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

Transient forebrain ischemia was induced in rats whose brain temperature was 31, 33, 35, 38, or 40 degrees C. The development of regional injury was followed using magnetic resonance (MR) imaging, with the ultimate extent of neuronal injury quantified histopathologically. Animals in the hypothermic groups showed minimal changes in MR images over 4 days; normothermic animals showed intensity enhancement attributed to progressive edema developing in the striatum and, later, in the hippocampus. Ischemia at 40 degrees C resulted in widespread edema formation by 1 day post-ischemia; animals in this group did not survive beyond 30 hours. Histopathological analysis at 4 days (1 day for the hyperthermic group) post-ischemia showed that neuronal damage in the normothermic group was confined to the hippocampus and striatum. Minimal damage was found in the hypothermic groups; damage in the hyperthermic group was severe throughout the forebrain. There were no differences in the pre-ischemia 31P MR spectra for the different groups. During ischemia, the increase in intensity of the Pi peak and the fall in tissue pH increased with temperature in the order hypothermic less than normothermic less than hyperthermic group of animals. Post-ischemia energy recovery was similar in all groups, while pH recovered more rapidly in hypothermic animals.
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PMID:Magnetic resonance imaging and 31P magnetic resonance spectroscopy study of the effect of temperature on ischemic brain injury. 139 40

PD--the electric potential difference across the gastric mucosa--is a variable used to describe the gastric mucosal integrity and function. A new, reliable, and easily applied method for gastric PD measurements corrected for the disturbing liquid junction potentials between gastric juice and the PD measuring probe is presented. PD is measured with the gastric lumen negative, and a numeric reduction in PD is used as an expression of an injured mucosal condition. A reduced gastric PD is found along with a reduced gastric mucosal blood flow after intravenous indomethacin in anesthetized dogs. Increasing the FFA/albumin ratios in mini-pigs causes vasoconstriction and PD reduction. Short hypoxia and selective gastric ischemia cause a reversible PD reduction and no morphologic changes in anesthetized dogs, but ischemia for 1 h causes more permanent changes in PD, pH, and morphology. This damage can be reduced by allopurinol pretreatment, possibly due to the inhibition of oxygen-derived free radical formation. Gastric PD and pH were measured in volunteers and duodenal ulcer patients during Stroop's color word conflict test, in which mental stress causes sympathetic activation. A PD reduction and a pH increase were found along with stress induction, thereby indicating an influence of mental stress on stomach mucosal function. It is concluded that gastric PD measurement may be useful in ulcer pathogenetic research, and a sufficient gastric mucosal blood flow is stressed as being important for the mucosal defense.
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PMID:Gastric potential difference measurements. The gastric mucosal integrity and function studied with a new method for measurement of the electric potential difference across the stomach wall. 192 6

Experiments were conducted on 14 mongrel dogs to appraise the validity of the results of intraoperative pH-metry in the control of vagotomy completeness depending on the force of pressure exerted on the pH electrode with consideration for the type of a pH catheter used. The level of parietal pH increased with elevating pressure force due to diminished circulation in the gastric wall. The encountered diminution of circulation in the gastric wall after SPV increases still more the pH level and reduces the amplitude of its growth even in areas with maintained parasympathetic innervation with the use of histamine, which raises the probability of incomplete vagotomy. The authors conclude that pH-metry by slight application of the pH electrode to the gastric wall raises the validity of the values recorded and reduces the frequency of incomplete vagotomy in patients operated on in the clinic by 4.7 times. Increase of parietal pH to more than 6.7, irrespective of the force of the exerted pressure, is an indirect sign of ischemia of the gastric wall.
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PMID:[Intraoperative pH-metry in the prevention of incomplete vagotomy and ischemia of the gastric wall in selective proximal vagotomy]. 259 72

Phosphorus-31 magnetic resonance spectroscopy (MRS) was used to monitor regional changes in high-energy phosphorus compounds and intracellular pH during 60 min of acute regional ischemia (acute occlusion of left anterior descending artery) and reperfusion in open-chest cats using a 1.2-cm two-turn coil sutured to the myocardium. During the 60-min ischemic phase, phosphocreatine (PCr) intensity was reduced to 47 +/- 4.9% (mean +/- SE) of control (p less than 0.01) by 15 min postocclusion while adenosine triphosphate (ATP) intensity decreased more slowly with the decrease (66 +/- 5.6%) achieving significance (p less than 0.05) only at 60 min postocclusion. Inorganic phosphate (Pi) increased to a maximum of 397 +/- 42% of control (p less than 0.01) while the pH decreased progressively from 7.36 +/- 0.02 to 6.02 +/- 0.14 (p less than 0.01). After release of occlusion PCr intensity recovered to 86 +/- 12% of the initial control value at 15 min postreperfusion but showed a subsequent downward trend to 79 +/- 8.8%. The ATP did not recover but tended to decline further during reperfusion. The Pi intensity decreased to 260 +/- 38% of control while the pH increased to 7.01 +/- 0.23 by 15 min postreperfusion. Thus, the reperfused irreversibly injured myocardium is characterized by persistent depletion of PCr and ATP and elevation of Pi. Phosphorus-31 MRS provides a nondestructive method for characterizing the reperfused irreversibly damaged myocardium.
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PMID:Characterization of high-energy phosphate compounds during reperfusion of the irreversibly injured myocardium using 31P MRS. 339 64

During myocardial ischemia in dogs effects of NCO-700, a protease inhibitor on myocardial pH, were investigated. Ischemia was produced for 90 min by partial occlusion of the left anterior descending coronary artery (LAD). Myocardial pH was measured by a micro glass pH electrode inserted in the subendocardium of the LAD area. Before partial occlusion, myocardial pH was 7.50-7.67. It decreased by 0.65 to 0.86 pH units after partial occlusion. NCO-700 was injected intravenously after 30 min partial occlusion. At a dose of 5 or 20 mg/kg NCO-700 increased myocardial pH, which had been decreased by LAD partial occlusion, by 0.26 or 0.31 pH units, respectively. In the nonischemic myocardium pH increased only 0.03 units. Drug-induced restoration of myocardial [H+] was then calculated. At a dose of 5 or 20 mg/kg NCO-700 restored myocardial [H+], which had been increased by partial occlusion. However, NCO-700 did not attenuate the ischemia-induced elevation of ST segment of the surface electrocardiogram. These observations demonstrate that NCO-700 attenuates myocardial pH depressed by partial occlusion of LAD.
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PMID:Effect of NCO-700, an inhibitor of protease, on myocardial pH decreased by coronary occlusion in dogs. 405 26

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 metabolic status of rat livers during hypothermia has been studied using 31P magnetic resonance spectroscopy. Perfusion with oxygenated buffer at 6-8 degrees C allowed maintenance of ATP, while pH increased to values in the range 7.7-7.9. In organs depleted of ATP by a short (2 h) period of cold ischemia, pH fell to 6.92 +/- 0.10. If these livers were reperfused with hypoxic buffer at hypothermia, two distinct responses were noted. In one group (responders), there was evidence of ATP resynthesis and in these organs pH returned to 7.90 +/- 0.28. In the second group (non-responders), there was no recovery of ATP synthesis and pH remained depressed at 6.97 +/- 0.07. In another group, adenine nucleotides were severely depleted by 24 h of cold ischemia, and in these livers there was again no significant recovery of ATP synthesis during hypoxic reperfusion and pH remained at 7.03 +/- 0.25. These results suggest that (a) there is an apparent relationship between energy metabolism and control of intracellular pH in the hypothermic mammalian liver, and (b) that intracellular pH may shift in liver at hypothermia to values predicted by the alpha-stat hypothesis.
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PMID:Control of intracellular pH in mammalian liver at hypothermia: evidence for a relationship with energy metabolism. 830 3

Gastrointestinal complications including acute stress ulcerations occur after burn injury. The causes of acute gastric derangements are multiple, and tissue ischemia in the acute period of burn shock may promote breakdown of the gastric mucosal protective barrier. We compared gastric pH in mice after 25% total body surface area, full-thickness murine burn injury with that in unburned control animals. Animals were anesthetized with methoxyflurane and were resuscitated with 1 ml normal saline solution immediately after burn. Animals were killed at intervals up to 24 hours after burn injury, stomachs were removed and opened, and gastric mucosal pH was measured by use of a surface pH probe. In other animals mixed venous blood was obtained via direct inferior vena cava puncture, and blood gas analysis was performed at intervals up to 24 hours after burn injury. Unexpectedly, gastric mucosal pH increased in burned mice compared with that in controls. The peak difference, greater than one log pH unit, occurred at 3 hours after burn injury (pH 4.45 burn vs pH 3.34 control, p < 0.00001), and this difference was maintained through 12 hours (pH 4.88 burn vs pH 3.20 control, p < 0.005). In this model, shock was observed to begin as early as 1 hour after burn injury and reached its maximal period (base deficit, -27.8 mEq/L) at 12 hours after burn injury. In view of the higher gastric pH in burned mice with concomitant profound shock, gastric acid production appears to be impaired during this time, which suggests acute postburn gastrointestinal ulcerations may be primarily due to ischemia. Prevention of organ ischemia may play a key role in the prevention of acute gastric ulcerations after burn injury.
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PMID:Burn injury results in decreased gastric acid production in the acute shock period. 858 42

In vitro data suggest that low tissue pH reduces, whereas extracellular alkalosis potentiates, cerebral anoxic injury via excitotoxic mechanisms. We tested the hypothesis that in vivo metabolic alkalemia potentiates defects in energy metabolism after global incomplete cerebral ischemia (12 min) and reperfusion (180 min) by an N-methyl-D-aspartate (NMDA) receptor-mediated mechanism. Brain ATP, phosphocreatine, and intracellular pH (pHi) were measured by 31P magnetic resonance spectroscopy in anesthetized dogs treated with 1) preischemic intravenous carbicarb buffer (NaHCO3+Na2CO3, Carb, n = 7); 2) carbicarb infusion plus NMDA receptor antagonist MK-801 (MK-801 + Carb, n = 7); 3) an osmotically equivalent volume of 5% NaCl (NaCl, n = 8); or 4) equivalent volume of 0.9% NaCl (Sal, n = 3). Sagittal sinus pH was raised to 7.82 +/- 0.04 before and 7.65 +/- 0.03 during ischemia in Carb vs. 7.72 +/- 0.01 and 7.60 +/- 0.01 in MK-801+Carb, 7.25 +/- 0.02 and 7.15 +/- 0.03 in NaCl, and 7.31 +/- 0.00 and 7.26 +/- 0.01 in Sal, respectively. Ischemic cerebral blood flow (CBF, radiolabeled microspheres), pHi, and ATP reduction were similar among groups. By 180 min of reperfusion, recovery of ATP was greater in MK-801+Carb (104 +/- 6% of baseline), NaCl (93 +/- 6%), and Sal (94 +/- 6%) than in Carb (47 +/- 6%). Intraischemic pHi was similar among groups, and pHi recovery did not vary among groups despite differences in sagittal sinus pH. In Carb, CBF was restored but with delayed hypoperfusion. We conclude that extracellular alkalosis is deleterious to postischemic CBF and energy metabolism, acting by NMDA receptor-mediated mechanisms.
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PMID:Alkalemia reduces recovery from global cerebral ischemia by NMDA receptor-mediated mechanism. 922 31

Muscle acidosis has been implicated as a major determinant of reflex sympathetic activation during exercise. To test this hypothesis we studied sympathetic exercise responses in metabolic myopathies in which muscle acidosis is impaired or augmented during exercise. As an index of reflex sympathetic activation to muscle, microneurographic measurements of muscle sympathetic nerve activity (MSNA) were obtained from the peroneal nerve. MSNA was measured during static handgrip exercise at 30% of maximal voluntary contraction force to exhaustion in patients in whom exercise-induced muscle acidosis is absent (seven myophosphorylase deficient patients; MD [McArdle's disease], and one patient with muscle phosphofructokinase deficiency [PFKD]), augmented (one patient with mitochondrial myopathy [MM]), or normal (five healthy controls). Muscle pH was monitored by 31P-magnetic resonance spectroscopy during handgrip exercise in the five control subjects, four MD patients, and the MM and PFKD patients. With handgrip to exhaustion, the increase in MSNA over baseline (bursts per minute [bpm] and total activity [%]) was not impaired in patients with MD (17+/-2 bpm, 124+/-42%) or PFKD (65 bpm, 307%), and was not enhanced in the MM patient (24 bpm, 131%) compared with controls (17+/-4 bpm, 115+/-17%). Post-handgrip ischemia studied in one McArdle patient, caused sustained elevation of MSNA above basal suggesting a chemoreflex activation of MSNA. Handgrip exercise elicited an enhanced drop in muscle pH of 0.51 U in the MM patient compared with the decrease in controls of 0.13+/-0.02 U. In contrast, muscle pH increased with exercise in MD by 0.12+/-0.05 U and in PFKD by 0.01 U. In conclusion, patients with glycogenolytic, glycolytic, and oxidative phosphorylation defects show normal muscle sympathetic nerve responses to static exercise. These findings indicate that muscle acidosis is not a prerequisite for sympathetic activation in exercise.
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PMID:Sympathetic activation in exercise is not dependent on muscle acidosis. Direct evidence from studies in metabolic myopathies. 954 95


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