/kg of lactic acid above 19 mmol/kg lactate without further changes in PtCO2 or [H+]o, H+ and HCO3- must have been heterogeneously compartmented. The continued lactic acid production occurred in a compartment that occupied 36% of neocortical space. This compartment is likely to represent glial cells.
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PMID:Carbonic acid buffer changes during complete brain ischemia. 308 19

Effects of ischemia and reperfusion on acid-base changes in relation to myocardial contractility, and the effects of correcting H+ were studied by lowering PCO2 or increasing HCO3- levels. The hearts were perfused by working heart mode and whole heart ischemia was induced by use of a one way valve followed by myocardial warming (37 degrees C, normothermia), cooling (18 degrees C, hypothermia) or warming plus 2.1 mM NaHCO3 for 15 min. The hearts were then reperfused for 20 min. Coronary effluent was collected through pulmonary artery cannulation and used for the measurement of acid-base changes. There were close correlations between the decrease in coronary flow and LV pressure, LV dP/dt. Close correlations were also observed between the decline in LV pressure and the rise in PCO2, H+, and the decline in HCO3-. A highly significant correlation was seen between H+ and lactate production. Myocardial contractility decreased to the same extent in 3 groups during ischemia, whereas its recovery rate in both the hypothermia and HCO3- -treated groups were significantly higher than in the normothermia group. The increment of H+ was significantly less in both the hypothermia and HCO3- -treated groups than in normothermia. These results indicate that lactate production is the major H+ producing source and the correction of H+ could minimize the ischemic insult and at the same time contribute to the reperfusion injury.
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PMID:Acid-base changes in ischemic myocardium and intervention with hypothermia or bicarbonate. 314 55

Intracellular pH (pHi) was measured with proton-sensitive liquid sensor microelectrodes in isolated Necturus antral mucosa, paying special attention to arranging experimental conditions to simulate conditions frequently associated with in vivo "stress ulceration." Intracellular pH in mucosas perfused under standard conditions (Ringer's solution containing HCO3-/CO2) was 7.22 + 0.02 (n = 27). Removal of Na+ and HCO3- or addition of amiloride or 4-acetamido-4-isothiocyanostillbene-2,2-disulfonic acid (blockers of Na+/H+ and Cl-/HCO3-exchangers) had no influence on steady-state pHi, suggesting that these ion exchangers do not significantly contribute to the maintenance of pHi in the presence of normal external pH. Acidification of mucosal (luminal) perfusate to pH 3 (mimicking the presence of gastric acid) had no influence on pHi, but mucosal pH 2 (10 mM HCl) acidified pHi to 6.93 +/- 0.07. Acidification of serosal (nutrient) perfusate to pH 6 (mimicking intramucosal acidosis caused by back-diffusion of luminal H+) acidified pHi to 6.72 +/- 0.10. Removal of Na+ from and addition of amiloride to the serosal perfusate during exposure to serosal pH 6.0 induced further acidification of pHi, suggesting that in this acidotic situation (with very low ambient HCO3- concentration) a Na+/H+ exchanger does contribute to the maintenance of steady-state pHi. Increased PCO2 (10% vol/vol in the gas) in a slightly acidic milieu (mimicking mucosal ischemia) likewise acidified pHi to 6.73 +/- 0.05. A combination of mucosal acid (pH 3), high PCO2 (10% CO2), and low serosal pH (pH 6) (mimicking conditions that prevail, for example, during hemorrhagic shock) acidified pHi and ultimately resulted in cell death. These derangements of intracellular acid-base balance may have pathogenetic importance also in in vivo stress ulceration.
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PMID:Intracellular pH in isolated Necturus antral mucosa in simulated ulcerogenic conditions. 316 88

During near complete hyperglycemic brain ischemia, brain lactate levels rise in excess of 16-18 mmol/K and are associated with severe brain infarction. Analyses of pHo, Pt(CO2), and total brain lactate under these circumstances suggest that H+, HCO3, and lactate become unequally distributed between cells and the interstitial space and, perhaps, even between different types of brain cells. In addition, to whatever physiological advantages it may generate, such compartmentalization may be a factor leading to cell death in brain ischemia.
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PMID:Compartmentation of acid-base balance in brain during complete ischemia. 324 68

ATP-MgCl2 X administration had been shown to accelerate the recovery of renal function following warm ischemia. However, since the major breakdown product of ATP is adenosine, the relative contribution of ATP vs. adenosine in improving renal function following ischemia remains to be determined. To study this, kidneys were subjected to 45 min of normothermic ischemia and then perfused at 100 mmHg with oxygenated Krebs-HCO3 buffer containing albumin, [3H]inulin, substrates, and either 0.3 mM ATP-MgCl2 or adenosine-MgCl2 for 110 min. Perfusate and timed urine samples were collected and analyzed for radioactivity and [Na+]. The functional parameters indicated that although adenosine-MgCl2 treatment provided a transient improvement, it failed to provide a sustained improvement in renal function or attain control values compared with ATP-MgCl2 treatment. Thus, the salutary effects of ATP-MgCl2 following warm ischemia in the kidney are not mediated by adenosine.
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PMID:Comparison of effects of ATP-MgCl2 and adenosine-MgCl2 on renal function following ischemia. 349 30

Transient renal tubular acidosis may complicate acute renal failure (ARF). To clarify this phenomenon, the present study examined tubular H+ ion secretory capacity in an ischemic model of ARF. Clearance studies were performed in dogs subjected to 60 minutes, unilateral renal artery clamping. The contralateral kidney served as control. One hour after release of clamp, mean glomerular filtration rate (GFR) was reduced by 50 to 70 percent in the ischemic kidney. Bicarbonate reclamation (mEq/liter GFR) was comparable in both kidneys. However, ischemia resulted in impaired distal acidification as judged by three separate maneuvers: minimal urinary pH following sulphate infusion was higher in ischemic than in control kidney (6.61 +/- 0.39 vs. 5.39 +/- 0.26, P less than 0.01), mean urine to blood PCO2 difference (U-B PCO2) was significantly lower during phosphate infusion (ischemic: 13.8 +/- 4.1 mm Hg, control: 37.2 +/- 6.8 mm Hg, P less than 0.01) and was completely abolished during isotonic NaHCO3 infusion in the ischemic kidney (-1.9 +/- 3.4 mm Hg) compared to control (40.1 +/- 14.8 mm Hg, P less than 0.05). Urinary potassium excretion was intact following ischemia and was appropriately suppressed by amiloride. Administration of 0.7 M NaHCO3 solution at a rate sufficient to produce maximally alkaline urine resulted in a similar U-B PCO2/UHCO3 relationship in both kidneys in the face of impaired distal acidification in the ischemic kidney. This suggests either that the defect may be reversed by massive bicarbonate infusion or, alternatively, that U-B PCO2 difference may be related to other factors in addition to distal H+ secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired renal acidification following acute renal ischemia in the dog. 382 Sep 40

Effects of forelimb tourniquet ischemia of 90 minute duration were investigated in six bulls aged two to three years. Studies were also conducted up to 150 minutes after release of the tourniquet. Parameters investigated were pH, PCO2, PO2, oxygen saturation and HCO3. In systemic circulation no variations in different parameters were observed during 90 minutes of ischemia. However, significant increase in arterial and venous pH were observed after 30 and 45 minutes of the release of tourniquet, respectively. These increases were accompanied by an increase in HCO3. In the affected limb, ischemia resulted in severe acidosis with a significant increase in PCO2 and a nonsignificant decrease of HCO3. There was a significant fall in PO2 and oxygen saturation. After release of the tourniquet, limb venous pH increased significantly due to a significant fall in PCO2 and a nonsignificant increase in HCO3. A significant increase in the limb venous PO2 and oxygen saturation post tourniquet was observed up to the end of the experiments. There was evidence of very poor oxygen exchange and utilization up to 150 minutes after release of the tourniquet. These results demonstrated that tourniquet ischemia of 90 minutes duration of the limb of cattle may not be safe.
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PMID:Effects of limb tourniquet ischemia on local and systemic acid-base and blood gases of cattle. 681 61

The objective of the present study was to discover whether or not intracellular alkalosis develops in the brain in the recovery period following transient ischemia. Forebrain ischemia of 15-min duration was induced by four-vessel occlusion in rats, with recovery periods of 15, 60, and 180 min. Intracellular pH was derived both by the HCO3- -H2CO3 method and from the creatine kinase equilibrium. The ischemia was associated with energy failure and marked accumulation of lactic acid in the cerebral cortex. Recirculation brought about rapid rephosphorylation of adenine nucleotides and gradual normalization of lactic acid levels. After 15 min of recovery, the HCO3- -H2CO3 method indicated persisting acidosis, but the creatine kinase reaction did not. After 60 min, a shift of pH in the alkaline direction was demonstrated in both methods. This alkalosis had disappeared after 3 h of recovery. It is concluded that resumption of ATP production after ischemia is followed by a rapid rise in intracellular pH, which transiently increases above normal.
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PMID:Intracellular pH in the brain following transient ischemia. 682 11

We studied the individual and combined effects of extracellular acidosis and increases in extracellular potassium on action potential characteristics and conduction in order to gain a better understanding of the effects of acute ischemia. At each level of potassium between 2.7 and 17 mm, acidosis induced by increasing Pco2 (respiratory acidosis) and by decreasing HCO3- (metabolic acidosis) decreased resting membrane potential, the maximum rate of rise of the action potential upstroke (Vmax), and slowed conduction. Metabolic acidosis consistently and significantly lengthened the steady state action potential duration whereas respiratory acidosis did not. Respiratory acidosis caused changes in resting membrane potential, Vmax, and conduction velocity; which occurred more rapidly and were of greater magnitude than the changes induced by metabolic acidosis. The changes in Vmax induced both types of acidosis were due to a change in the resting membrane potential-Vmax relationship as well as to the changes in the resting membrane potential. The conduction slowing induced by acidosis was greater when potassium was 9 and 13 mM than when potassium was 5.4 mm. Our results suggest that acidosis causes important changes in the electrophysiological properties of ventricular fibers and that many of the known electrophysiological effects of acute ischemia can be mimicked by the combined effects of extracellular acidosis and an increase in extracellular potassium.
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PMID:Interaction of acidosis and increased extracellular potassium on action potential characteristics and conduction in guinea pig ventricular muscle. 713 80

Paracorporeal rat hearts were supplied with blood derived from the abdominal aorta of a supporting rat. The circulatory stability and working capacity of the supporting animal was analyzed in the experimental situation in terms of PO2, SO2, PCO2, HCO3, pH and electrolytes, all of which were within the normal range before and during a 60 min period of paracorporeal perfusion. For evaluation of ischemic damage in this model studies were made on three groups of excised hearts. They were subjected to 10, 15 or 20 min of complete global ischemia at 37 degrees C (ambient temperature) and reperfused for 30 min, including ECG, observations of contractility and an analysis of creatine kinase efflux in the coronary effluent. The results showed good reproducibility and the data were in accordance with reports from similar studies on Langendorff preparations. The model, which is easily set up, inexpensive and based upon pulsatile blood perfusion, should be more physiologic than the conventional Langendorff preparation.
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PMID:A paracorporeal rat heart model for ischemic and reperfusion studies. 715 56


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