Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ASI-222 [3-beta-O-(4-amino-4,6-dideoxy-beta-D-galactopyranosyl) digitoxigenin HCl] is a semisynthetic aminosugar cardiac glycoside that has been shown to have a greater therapeutic index than ouabain or digoxin in dogs. We have compared the effects of ASI, digitoxigenin, digitoxigenin-beta-D-galactose, and digoxin in the dog heart-lung preparation. Minute work and stroke work were calculated. Controls were obtained before and after the hearts were failed with sodium pentobarbital. ASI-222 is about three times more potent than digitoxigenin and about twice as potent as digitoxigenin-beta-D-galactose in producing similar increases in the left ventricular stroke work. ASI-222 is about three times more potent than digoxin in creasing left ventricular stroke work. Our results indicate that the addition of an aminosugar group to the genin further increased potency over that observed with the addition of a single neutral sugar and prolonged the duration of activity in failing myocardial tissue.
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PMID:Structure-activity relationships of an aminosugar cardiac glycoside, ASI-222 HCl, in the heart-lung preparation of the dog. 9 11

The use of vasodilators represents a new approach in the treatment of heart failure. These drugs have the property of causing vasodilatation of either arterial or venous predominance or balanced between these two vascular beds. Arterio-dilators (phentolamine, hydralazine) increase stroke volume and cardiac output by decreasing ventricular afterload. Veno-dilators (nitroglycerine) have little effect on cardiac output but decrease ventricular filling pressure, thereby relieving pulmonary venous hypertension. Mixed vasodilators (Sodium nitroprussideate, trimetaphan) combine these two groups of properties in various degrees. The majority of these drugs can only be administered intravenously, with careful haemodynamic surveillance.
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PMID:[The treatment of congestive heart failure by using vasodilators. I. Physiological basis. Different vasodilators (author's transl)]. 9 22

Experimental regional cerebral ischemia was produced in the middle cerebral artery (MCA) territory in primates (M. mulatta) by macrosphere embolization. Determinations of percentage tissue dry weight and tissue sodium and potassium concentrations were obtained in samples from the ischemic and non-ischemic hemispheres at various time from 12 to 48 hours after the onset of cerebral ischemia. Samples from the cortex normally supplied by the occluded MCA showed maximal accumulation of edema fluid with fluxes in sodium and potassium in reciprocal directions at 12 hours and similar edematous changes in putamen at 24 hours after embolization By 48 hours after MCA occlusion and despite the presence of infarction, partial reversal was observed in the redistribution of water and electrolytes in these gray matter structures. In contrast to cerebral cortex and putamen, the adjacent subcortical white matter showed progressive increases in water content from 12 to 48 hours and definite increases in tissue sodium with decreases in potassium were not observed until 48 hours after MCA occlusion. This late severe white matter edema associated with cerebral infarction appears to be a major factor responsible for the hemispheric swelling observed at this state.
Stroke
PMID:Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 3: effects on brain water and electrolytes in the late phase of acute MCA stroke. 9 10

Echovirus 11 in the presence of fetal calf serum was exposed to six commonly used disinfectants for times of 10, 20 and 30 s. At the end of such exposure times, skim milk neutralized disinfectant activity and residual virus was assayed using the plaque technique. The six disinfectants studied were Javex, sodium hydroxide, ethanol, Wescodyne, One Stroke Ves-Phene, and Sonacide. Although 0.25% (w/v) sodium hydroxide and 95% (v/v) ethanol were equally virucidal and significantly more so than the other four disinfectants, causing 10(6) reduction in 20 s, they may not be practical to use in many instances. Javex at a dilution of 1/50 (1200 parts/10(6) chlorine) proved to be virucidal causing 10(3.5) reduction of echovirus 11 in 30 s. Wescodyne (1/50) and undiluted Sonacide were relatively ineffective causing 10 reduction or less of echovirus 11 in 30 s. One Stroke Ves-Phene (1/50) was ineffective causing no significant inactivation in 30 s.
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PMID:The relative effectiveness of commonly used disinfectants in inactivation of echovirus 11. 9 74

With a closed head primate stroke model, acute cerebral ischemia limited to the middle cerebral artery (MCA) territory was produced by macrosphere embolization of the internal carotid artery bifurcation. Measurements of the oxygen tension (PO2) at the cerebral cortical surface were obtained by continuous on-line mass spectrometry. Percentage of dry weight and tissue sodium, potassium, and chloride concentrations from ischemic and nonischemic hemispheres were determined at various times. With this preparation, we registered the precise onset of cortical surface PO2 depletion, which showed an exponential downward trend (fast component from 0 to 5 minutes, t 1/2 = 0.8 minute, rate of change = 89% per minute; slow component from 5 to 240 minutes, t 1/2 = 285 minutes, rate of change = 0.3% per minute). After the onset of cerebral ischemia, there was an immediate fall of the cortical surface PO2 with reductions of more than 45% at 5 minutes before definite hemiparesis and electroencephalographic abnormalities were recognized. During the secondary phase from 5 to 240 minutes the cortical surface PO2 fell by only an additional 23% of the steady state. Even so, when cortical surface PO2 was maintained at this critically low level, the earliest cerebral cortical edema was evident 180 minutes after MCA occlusion. Thereafter, progressive accumulation of edema fluid in the cortex (90 to 170.8 microliters per g of tissue) and in the white matter (19 to 46.2 microliter per g of tissue) was detected by the end of 240 minutes of cerebral ischemia.
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PMID:Alterations in cortical oxygen tension during the development of ischemic cerebral edema in primates (Macaca mulatta). 11 Nov 52

Coxsackievirus B5 in the presence of fetal calf serum was exposed to six commonly used disinfectants for times of 10, 20 and 30 s. At the end of exposure times skim milk neutralized the disinfectant activity, with residual virus assayed by the plaque technique. The six disinfectants considered were Javex, sodium hydroxide, ethanol, Wescodyne, One Stroke Ves-Phene and Sonacide. Although 95% (v/v) ethanol was significantly more virucidal than dilutions of the other five disinfectants tested causing a 10(6) reduction in 20 s, it may not be practical to use in many instances. Next to 95% (v/v) ethanol, 1/75 (800 parts/10(6) Javex, 0.25% (w/v) sodium hydroxide and 1/200 Wescodyne were the most effective virucides. These disinfectants were equal in effectiveness causing a 10(5) reduction of coxsackievirus B5 in 30 s. Of these three disinfectants Javex is the most practical to use since sodium hydoroxide is caustic and Wescodyne is selective in its virucidal action. Undiluted Sonacide was a less effective virucide causing a less than 10-fold reduction of coxsackievirus B5 in 30 s. A 1/50 dilution of One Stroke Ves-Phene was the least effective virucide tested since it did not significantly inactivate coxsackievirus B5 in 30 s.
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PMID:The relative effectiveness of commonly used disinfectants in inactivation of coxsackievirus B5. 21 74

A homogeneous amidophosphoribosyltransferase (EC 2.4.2.14) preparation, which was sensitive to purine nucleotide inhibitors, was obtained from chicken liver. From the result of sodium dodecyl sulfate polyacrylamide gel electrophoresis, the subunit weight was estimated to be approximately 58 000. In Tris-HCl buffer, the predominant form of the enzyme had an S20,w of 6.5, Strokes radius of 40 A, and estimated molecular weight of 110 000. Incubation with 5-phosphoribosyl 1-pyrophosphate or Pi resulted in an increase in the S20,w to 9.1--9.5, Strokes radius 50 A, and estimated molecular weight to 200 000. Incubation of the large form with AMP led to a decrease in the molecular wight of the enzyme. It is concluded that chicken liver amidophosphoribosyltransferase is an allosteric protein whose activity is regulated by a series of conformational changes induced by a number of ligands.
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PMID:Chicken liver amidophosphoribosyltransferase. Ligand-induced alterations in molecular properties. 22 44

1. The effects of long-term treatment with the angiotensin I converting-enzyme inhibitor YS 980 were examined in stroke-prone spontaneously hypertensive (sp-SH) rats. Development of hypertension was markedly blunted in the YS 980-treated animals. 2. Effective converting-enzyme inhibition was confirmed by significant increases in plasma angiotensin I (ANG I) and plasma renin concentration, inhibition of the pressor responses to intravenous ANG I and potentiation of the depressor responses to intravenous bradykinin. 3. Urinary free aldosterone excretion was decreased but no changes in urinary sodium and potassium excretion were observed. 4. The pressor responses to intravenous leucine-enkephalin were reduced. 5. The pressor responses to injection of ANG I and bradykinin into the lateral brain ventricle were unaltered. 6. We conclude that the antihypertensive action of YS 980 in sp-SH rats cannot be explained by the inhibition of the plasma renin-angiotensin system alone. Effects on other peptide systems must be considered.
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PMID:A novel orally active converting-enzyme inhibitor YS 980: effects on blood pressure in spontaneously hypertensive rats. 23 20

Stupor in patients with nonketotic hyperglycemia has been ascribed to hyperosmolarity, but the cause of depressed consciousness in patients with ketoacidosis has been puzzling. In this study, blood pH, serum glucose and sodium concentrations, and serum osmolality were measured in eighty-five consecutive episodes of diabetic ketoacidosis and forty-seven of nonketotic hyperglycemia. In the acidotic patients, as in those with nonketotic hyperglycemia, stupor closely paralleled hyperosmolarity and not the severity of acidemia. Indeed, the mean elevations of serum osmolarity were almost the same in the ketotic and in the nonketotic patients who were deeply obtunded. It seems likely that depression of consciousness in patients with severely uncontrolled diabetes mellitus, if not due to a nonmetabolic disorder, such as acute stroke, is attributable to hyperosmolarity, whether or not ketoacidosis is present.
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PMID:Hyperosmolar nature of diabetic coma. 23 99

Afterload reduction with sodium nitroprusside was performed in a patient with idiopathic lactic acidosis in whom sodium bicarbonate therapy had precipitated pulmonary edema. The drug reduced mean pulmonary-artery wedge pressure from 28 to 12 mm Hg, accompanied by a modest rise in left ventricular stroke work index from 33 to 43 g-m per square meter. Concomitantly, there was dramatic resolution of the metabolic acidemia, the arterial pH rising from 7.19 to 7.61, arterial carbon dioxide tension from 13 to 26 mm Hg, and bicarbonate content from 6 to 28 mEq per liter, and the anion gap falling from 32 to 11 mEq per liter. Metabolic improvement occurred despite a fall in cardiac output from 5.5 to 4.8 liters per minute. These findings support the concept that regional vasoconstriction plays a part in idiopathic lactic acidosis, and suggests that vasodilators may be an effective form of therapy for this almost uniformly fatal disorder.
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PMID:Vasodilator therapy of idiopathic lactic acidosis. 23 36


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