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

Long-lasting hypophosphatemia was previously found to diminish myocardial performance. The present study aimed to elucidate if postoperative glucose-induced hypophosphatemia is of importance for myocardial performance. Sixteen patients undergoing elective colonic or rectal surgery were given 100 g glucose intravenously (as 20% glucose solution) on the first and second postoperative days. The infusion rate was 0.3 g/kg/hour. On both days the glucose infusion caused significant fall in P-phosphate (0.94 to 0.67 and 0.71 to 0.47 mmol/l, respectively). No changes were seen in P-calcium, P-potassium or P-sodium. Measurements of stroke volume and frequency, central venous pressure and mean arterial pressure were made immediately before and after the glucose infusions. Stroke volume and cardiac output were unaffected during the infusions, and also from the first to the second postoperative day. As the preload (central venous pressure) and the afterload (arterial pressure) similarly were unchanged by the glucose infusion, glucose-induced hypophosphatemia following elective surgery was judged to lack importance for the myocardial performance.
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PMID:Postoperative myocardial performance during glucose-induced hypophosphatemia. 398 50

Brain energy state and glycolytic metabolites were measured in young (6 month) and aged (28 month) male rats under normoxic (70% nitrous oxide, 30% oxygen) or hypoxic (PaO2 = 25 mm Hg) test conditions. Hypoxic ischemia was induced in one cerebral hemisphere by ligation of one carotid artery. Under normoxic test conditions brain energy metabolite concentrations were similar between young and aged rats. Brain tissue glucose, glycogen, glucose-6-phosphate and critic acid cycle intermediate concentrations were decreased in aged rats during normoxia while fructose-6-phosphate and pyruvate were increased. Decreases in brain energy state and increases in lactate/pyruvate ratios were significant in both young and aged rats during hypoxia and were greater in aged animals in hypoxic-ischemic tissues. These results indicate that brain energy state is normal in aged rats under normoxic conditions but that hypoxic-ischemia produces a greater degree of brain energy failure compared to younger animals.
Stroke
PMID:Brain metabolic changes in young vs aged rats during hypoxia. 404 50

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

Rats were subjected to a 30 minute period of combined hypoxia (F1o2 = .08) and hemorrhagic hypotension (MAP = 30 mm Hg), then resuscitated by restoration of F1o2 = .30 and reinfusion of shed blood and saline. Intracranial blood volume, hemoglobin saturation, and the cytochrome alpha, alpha 2 redox state were monitored through the intact skull during hypoxic hypotension and after resuscitation utilizing reflectance spectrophotometry. Although resuscitation returned arterial blood pressure, arterial pO2, and hemoglobin saturation toward normal, a sustained, significant (p less than .005) reduction in cytochrome alpha , alpha 2 remained. A parallel series of rats was subjected to identical hypoxic hypotension. At designated intervals the animals were sacrificed to determine brain ATP, ADP, and inorganic phosphate (P1). The data are discussed in terms of relationships between high energy phosphate metabolism and recorded changes in cerebral cytochrome alpha , alpha 2 redox state.
Stroke
PMID:Failure of brain cytochrome alpha , alpha 3 redox recovery after hypoxic hypotension as determined by in vivo reflectance spectrophotometry. 627 81

The intensity of parenchymal brain lesions was compared using Tc-99m pertechnetate and Tc-99m phosphate. The following conclusions were made: 1. If the Tc-99m phosphate intensity is greater than the intensity of the Tc-99m pertechnetate scan, and the patient is evaluated within four weeks of ictus, the lesion is a CVA (P less than .001). 2. If the Tc-99m phosphate intensity is less than or equal to the intensity of the Tc-99m pertechnetate scan, and the patient is evaluated within four weeks of ictus, the parenchymal lesion is not a CVA (P less than .001). 3. If the evaluation takes place longer than six weeks after ictus, then no evaluation about the nature of the lesion can be made based upon uptake of Tc-99m phosphate and Tc-99m pertechnetate.
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PMID:Imaging of brain tumors and other lesions utilizing Tc-99m phosphates and Tc-99m pertechnetate. 629 48

The effects of glucose-insulin-potassium (GIK) on hemodynamics, oxygen transport, P50, 2,3-diphosphoglycerate (2.3-DPG), and adenosine triphosphate (ATP) were evaluated in canine endotoxin shock. Ten dogs were studied under general anesthesia and controlled ventilation. Shock was induced with Escherichia coli endotoxin (1.5 mg/kg body wt). Thereafter two groups of five dogs each were formed by randomization. The one group received GIK (glucose 50%, 2 g/kg, insulin 3 U/kg, and 10 mmole K) in the period between 90 and 120 min after endotoxin. The other group received an equal amount of NaCl infusion and served as a control group. Observations were completed at 180 min after endotoxin. GIK resulted in a significant increase of cardiac output, stroke volume, mean arterial pressure, and oxygen consumption. Serum phosphate levels decreased. No changes were observed of P50 in vitro (at 37 degrees C and pH 7.40) and of P50 in vivo, nor of 2.3-DPG and ATP in the red cells. The data suggest that the increased oxygen consumption after GIK in canine endotoxin shock is caused only by improvement of cardiac output and oxygen availability and not by an effect on oxygen unloading capacity of hemoglobin.
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PMID:Effects of glucose-insulin-potassium (GIK) on the position of the oxyhemoglobin dissociation curve, 2.3-diphosphoglycerate, and oxygen consumption in canine endotoxin shock. 633 16

Considerable experimental evidence has accumulated to indicate that brain ischemia or stroke-like events will lead to rapid losses of brain potassium, magnesium, ATP, creatine phosphate and glucose. These events are usually followed by an uptake of sodium and calcium ions. Increased uptake or excess Ca2+ uptake in neuronal cells is thought to be the prime cause of neuronal death in the brain. Mg2+ deficiency is known to produce a host of neurological disturbances in man; experimentally, Mg2+ deficiency leads to excess uptake of Ca2+ in the brain. Strokes and transient ischemic attacks also are known to be associated with neurological disturbances and ionic changes in the brain. Stroke patients have been reported to exhibit deficits in serum and CSF [Mg]. Acute Mg or K deficiency can produce cerebrovasospasm, at least experimentally. The lower the extracellular concentration of either Mg2+ or K+, the greater the magnitude of cerebral arterial contraction. These cerebrovascular contractions induced by lowering either the [Mg2+]0 or [K+]0 cannot be antagonized or attenuated by known pharmacologic antagonists. The cerebrovasospasms produced upon lowering [Mg2+]0 can be modulated by [K+]0 and vice versa; e.g. the lower the [K+]0, the greater the degree of vasospasm upon withdrawal of [Mg2+]0 and vice versa. Lowering [Mg2+]0 in situ and in vitro results in increased uptake of Ca2+ in the brain and the cerebral arteries. Cerebrovasospasms induced by substances that are known to be released in the brain on injury, such as prostanoids and serotonin, are relaxed dramatically by addition of [Mg2+]0. Infusions of MgSO4 into the brain via the internal carotid artery produces dose-dependent lowering of systolic and diastolic blood pressure as well as dose-dependent vasodilatation of arterioles (17-30 micron) and venules (18-40 micron) in the cerebral microcirculation, as observed by direct in situ high-resolution TV image-intensification microscopy. In clinical studies, infusion of MgSO4 has been reported to alleviate cerebrovasospasms. Epidemiological evidence is accumulating to suggest that consumption of fruit and vegetables (foodstuffs relatively high in K and Mg, and low in Na) is associated in certain geographic regions with a lower than normal incidence of strokes, particularly that of cerebral hemorrhage. On the basis of such data, and the findings reported herein, we believe one must consider that certain types of cerebrovascular accidents, transient ischemic attacks and 'classical' migraine attacks may be associated with a 'true' Mg deficiency and altered fluxes of K+ ions in the brain and CSF.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions of Mg and K on cerebral vessels--aspects in view of stroke. Review of present status and new findings. 639 42

In specimens from the superficial temporal artery (STA) and middle cerebral artery (MCA), obtained during STA-MCA anastomosis, green fluorescent varicose fibers of sympathetic nerves were clearly visible with both formaldehyde-glutaraldehyde and sucrose-potassium phosphate-glyoxylic acid wet-histofluorescent techniques. These fibers were fairly thick, were densely packed and had a meshwork-like arrangement. Fluorescent terminals were seen both in the adventitia and in the outer muscular layer of the media in both STA and MCA specimens. They were more often observed in patients with prominent atherosclerosis in these vessels. The present study suggests the possible role of sympathetic nerve terminals in the development of vasospasm and occlusive lesions in cerebral vessels. It may also help to explain the marked constriction and transient occlusion following a STA-MCA bypass procedure.
Stroke
PMID:Sympathetic nerve terminals in the tunica media of human superficial temporal and middle cerebral arteries: wet histofluorescence. 640 79

In helically-cut strips of dog basilar and mesenteric arteries, the isometric tension developed by application of ghost-free hemolysate from dog erythrocytes was recorded. The hemolysate contracted basilar arteries in a concentration-dependent fashion, the response being attenuated by treatment with either aspirin or polyphloretin phosphate, a prostaglandin antagonist. Mesenteric arteries were contracted only slightly by high concentrations of hemolysate. When the mesenteric arteries had partially been contracted with prostaglandin F2 alpha or norepinephrine, the hemolysate induced relaxations, which were abolished by aspirin in approximately half the preparations used. Studies on rat stomach strips exposed to superfusate of dog cerebral arteries showed a release of prostaglandin-like substance by the hemolysate application. It may be concluded that the hemolysate contracts basilar arteries and relaxes mesenteric arteries, mainly through prostaglandins synthesized in and released from the vascular wall. Such a mechanism may be involved in the pathogenesis of cerebral vasospasm following a subarachnoid hemorrhage.
Stroke
PMID:Role of intrinsic arachidonate metabolites in the vascular action of erythrocyte breakdown products. 642 Sep 46

The cardioprotective effects of lidoflazine, a calcium entry blocker, were tested in patients undergoing multiple aorta-coronary bypass grafting (at least four grafts). Intermittent aortic cross-clamping at 25 degrees to 28 degrees C was used. Mean cross-clamp time was 11 minutes for one distal anastomosis. Patients were randomized into three groups: a control group (I), a group (II) pretreated with 0.5 mg . kg-1 lidoflazine intravenously before cardiopulmonary bypass (CPB), and a group (III) pretreated with 1 mg . kg-1 lidoflazine intravenously. The following markers of ischemia are used: (1) adenosine triphosphate (ATP), creatine phosphate (CP) and glycogen determined in transmural left ventricular biopsy specimens taken at the beginning and end of CPB; (2) ultrastructure in a similar pair of specimens; and (3) hemodynamic recovery 15 minutes after cessation of CPB. At the end of the intervention, ATP decreased to 73% in Group I but remained unchanged in Groups II (98%) and III (88%). CP decreased to 82% in Group I and remained unaltered in Groups II (100%) and III (110%). Glycogen decreased in Group I (to 44%) and in Group II (78%) but remained unchanged in Group II (138%). Ultrastructural study showed better preservation of the glycocalyx and sarcolemma in Group III than in Group I. Left ventricular stroke work index remained unaltered after CPB in Group III but decreased in Groups I and II to about 60% of its initial value. Thus lidoflazine pretreatment protects the myocardium in a dose-dependent manner against deterioration of myocardial function and structure.
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PMID:Cardioprotective effects of lidoflazine in extensive aorta-coronary bypass grafting. 660 46


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