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

In 61 patients in whom high doses of corticoids had been administered owing to various indications, the hemodynamic modifications caused by this injection were studied. The corticoids administered were : hydrocortisone hemisucccinate (150 mg/kg), methyl prednisolone sulfate (30 mg/kg), prednisone sodium m sulfobenzoate (50 mg/kg), prednisolone sodium m sulfobenzoate (35 mg/kg) and dexamethasone phosphate (2 mg and 6 mg/kg). The results study the modifications caused by each drug on heart rate, arterial blood pressure, cardiac output, systolic stroke volume and peripheral vascular resistance. The expression of the results is given as a percentage of the variation with statistical study. Methyl-prednisolone sulfobenzoate only leads to slightly marked hemodynamic effects : the four other compounds studied have definite hemodynamic effects, of variable intensity and duration. The most important variations are noted with dexametasone phosphate. From these results, the indications and results of the use of corticoids in states of shock are discussed.
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PMID:[Hemodynamic effects of high-dosage corticoids. Their justification in the treatment of shock]. 0 83

Myocardial performance was evaluated intraoperatively in 20 patients undergoing myocardial revascularization when hypothermic potassium cardioplegic arrest was used. High concentrations of potassium (20 mEq/L) were compared to normal concentrations of potassium (5 mEq/L) in hypothermic cardioplegic solutions. The cardioplegic arrest period averaged 53 +/- 3 minutes in the high potassium group and 54 +/- 4 minutes in the low potassium group, Intraoperative calculation of ejection fraction and end-diastolic volume was accomplished by the technique of radiocardiography. All data were grouped according to end-diastolic volume index (EDVI) for both high (HK) and low (LK) potassium comparisons. Comparisons between high and low potassium groups demonstrated no significant differences in ejection fraction (HK = 66%, LK = 61%), cardiac index (HK = 2.74 L/min/m2, LK = 3.0 L/min/m2), stroke work (HK = 36 gm.m/m2, LK = 30 gm.m/m2), oxygen consumption as measured by left heart double product (HK = 9,438; LK = 9,209), and myocardial compliance (HK = 2.8 cc/torr, LK = 4.2 cc/torr at the post-cardioplegic arrest period). The role potassium plays in producing a rapid cardiac arrest is well accepted. Its protective effect on the preservation of high-energy phosphate stores is postulated, but its addition to perfusion hypothermia does not appear to enhance the protective effect observed with perfusion hypothermia alone.
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PMID:Protection of myocardial function not enhanced by high concentrations of potassium during cardioplegic arrest. 49 23

Cardiac performance and some parameters of glycolytic and oxidative metabolism were analyzed in isolated perfused guinea pig hearts performing pressure-volume work. Perfusion medium was an oxygenated Krebs-Henseleit bicarbonate buffer (pH 7.4) which contained glucose and physiological concentrations of pyruvate and insulin. The pressure-flow relationship in the coronary vascular bed indicated autoregulation of coronary flow. Left ventricular function was influenced by aortic pressure (Pa) and venous filling pressure (Pv) in accordance with the Frank-Starling principle, i.e. stroke work increased as a function of Pa or Pv to a certain maximum and then decreased. Myocardial oxygen consumption (MVO2), on the other hand, was linearly correlated with Pa and Pv, respectively, over the entire pressure range. Efficiency of the left ventricle, therefore, increased to an optimum (16%) and decreased at higher pressures. Myocardial contents of glycogen, ATP and creatine phosphate were not markedly influenced by a change in Pa or Pv. L-Noradrenaline (0.08 micrometer, NA) stimulated stroke work and MVO2 at a all Pv tested; efficiencies reached physiologic values (21%) at high volume loads. The increased MVO2 was associated with an acceleration of pyruvate decarboxylation and lactate release up to 10- and 15-fold, respectively, at elevated but physiological NA concentrations (0.2 micrometer). Our results demonstrate that the isolated perfused working guinea pig heart compares favourably with the non-failing Starling heart-lung preparation and hearts in situ, as far as coronary function, left ventricular performance and oxidative metabolism are concerned.
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PMID:Functional and metabolic features of an isolated perfused guinea pig heart performing pressure-volume work. 57 65

Severe heat stroke may be associated with hypophosphatemia and hypocalcemia. Hypophosphatemia is generally observed within hours after onset, but hypocalcemia usually occurs on the second or third day, and after hypophosphatemia has undergone spontaneous correction. A young man displayed respiratory alkalosis during the course of severe heat stroke. The hypophosphatemia abated spontaneously as metabolic acidosis and acute renal failure supervened. Hypocalcemia became prominent and was more severe than that ascribable to uremia. Hypocalcemia was probably the result of calcium phosphate and calcium carbonate deposition in injured skeletal muscle.
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PMID:The mechanism of hypophosphatemia in acute heat stroke. 57 61

In helically cut strips of dog cerebral, coronary, mesenteric and femoral arteries, the contractile response to prostaglandin (PG) F2alpha, and E2, relative to contractions induced by 30 mM K+, did not appreciably differ, whereas relaxations induced by PGE1 relative to those induced by 10(-4) M papaverine were significantly different; the least in cerebral arteries and the greatest in mesenteric arteries. The relaxation of human cerebral arteries in response to PGE1 was similar to that of dog cerebral arteries. Treatment for 60 min with polyphloretin phosphate (3 X 10(-5) and 10(-4) g/ml) suppressed the contractile response to PGF2alpha and E2 but did not alter the response to 25 mM K+. The relaxing effect of PGE1 was not influenced. Aspirin (5 X 10(-5) and 2 X 10(-4) M) significantly potentiated the contractile response to PGF2alpha and E2 but did not alter the relaxation induced by PGE1. In contrast, contractions induced by serotonin were attenuated. It is concluded that dog cerebral, coronary, mesenteric and femoral arteries relaxed differently in response to PGE1. It appears that arterial responses to vasoconstricting PGs, but not to the vasodilating PG, are significantly attenuated by polyphloretin phosphate and potentiated by aspirin.
Stroke
PMID:Responses of isolated dog cerebral and peripheral arteries to prostaglandins after application of aspirin and polyphloretin phosphate. 70 32

Haemodynamics and renal function have been investigated in 12 patients with valvular heart disease before and after injection of 2 mg bumetanide in the right heart catheter. There were no significant changes in oxygen consumption, arteriovenous oxygen difference, cardiac index, heart beats per minute, stroke volume or right and left ventricular stroke work 35 min after the injection, whereas pulmonary and systemic arteriolar resistance showed a slight but insignificant reduction. Mean pulmonary capillary venous pressure, left ventricular end-diatolic pressure, mean pulmonary arterial pressure and mean pressure in the right atrium were highly significantly reduced after injection, systolic left ventricular pressure showing a significant but slight decrease. The creatinine and urea clearances increased considerably during the first 50 min after injection of bumetanide, but diminished during the second period to levels somewhat lower than the initial values. There was also a marked increase in the clearance of sodium potassium, calcium, magnisium and phosphate. It is concluded that bumetanide is a very potent diuretic which changes haemodynamic parameters towards normal values.
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PMID:Haemodynamics and renal function following injection of bumetanide. 89 69

Severe hypophosphatemia is associated in man with low intracellular stores of ATP and a set of specific cellular dysfunctions. To investigate whether hypophosphatemia affects myocardial performance, we measured cardiac output by thermodilution and calculated stroke work in seven patients with severe hypophosphatemia before, during and after repletion with an intravenous potassium phosphate solution. Mean left ventricular stroke work for these patients increased from 49.57 to 71.71 g-m per beat (P less than 0.01) at the same or higher afterload whereas pulmonary-artery wedge pressure fell from a mean value of 10.1 to 6.7 torr (P less than 0.02). Return of serum phosphate to normal, therefore, improved myocardial stroke work independently of the Starling effect. The mechanism of this improvement in contractile force is unknown but may be related to intracellular availability of ATP.
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PMID:Effect of hypophosphatemia on myocardial performance in man. 90 68

In 6 open chest dogs, regional myocardial function und metabolic changes (ATP, creatine phosphate, lactate) were studied during coronary flow reduction in LAD by ultrasonic dimension gauges and transmural biopsies. After reduction of the perfusion pressure from 108 to 50 mm Hg the ischemic segment showed a marked dyskinesis: the enddiastolic segment length increased by 7%, and segment shortening and segment stroke work decreased by 22% and 63% respectively. Left ventricular (LV) enddiastolic pressure rose from 5 to 8 mm Hg (p less than 0.05). Heart rate, LV systolic pressure, LV max dP/dt and Vpm did not change significantly.
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PMID:[Myocardial function and metabolism during local coronary flow reduction]. 91 15

Administration of disopyramide phosphate (DE) i.v. in two doses, 30 min apart, to a patient with ventricular tachycardia was accompanied by no, or only slight, changes in systemic arterial pressure (SAP), cardiac output (Q), stroke work (SW), and pulmonary artery diastolic pressure (PADP). Heart rate fell from 123 to 103/min. Following reversion to sinus rhythm, which occurred 60 min after the second dose of DE at a serum concentration greater than 4.3 mug/ml, Q ans SW showed significant increases above their control values. PADP fell from 20 to 6 mmHg whereas the mean SAP remained largely unchanged. There seemed to be no adverse effects of drug administration. In this patient, recurrent attacks of ventricular tachycardia not responding to conventional antiarrhythmic treatment could be prevented by oral DE in a dose of 800 mg/day.
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PMID:Disopyramide in ventricular tachycardia. 97 Feb 27

The effect of intravenous infusion of 10 per cent glycerol on regional cerebral blood flow (using hydrogen bolus and Xenon-133 (133Xe) clearance methods) and metabolism was investigated in 57 patients with recent cerebral infarction. Hemispheric blood flow (HBF) increased, together with increase in regional cerebral blood flow (rCBF) and cerebral blood volume (rCBV), in foci of brain ischemia. Hemispheric oxygen consumption (HMIO2) decreased together with hemispheric respiratory quotient. Systemic blood levels of glucose, lactate, pyruvate, and triglycerides also increased after glycerol while free fatty acids (FFA) and inorganic phosphate (Pi) decreased. Hemispheric glucose consumption was unaltered after glycerol so that hemispheric glucose to oxygen ratio tended to rise. Pyruvate and lactate production by brain was unchanged. Glycerol moved across the blood brain barrier into brain and cerebrospinal fluid (CSF). Release of FFA and Pi from infarcted brain was reversed by glycerol. Total phosphate balance was maintained actoss brain both before and after glycerol infusion. Triglycerides increased in CSF after glycerol, originating either from cerebral blood or as a result of lipogenesis in cerebral tissue. The EEG Recording and neurological status of the patients improved despite decreased brain oxygen consumption. Results of this study suggest that after intravenous infusion of 10 per cent glycerol in patients with recent cerebral infarction, glycerol rapidly enters the CSF and brain compartments and favorably affects the stroke process in two ways: first, by redistribution of cerebral blood flow with increase in rCBF and rCBV in ischemic brain secondary to reduction in focal cerebral edema; and second glycerol may become an alternative source of energy either by being directly metabolized by the brain, or indirectly, by enhancing lipogenesis, or by both processes. Involvement of glycerol in lipogenesis with esterification to accumulated FFA might lead to improved coupling of oxidative phosphorylation, a hypothesis that fits the finding of improved neuronal function despite further decrease in cerebral hemispheric oxygen consumption.
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PMID:Circulatory and metabolic effects of glycerol infusion in patients with recent cerebral infarction. 109 Mar 93


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