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

Experiments were performed on 2 groups of baboons anesthetized with Sernylan. One group served as control and the other was premedicated with 5 mg/kg phenoxybenzamine (PBZ). A 2-step hypovolemic shock model was used followed by retransfusion of the shed blood. Cerebral blood flow was measured by the 133Xe clearance method. Arterial and cerebral venous samples were taken and analyzed for blood gases as well as glucose and lactate content. The cerebral metabolic rates of oxygen, glucose, and lactate were calculated. In addition, the effect of CO2 inhalation was studied before shock was induced. PBZ produced no effect on either CBF or the flow response to CO2 prior to bleeding. PBZ pretreatment prevented the fall in cerebral blood flow and CMRO2 produced by systemic hypotension due to bleeding. Lactic acid showed no evidence of change either in production or uptake by the brain during the experimental procedure. The cerebral metabolic pathway of glucose, however, seemed to be affected by PBZ both before and during shock.
Stroke
PMID:Effect of phenoxybenzamine on cerebral blood flow and metabolism in the baboon during hemorrhagic shock. 11 93

Effects of angiotensin-induced acute hypertension on cerebral metabolism were studied in normotensive (NTR), spontaneously hypertensive (SHR) and experimental renovascular hypertensive rats (RHR). Lactate, pyruvate and adenosine triphosphate (ATP) concentrations in the brain frozen in situ at 18--20 min after angiotensin infusion, which raised mean arterial pressure (MAP) by 28--62% of control, were determined by enzymatic methods. Supratentorial lactate was significantly increased to 135% of control in RHR, its increase being correlated with the degree of hypertension, wherease it remained unchanged in NTR or SHR. Furthermore, RHR showed a tendency toward increase in lactate/pyruvate ratio with a decrease in ATP despite no change of arterial acid-base balance measured simultaneously before and after acute induced hypertension. From the present study, it is postulated that some renal factor seems to contribute ischemic metabolic changes in RHR following acute hypertension. The possible effect of renin on the vascular permeability is discussed as the pathogenesis of hypertensive encephalopathy.
Stroke
PMID:Effects of acute hypertension on brain metabolism in normotensive, renovascular hypertensive and spontaneously hypertensive rats. 67 45

The study was conducted in 80 patients with ischaemic and 29 with haemorrhagic cerebral stroke. Lactate, pyruvate, the lactate/pyruvate ratio and glucose were determined in the arterial blood and lumbar CSF. A high prognostic value of the CSF lactate content was found in cases of ischaemic stroke. According to the data obtained, an elevation of the CSF lactate concentration above 4.0 mEq/l should be considered life-threatening. Haemorrhagic stroked was found to be accompanied by a reduced CSF glucose level and an elevated lactate content, as well as by a significant proportional elevation of the lactate and red blood cells count in the CSF. The conducted calculations demonstrated that 1/4 to 1/3 of the CSF lactate is formed at the expense of the glycolytic metabolism in the CSF erythrocytes. This constitutes the main reason of the discordance between the CSF lactate content in haemorrhagic stroke and the routine criteria of prognosis in ischaemic stroke. The lactate/pyruvate ratio in the CSF is of no prognostic importance in both forms of cerebral stroke.
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PMID:[The prognostic value of the lactate concentration and lactate/pyruvate ratio in cerebrospinal fluid following acute cerebral circulatory disorders]. 93 57

To study the efficacy of isosorbide dinitrate in prevention of myocardial ischemia, 20 patients with angiographically proved coronary artery disease underwent atrial pacing (mean rate 138/min) before (P1), 10 minutes after (P2) and 65 minutes after (P3) sublingual administration of 5 mg of isosorbide dinitrate. The symptomatic, hemodynamic and metabolic responses were evaluated at rest and during each pacing period. Angina occurred in all subjects during P1. Angina did not recur or was less severe in 17 of 19 patients during P2 and in 19 of 20 patients during P3. Resting left ventricular end-diastolic pressure for the group was normal at 11 plus or minus 4 mm Hg (mean plus or minus standard deviation). On interruption of pacing at 4.5 minutes during P1, average end-diastolic pressure during sinus rhythm was abnormal (18 plus or minus 6 mm Hg). After administration of isosorbide dinitrate mean left ventricular end-diastolic pressure was significantly decreased at rest and remained normal when pacing was interrupted during P2 and P3. Brachial arterial pressure, cardiac index, tension-time index, left ventricular stroke work index and maximal rate of rise of left ventricular pressure were all diminished at rest before and during P2 and P3. S-T segment depression was less during P2 and P3 than during P1. Before isosorbide dinitrate was given, resting myocardial lactate extraction was 15 plus or minus 11 percent during P1 lactate extraction decreased to minus2 plus or minus 25 percent. Lactate extraction was significantly greater during P2 and P3 than during P1. This study demonstrates that sublingual administration of 5 mg of isosorbide dinitrate has a significant protective effect against pacing-induced myocardial ischemia at 10 and 65 minutes after administration.
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PMID:Effects of isosorbide dinitrate on the response to atrial pacing in coronary heart disease. 115 42

Lactate and pyruvate concentrations and acid-base balance in cerebrospinal fluid (CSF) and arterial blood were determined in patients with intracranial hemorrhages (28 subarachnoid hemorrhages and 15 intracerebral hemorrhages). A greater increase in CSF lactate and lactate-pyruvate ratio (L/P ratio) was observed in patients with impairment of consciousness, focal neurological deficits, poor prognosis, or CSF pressures higher than 300 mm H2O. A combination of CSF lactate greater than 2.5 mM per liter, L/P ration above 20, bicarbonate less than 20.4 mEq per liter, pH below 7.276, or arterial PCO2 below 31.5 mm Hg seems to indicate poor prognosis from intracranial hemorrhage. The mechanism of hyperventilation in acute cerebrovascular diseases and of CSF pH regulation in acid-base disturbances was also discussed.
Stroke
PMID:Cerebrospinal fluid and arterial lactate, pyruvate and acid-base balance in patients with intracranial hemorrhages. 119 37

Hemodynamic and metabolic responses to pacing from either the coronary sinus or right atrium were evaluated in 41 patients with chest pain and normal coronary arteriograms. A group of patients (group II) with angina, lactate production, or significant ST segment depression had a significantly higher mean pulmonary capillary pressure on peak pacing or angina than did a group of patients considered to have a normal pacing response (group I). In 6 of 9 group II patients, the left ventricular end-diastolic pressure either rose abnormally with pacing or was greater than 14 mm Hg immediately after pacing and resembled that of a group of patients with coronary artery disease; Patients with a prolapsing mitral valve (group III) also had a significantly higher pulmonary capillary pressure on peak pacing as compared to those of group I, although abnormal left ventricular pressure responses occurred in only 2 of 9 of these patients. The stroke index was significantly lower in group III on peak pacing while group II was no different from group I. Lactate production occurred in 6 of 9 group II patients. However, only 1 of 6 patients with a prolapsing mitral valve who were studied for lactate production was found to produce lactate, suggesting a different mechanism for their pain.
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PMID:Hemodynamic and metabolic responses to pacing in patients with chest pain and normal coronary arteriograms. 120 72

Proton nuclear magnetic resonance spectroscopy is a noninvasive technique allowing the localized, in vivo detection of proton-containing brain metabolites. We used this technique to study eight patients with cerebral infarction or ischemia. A stimulated echo-pulse sequence with chemical shift imaging was used to acquire spectra from multiple contiguous 4-cc volumes extending from the site of ischemia to the opposite hemisphere. Six patients had a reduction in the signal from N-acetyl groups (NAG) in the stroke area compared with controls, and those with the lowest NAG to phosphocreatine/creatine ratios had the least recovery of function. Lactate was observed within the infarcted region in two patients at 9 and 11 days after infarction and may have been present in other patients up to 15 weeks after stroke.
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PMID:Multivoxel 1H-MRS of stroke. 132 Feb 20

As the myocardial carnitine content, a key control factor in myocardial oxidative metabolism and energy transfer, is reduced in heart failure, administration of L-propionylcarnitine (LPC), a potent analogue of L-carnitine, potentially may improve cardiac function, possibly through a positive inotropic effect. As its hemodynamic profile is unknown in humans, 32 fasting normotensive patients with coronary artery disease received either 15 mg/kg of LPC (n = 16) or vehicle (mannitol/acetate, n = 16) infused over 5 min. Hemodynamic, radionuclide [peak ejection and filling rates (PER and PFR, respectively)], and metabolic variables (myocardial O2, lactate, and carnitine uptake) were studied at baseline and 1, 3, 5, 10, 15, and 45 min postdrug. The baseline ejection fraction was depressed in LPC patients (40 +/- 3% vs. 48 +/- 4% in the vehicle group, p less than 0.05) as a result of a significant high incidence of previous infarctions. Immediately following LPC, the cardiac total carnitine uptake changed from 102 +/- 181 to 5,335 +/- 1,761 mumol/L (p less than 0.05). In both groups, left ventricular systolic and end-diastolic pressures increased significantly by 5 and 20%, respectively, during the first 5 min. In the vehicle group, contractility decreased by 5%, accompanied by a significant 11% fall in the stroke volume. In contrast, following LPC, isovolumetric contractility indices remained unaltered. Instead, both the PER and PFR improved by 16% at 45 min. Moreover, the cardiac output increased by 8%. LPC did not affect systemic or coronary hemodynamics. Lactate uptake increased by 42%, but myocardial O2 consumption did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute improvement of cardiac function with intravenous L-propionylcarnitine in humans. 138 25

Lactate, glycerol, and catecholamine in the venous blood were determined in 8 recreational swimmers following 60 sec of supramaximal arm strokes, kicks and the whole swim. The mean velocity of a whole stroke was higher than both arm strokes and kicks, and the mean velocity of arm strokes was higher when compared with kicks. There was a significant relationship between the mean velocity of arm strokes and the whole swim (r = 0.90; p less than 0.01). Peak blood lactate in the whole swim was higher than arm strokes (p less than 0.01) and kicks (p less than 0.01), and peak blood lactate in arm strokes was higher compared to kicks (p less than 0.01). The correlation coefficients between mean velocity and peak blood lactate in arm strokes, legs kick and whole swim were r = 0.72 (p less than 0.05); r = 0.61 (n.s.) and r = 0.35 (n.s.), respectively. These results suggest (1) that lactate in the blood during the whole crawl stroke originates predominantly from the muscle groups which work the arm and (2) that glycogen included in the muscles of the upper body which is used during arm strokes was easily convertible into the propelling force during arm swim, while additional energy from the leg muscles is not fully sufficient to increase propulsion force in a linear manner.
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PMID:Blood lactate, glycerol and catecholamine in arm strokes, leg kicks and whole crawl strokes. 140 72

Previous studies of human stroke by 1H nuclear magnetic resonance spectroscopy have shown elevation of lactate lasting 3 to 6 months. Complete metabolic turnover of the elevated lactate pool has been demonstrated 5 weeks after a stroke. Its cellular localization is among the first questions requiring clarification. Information pertinent to this question came to us from a patient with a 2-week-old stroke by 1H nuclear magnetic resonance spectroscopic imaging 1 week before his death led to neuropathologic examination of the brain. 1H spectra from voxels including the infarcts showed increased lactate and decreased N-acetylaspartate. Histopathology showed sheets of foamy macrophages in the infarct, but few neurons. Macrophage density ranged from 196 cells/mm2 near the surface of the infarct to 788 near its medial margin. Glial density was 500 to 800 cells/mm2. Lactate concentration in voxels including portions of the infarct was estimated at 7 to 14 mM. Voxels showing low N-acetylaspartate and high lactate on spectroscopic imaging were associated with histopathologic sections containing foamy macrophages. Brain macrophages--which begin to appear 3 days after infarction and gradually disappear over several months--could be a major source of elevated lactate signals that persist for months after stroke.
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PMID:Spectroscopic imaging of stroke in humans: histopathology correlates of spectral changes. 162 Mar 45


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