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

The effects on central hemodynamics and skeletal muscle metabolism during surgery for abdominal aortic aneurysm were compared in 6 patients given a preoperative adrenergic block (group B) and in 6 patients who additionally had a temporary brachio-femoro-femoral by-pass during the aortic clamping (group B + S). The cardiac output, heart rate, arterial and pulmonary artery pressures and the cardiac filling pressure were studied. Biopsy specimens from the lateral vastus muscle and blood samples from the radial artery and the iliac vein were taken before aortic clamping and also before and 30 minutes, 4 and 16 hours after the aortic declamping. Intramuscular temperature and pH were measured. The glycogen, glucose, lactate, pyruvate, ATP, ADP, AMP, phosphocreatine (PCr) and creatine (Cr) contents of the muscle and the lactate and pyruvate concentration in iliac venous and radial arterial blood were determined, using enzymatic fluorometric techniques. In group B, aortic clamping induced severe temporary incomplete ischemia with a 300% increase in lactate/pyruvate (L/P) ratio and a fall in intramuscular pH (pHm). The adenylate energy charge (EC) decreased, but the creatine (PCr + CR) and the adenylate (ATP + ADP + AMP) pool remained unchanged. After aortic declamping, the L/P ratio, EC and pHm regained their preclamping values, but the pools of energy phosphate compounds were reduced, indicating dysfunction or damage of the muscle cells. In group B + S there were no major muscle metabolic changes during clamping or after declamping of the aorta. In group B the systemic vascular resistance (SVR), mean arterial blood pressure (MAP) and left ventricular stroke work (LVSW) increased during the occlusion. On release of the clamp, cardiac output rose, possibly due to the sudden reduction of SVR. A temporary marked fall of MAP occurred. In group B + S, no increase of SVR, MAP or LVSW was observed during aortic clamping. After the declamping, only a minor MAP drop was observed. In both groups, a brief rise in pulmonary vascular resistance after the aortic declamping suggested transient pulmonary microembolism. If a high-risk patient is to undergo reconstructive surgery of the abdominal aorta and/or technical difficulties can be expected to necessitate prolonged cross-clamping during the operation, a temporary extracorporeal by-pass may be a favorable adjuvant, improving cardiac performance and preventing derangement of muscle metabolism.
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PMID:Temporary incomplete ischemia of the legs induced by aortic clamping in man. Metabolic and hemodynamic effects of temporary extracorporeal by-pass. 613 73

The potential efficacy of the calcium channel blocker verapamil in modifying ischemic brain injury was evaluated in anesthetized rats subjected to 60 or 90 min of diffuse forebrain ischemia produced by bilateral occlusion of the carotid and vertebral arteries. Treated animals received verapamil, 2 mg/kg intravenously, prior to ischemia. Four hours of postischemic recirculation was permitted by reversing the carotid occlusions. Intermittent high-voltage slow-wave activity was noted on electroencephalograms shortly after verapamil infusion, prior to ischemia. The ischemic insult induced an isoelectric EEG, which tended to persist during recirculation in both treated and untreated animals. Similarly, verapamil pretreatment failed to influence brain water content or cerebral energy metabolites (phosphocreatine, ATP, ADP, AMP) or cerebral energy charge when assayed after four hours of recirculation. Thus, verapamil failed to confer a protective effect on brain electrical activity, water content, or energy metabolites following ischemia in this model.
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PMID:Verapamil: failure of metabolic amelioration following global forebrain ischemia in the rat. 643 33

31P NMR technique was applied to monitor changes in the energy metabolism of the brain and heart of unanesthetized cats during shock, stroke, hypoxia and increased functional activity. The results show that in these tissues content of inorganic phosphate, sugar phosphates, phosphocreatine and of ATP can be measured decently in awake animals. At the same time this technique has the great advantage over the disruptive biochemical methods that it gives a semi-continuous reading and it is non-invasive. Our findings are summarized as follows: Hemorrhagic shock resulted in an irreversible deterioration of the energy state of the brain. Our stroke model led to a very marked increase in Pi and a decrease CP in the brain but these changes were reversible. The ATP levels of the brain as it was indicated by 31p NMR spectra were not affected by hemorrhagic shock and stroke which can be attributed probably by the reduced rate of ATP consumption. The verification of this hypothesis needs further work. During increased mechanical performance the levels of SP, and Pi increased, ATP decreased, while CP was not influenced in the heart.
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PMID:31P NMR spectroscopy of brain and heart. 663 19

The effect of arterial hypotension on cerebral cortical tissue levels of adenosine triphosphate (ATP), phosphocreatine (PGr), lactate, and reduced nicotinamide adenine dinucleotide (NADH) was studied in male Wistar rats with unilateral carotid ligation exposed to arterial by hypoxia (PaO2 25 torr) for 20 min. while the body temperature was maintained at 32 degrees C and 27 degrees C. Brain metabolite levels were normal in normotensive hypothermic animals exposed to hypoxia, but reduction in arterial pressure to 75 torr caused a significant (p less than 0.05) decrease in ATP and PCr values and a significant increase in lactate and NADH levels. These changes were comparable to those of normothermic normotensive, hypoxic animals. Furthermore, there was no significant differences in the brain metabolite levels between the two hypotensive hypoxic groups. These results indicate that arterial hypotension severely alters the cerebral protective effect of hypothermia against injury caused by hypoxia, and that further reduction in body temperature (from 32 degrees C to 27 degrees C) will not prevent the harmful effect of hypoxia upon the brain in hypotensive rats.
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PMID:Reduction of the cerebral protective effect of hypothermia by oligemic hypotension during hypoxia in the rat. 680 24

Cerebral ischemia was induced in cats using bilateral carotid artery occlusion coupled with hemorrhagic hypotension. Thirty minutes of ischemia, which depleted levels of ATP and phosphocreatine throughout the cerebral cortex, was followed by 2-4 hours of recirculation. During the recovery period, cortical perfusion and NADH fluorescence were monitored through a cranial window. Postischemic perfusion, as indicated by transit time, was initially higher than control, but declined to subnormal levels by 60 minutes. NADH fluorescence transients, induced by brief anoxia, also decreased steadily during recirculation, indicating a failure of oxidation-reduction capability. The disappearance of anoxic-NADH transients usually preceded the decline of flow, suggesting that O2 delivery was not the factor limiting redox reactions. Furthermore, tissue levels of NADH, which were nearly normal after 2-4 hours of recirculation, did not indicate tissue hypoxia. In spite of normalization of NADH, resynthesis of high energy phosphates were severely impaired. The degree of ATP recovery varied widely in different cortical regions; however, there were two general groups of ATP values--one at 5% and the other at 70% of control levels. In the energy-depleted areas, NADH levels were normal, but the total pool of NAD (NADH + NAD+) and the tissue content of K+ were 43% lower than control. In contrast, the NAD pool and K+ content were only slightly diminished in the regions with greater ATP restitution. The results suggest that postischemic resynthesis of ATP may be limited not by inadequate delivery of O2, but rather by defective production of NADH.
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PMID:Factors limiting regeneration of ATP following temporary ischemia in cat brain. 706 95

Glucose metabolites in the rat brain were measured under various stages of ischemia. In acute ischemia induced by bilateral carotid artery ligation, phosphocreatine and ATP levels were significantly decreased and lactate levels were significantly increased in stroke-prone spontaneously hypertensive rats (SHRSP). These extreme changes were not observed in normotensive Wistar-Kyoto rats (WKY) and stroke-resistant spontaneously hypertensive rats (SHRSR), under the same conditions. In chronic ischemia induced by long-lasting regional cerebral blood flow reduction due to severe hypertension, similar changes were observed only in SHRSP at the advanced stage. The levels of glucose metabolites in the brain were confirmed to be well maintained within control ranges even though the cerebral tissues were subjected to the chronic ischemia related to severe hypertension.
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PMID:Effect of acute and chronic reduction of cerebral blood flow on glucose metabolite levels in SHRSP. 730 59

Focal ischemia was produced in cat brain by occluding the middle cerebral artery. After 60 min of ischemia the rate of glucose utilization, as measured by the uptake of [14C] deoxyglucose ([14C]DG), was correlated with tissue levels of ATP, phosphocreatine, and lactate measured in the same regional samples. Ischemia caused local increases of [14C]DG uptake which were associated with mild to moderate anaerobic perturbations of metabolite levels. Altered metabolite levels also occurred in regions in which the rate of glucose consumption was not markedly different from that of the non-ischemic hemipshere. In addition, there were regions with decreased [14C] DG uptake which invariably were depleted of ATP and phosphocreatine. Thus, suppression of glucose metabolism was restricted to the most severely ischemic areas, where the delivery of glucose may be rate-limiting.
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PMID:Correlation between glucose utilization and metabolite levels during focal ischemia in cat brain. 735 35

Cerebral hypoxia-oligemia was produced by lowering of the arterial PO2 to 30 mm Hg and by right common carotid artery occlusion in rats who were pretreated with intravenous Krebs' solution, gamma-hydroxybutyrate (GHB) (500 mg/kg) or gamma-butyrolactone (GBL) (300 mg/kg). At 0.5 h exposure the right cerebral hemisphere of animals receiving Krebs', GHB or GBL showed equivalent decreases of ATP and phosphocreatine and increase of ADP, AMP and lactate which indicated that these depressant drugs had no beneficial effect on the energy metabolism of the acutely hypoxic-oligemic brain. In a second series of rats in which Krebs' solution, GHB or GBL were administered to animals during the early recovery period from 0.5 h hypoxic-oligemic exposure, the brain metabolic patterns of the right hemisphere indicated that GHB retarded the restitution of energy phosphates and the oxidation of the accumulated lactate; whereas, GBL led to a delayed metabolic deterioration. It is concluded that GHB and GBL do not beneficially alter cerebral energy metabolism during acute hypoxia-oligemia and that their administration during restitution may result in metabolic alterations which suggest an unfavorable effect.
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PMID:Effects of gamma-hydroxybutrate and gamma-butyrolactone on cerebral energy metabolism during exposure and recovery from hypoxemia-oligemia. 739 64

Glucose was infused intravenously into cats prior to cerebral ischemia. Brain concentrations of glucose, measured in 7 regions, were elevated 2.5-fold compared to those of non-infused animals. Ischemia of 15 or 30 minutes duration caused a greater accumulation of lactic acid in the brain of glucose-infused animals. Post-ischemic restitution of cerebral ATP, phosphocreatine, and lactate during 90 minutes of recirculation was severely impaired in the brain of animals pretreated with glucose compared to untreated animals. Thus, excess lactic acidosis may be a major factor interfering with metabolic restitution following cerebral ischemia.
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PMID:Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. II. Regional metabolite levels. 741 63

The hemodynamic changes which occur when clamping and unclamping the aorta during reconstructive surgery might be a threat to the elderly patient with concomitant cardiac disease. In addition, the cross-clamping induces a temporary ischemia of the legs, with severe metabolic derangement after the release of the aortic clamp. We have studied the effect of a intraoperative adrenergic block (phenoxybenzamine plus metoprolol) on the central circulation and the skeletal metabolism in 14 patients undergoing aortic reconstruction to treat occlusive arteriosclerotic disease. Cardiac output, heart rate, arterial and pulmonary artery pressures, and cardiac filling pressures, as well as femoral venous blood flow were studied. Biopsy specimens of the lateral vastus muscle and blood samples from the radial artery and iliac vein were taken before aortic clamping, and before, 30 minutes, four and 16 hours after the aorta was unclamped, as well as five days postoperatively. In addition, intramuscular temperature and pH were measured. Glycogen, glucose, lactate, pyruvate, ATP, ADP, AMP, phosphocreatine (PCr) and creatine (Cr) contents of the muscle and lactate and pyruvate concentrations in iliac venous and radial arterial blood were determined using enzymatic fluorometric techniques. Mean arterial blood pressure (MAP) averaged 80 mmHg before clamping, chiefly because of the low systemic vascular resistance (SVR), and left ventricular stroke work (LVSW) was normal. At clamping MAP, SVR, LVSW, remained unchanged. MAP and LVSW were unaffected even though SVR decreased slightly after the aorta was unclamped and resulted in an increased cardiac output, mainly due to a higher stroke volume. No major change in the pulmonary circulation was observed. During clamping the muscle lactate/pyruvate ratio increased, intramuscular pH and femoral venous blood flow decreased indicating insufficient tissue perfusion. Energy charge (EC), the adenylate (ATP + ADP + AMP) and creatine (PCr + Cr) pools were, however, unchanged. In spite of a restored blood flow to the legs, a severe metabolic derangement of the muscle was observed after declamping, with lowered EC, ATP + ADP + AMP and PCr + Cr indicating cellular damage. No improvement in the condition of the cells was observed 16 hours after operation. In conclusion, we found that by using neurolept anesthesia and an intraoperative adrenergic block in combination with a differentiated fluid therapy the central circulation stabilized and was largely unaffected by the clamping and unclamping procedures. In spite of the improved central hemodynamics no favorable effect on the skeletal muscle metabolism was observed.
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PMID:Temporary incomplete ischemia of the legs induced by aortic clamping in man: effects on central hemodynamics and skeletal muscle metabolism by adrenergic block. 745 55


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