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)

Sotalol is a nonselective, water-soluble beta-adrenoceptor antagonist with no membrane-stabilizing activity or intrinsic sympathomimetic activity. Sotalol is, essentially, completely absorbed and is not metabolized. Consequently, bioavailability is close to 100%. Age and food have slight but unimportant effects on bioavailability. Cmax of sotalol is 2 to 3 hours with a t1/2 between 7 and 15 hours. Excretion of sotalol is primarily through the kidneys, with no metabolism by liver and no first-pass effect. Therefore, sotalol plasma levels and half-life are directly related to creatinine clearance and glomerular filtration rate. Appropriate dose adjustments must be made for patients with impaired renal function or increased renal blood flow, as in pregnancy. The beta-adrenoceptor antagonistic effects of sotalol are directly related to plasma levels, which, in turn, are directly related to dose. However, the beta-adrenoceptor antagonism t1/2 is longer than the sotalol plasma t1/2. As a consequence of its ability to prolong the action potential duration, sotalol also increases cardiac contractility in isolated ventricular, but not atrial, preparations by 20 to 40%. This positive inotropic effect is not blocked by beta or alpha blockade or reserpine pretreatment and seems to be related to sotalol's effects on cardiac ionic currents. Like the effects of sotalol on action potential duration, the positive inotropic effects are inversely proportional to rate. The hemodynamics of sotalol indicate a relative lack of direct cardiac depressant activity in both animals and humans. The typical hemodynamic effects of sotalol in normotensive humans, even with depressed myocardial function, are a reduction in heart rate with little or no change in blood pressure, a reduction in cardiac output with no change in stroke volume, and little or no change in pulmonary wedge pressure and left ventricular end-diastolic pressure or volume, and little or no change in ejection fraction either at rest or during exercise.
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PMID:Pharmacology, pharmacodynamics and pharmacokinetics of sotalol. 240 31

The incidence of second wave of platelet aggregation induced by a small dose of ADP (1 mumol/l) was compared with plasma levels of beta-thromboglobulin in 81 normal individuals, 34 patients with acute myocardial infarction, 11 patients with acute cerebrovascular disease and 26 patients with renal disease. Platelet hyperaggregability was observed in 7% of normal individuals. Plasma levels of beta-thromboglobulin were higher in normal individuals over 60 years of age (48 vs. 32 micrograms/l). In contrast, hyperaggregability was observed in 79% of patients with acute myocardial infarction and in 64% of those with acute cerebrovascular disease. Median plasma levels of beta-thromboglobulin were also significantly elevated in patients with acute myocardial infarction (82 micrograms/ml) or acute cerebrovascular disease (99 micrograms/l). Levels of beta-thromboglobulin in plasma were significantly higher in those patients who demonstrated hyperaggregability. In patients with renal disease only 12% had signs of hyperaggregability. Nevertheless their plasma levels of beta-thromboglobulin were elevated (76 micrograms/l) and correlated with the serum creatinine values. These investigations indicate that patients with acute myocardial infarction or stroke have hyperreactive platelets and evidence of increased platelet inactivation in the circulation. However, evaluation of increased levels of beta-thromboglobulin requires consideration of renal function.
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PMID:Relationship between platelet aggregation and plasma beta-thromboglobulin levels in arterio-vascular and renal diseases. 240 89

A previous article (Part I) described the patient population and operative management of 666 patients who had surgery for nonruptured abdominal aortic aneurysms. This article details the perioperative complications and, by chi-square and logistic regression analysis, identifies the variables that are associated with each complication. In summarizing the results (below) the incidence of each complication is listed, along with the predictive risk factors in parentheses that have significance levels less than 0.05. Vascular morbidity data are as follows: intraoperative bleeding, 4.8%; postoperative bleeding requiring transfusion, 2.3% or repeat operation, 1.4% (large volume of blood transfusion and/or use of an autotransfusion device); intraoperative limb ischemia, 3.5%; graft thrombosis, 0.9% (femoropopliteal disease and/or distal anastomosis at the femoral level); distal thromboembolism, 3.3% (male sex, femoral popliteal disease, and/or intraoperative graft thrombosis); amputation, 1.2%; graft infection, 1 case. General morbidity data are as follows: cerebrovascular event, 0.6%; paraplegia, 1 case; cardiac event, 15.1% (age, previous episode of congestive heart failure, and/or electrocardiogram [ECG] evidence of a previous myocardial infarction); myocardial infarction, 5.2% (advancing age, angina, and/or prolonged aortic cross-clamp time); congestive heart failure, 8.9% (previous history of congestive heart failure, ECG evidence of ischemia, and/or chronic obstructive lung disease); arrhythmia requiring treatment, 10.5% (preoperative ventricular premature beats and/or respiratory failure requiring ventilation for more than 48 hours); new arrhythmia, 8.4% (angina and/or chronic obstructive lung disease); respiratory failure, 8.4% (chronic obstructive lung disease, large volume of blood transfused, and/or occurrence of postoperative bleeding, cerebrovascular accident, congestive heart failure, or myocardial infarction); renal damage with rise in creatinine or blood urea nitrogen, 5.4% and/or renal failure requiring dialysis, 0.6% (elevated preoperative creatinine, suprarenal aortic cross-clamping, and/or renal vein ligation); diarrhea without evidence of ischemia colitis, 7.1% and ischemic colitis, 0.6% (pelvic flow interrupted); prolonged ileus, 11.0% (aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and/or preoperative history of angina); superficial wound infection, 1.5% and deep infection, 0.5% (femoral anastomosis and/or female sex); coagulopathy, 1.1% (large volume of blood transfused).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality. 264 60

This study aims to clarify the neurohumoral regulation of cardiovascular circulatory adjustments and to analyze changes in renal function and their relationship to cardiovascular hemodynamics in the early stage of heart failure. Cardiac and peripheral (calf segment) hemodynamics, neurohumoral factors and renal function were investigated in totally 139 patients with acute myocardial infarction (AMI). Capacitance vessel constriction was observed in patients with uncomplicated AMI (Killip-I, Forrester HS-I) and constriction of capacitance and resistance vessels in patients complicated by heart failure (Killip II, Forrester HS-II) or cardiogenic shock (Killip III-IV, Forrester HS-IV). Augmented sympathoadrenal discharge significantly related to the degree of pump dysfunction (elevation of heart rate, central venous pressure, pulmonary capillary wedge pressure (PCWP) and decrease of stroke volume index (SVI] and activation of the renin-angiotensin-aldosterone system significantly related to fall in tissue perfusion pressure (mean blood pressure and calf vascular resistance) would be a possible mechanism for these compensatory mechanisms. However these would contribute to excessive vasoconstriction in limbs resulting in exercise intolerance or renal glomerular function impairment. The derangement of creatinine clearance, serum creatinine (Scr), blood urea nitrogen and beta 2-microglobulin were related to Killip classification, and it was clarified that PCWP tended to elevate more in patients with preexisting renal function disturbance, and when cardiac output (CO) depressed much lower, reduction of CO per se caused more severe prerenal renal insufficiency. That is, there were significant correlations between renal function parameters and cardiovascular hemodynamics. The Cardio-Renal Subset (CRS) was originally developed according to the initial SVI and Scr, and it was demonstrated that the CRS would be of definite predictive value in early identification of high risk patients.
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PMID:Cardiovascular circulatory adjustments and renal function in acute heart failure. 265 39

Heat stroke is the most serious entity amongst the heat disorders. Whilst potentially fatal, it is preventable and salvageable. A retrospective study involving 27 patients admitted for exertional heat stroke to the Medical Unit, Toa Payoh Hospital, Singapore from January, 1984 to January, 1987 was carried out. These patients presented with a rectal temperature of greater than 40 degrees C and central nervous system disturbances. All were males and, except for three, were local born. All except two were below thirty years old. The patients were treated with a standard regime of IV fluids and sponging in the ICU. 19 patients (70.4%) presented in coma whilst abnormal behaviour, e.g. aggression and mental confusion was seen in the remainder. Fits were seen in only 5 patients (18.5%). Metabolic acidosis was seen in 93.3%. Hypokalaemia was present in 3 patients (11.1%). Of the enzymes, creatinine phosphokinase was elevated in all except 1 patient (mean: 4868.8, range: 146-28850). There were no deaths recorded in this series. Complications include reversible DIVC (3 instances), oliguric renal failure (4 instances) and residual neurological deficit (2 instances). 9 patients (39.1%) took more than 4 hours for the rectal temperature to attain 37.5 degrees C. All the above complications except for 1 instance of DIVC occurred in this group with delayed cooling. Heat stroke is a serious condition with serious complications and require prompt treatment.
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PMID:Heat stroke: a clinical review of 27 cases. 260 67

Clinical studies using 31P and 1H MRS with a whole body 2.0 T MRI/MRS system are described. In most cases, techniques to quantitate absolute molar concentrations of metabolites in various organs were used. In the brain, AIDS, chronic stroke, and white matter lesions were associated with alterations of brain 31P metabolites. Epilepsy was associated with increased pH in the seizure focus. In the heart, dilated cardiomyopathy was associated with increased PDE/ATP while PCr/ATP was unchanged. In the liver, alcoholic hepatitis and cirrhosis were associated with diminished hepatic ATP while alcoholic hepatitis had increased pH and cirrhosis had decreased pH. This allowed differentiation of normal liver, alcoholic hepatitis, and alcoholic cirrhosis without biopsy. In the prostate, malignancy was associated with increased PME/ATP and decreased PCr/ATP. The PME/PCr was greatly increased in malignant prostate with no overlap in normals. Other cancers outside the brain had increased PME and effective treatment was often associated with diminished PME. 1H MRS of the brain was performed using ISIS and outer volume suppression pulses for volume localization. Excellent high resolution 1H water-suppressed spectra were obtained at echo times as short as 30 ms, showing well resolved peaks for lactate, N-acetylaspartate, glutamate, choline, creatinine, and inositol. 1H MRS demonstrated that the uptake of ethanol by the brain was slower than the rise of ethanol in blood. 31P spectroscopic imaging of the brain with resolution of 2.25 x 2.25 x 2.5 cm produced metabolic images and high resolution spectra from desired regions of interest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical magnetic resonance spectroscopy of brain, heart, liver, kidney, and cancer. A quantitative approach. 270 9

A group of 25 patients in III-IV haemodynamic period of chronic stagnant circulatory failure (pzns) in clinical conditions for two weeks were administered digoxin and furosemide (DF), then for the following two weeks DF therapy was combined with nifedipine (N), in the following 4 weeks the DFN therapy was combined with captopril (DFNK), in the last two weeks DFN therapy was applied again. The authors used the following doses per 24 h: D--0.29 +/- 0.96 mg, F--13.5 +/- 4.8 mg, N--40.8 +/- 12.8 mg and K 75.0 +/- 28.8 mg. Each cycle of the therapy was followed by a precise clinical evaluation, analysis of the function of the left ventricle by means of two-dimensional echocardiography, the evaluation of the tolerance of physical effort and the evaluation of chest radiograms. Besides, blood was studied for the concentrations of potassium, sodium, chloride, urea, creatinine, uric acid, haematocrit value and pH value. The addition of nifedipine to the classical therapy did not give significant improvement in the clinical condition, haemodynamic parameters and the tolerance of physical effort in patients with pzns. In comparison to DF period, the use of captopryl brought about a statistically significant increase (p less than 0.05) in ejection fraction (EF) from 43.0 +/- 15.3% up to 45.2 +/- 11.7%, in effort power from 36.5 +/- 16.4W up to 47.1 +/- 17.5W, in effort duration from 3.5 +/- 1.6 min. up to 4.5 +/- 1.8 min. and a significant decrease (p less than 0.05) in body weight from 68.1 +/- 13.8 down to 66.9 +/- 13.0 kg and heart volume from 1175.5 +/- 487.3 cm3 down do 1074.6 +/- 380.9 cm3. One could notice, though statistically not significantly (p greater than 0.05) an increase in stroke volume index and cardiae index. Besides, the authors noticed a tendency to an increase in potassium concentration in blood serum. Eliminating captopryl caused fast regression of positive haemodynamic effects, decrease in physical effort tolerance, and clinical condition resumed the condition observed in the period of DFN therapy.
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PMID:[Evaluation of nifedipine and captopril as adjuvant drugs in the standard treatment of chronic heart failure]. 270 93

Autologous blood clot was injected into six dogs to produce a graduated decrease in cardiac output (CO). The effects of an infusion of norepinephrine, titrated to specific end points, were recorded before embolization and at two levels of pulmonary hypertension. Simultaneous measurements of systemic and renal hemodynamics were made. Sequential blood clot injection increased (p less than .01) pulmonary vascular resistance (PVR) from 1.3 to 13 to 33 mm Hg.L-1.min and reduced CO 45 percent and 75 percent (p less than .01). Norepinephrine increased both stroke volume and CO (p less than .01) in each condition and did not increase PVR. Since the biventricular filling pressures remained constant or fell slightly with norepinephrine, the increase in CO is best explained by an improvement in pump performance. There was no deterioration in renal blood flow or creatinine clearance with norepinephrine. The data suggested that in this model of right ventricular dysfunction, norepinephrine consistently improved myocardial performance without provoking further vasoconstriction in either the pulmonary or renal circulations.
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PMID:The cardiopulmonary and renal hemodynamic effects of norepinephrine in canine pulmonary embolism. 272 Dec 72

Arterial and pulmonary artery catheters were used to monitor the cardiopulmonary effects of recombinant interleukin-2 (rIL-2) given iv at a dose of 100,000 U/kg every 8 hours on days 1-5 to 10 patients with metastatic solid tumors. As anticipated, a severe capillary leak syndrome developed in all patients. Myocardial infarction (MI) occurred unexpectedly in three patients, as evidenced by a focal injury pattern on ECG and elevations of creatinine phosphokinase myocardial band fractions. All patients receiving rIL-2 exhibited major reductions in their left ventricular stroke work index (47 +/- 11 g.m/m2 to 29 +/- g.m/m2), an index of cardiac contractility. It remains uncertain whether the MIs were a byproduct of the capillary leak syndrome in patients with underlying coronary artery disease or whether rIL-2 directly or indirectly damages cardiac muscle.
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PMID:Myocardial toxic effects during recombinant interleukin-2 therapy. 278 57

Enalapril 40 mg or tolerated dose was given once daily to 21 patients with congestive heart failure (CHF), NYHA class III, in addition to treatment with digoxin and/or diuretics. After an 8-week open period, 19 patients were randomized to continue enalapril or to receive a placebo in a double-blind manner. After the first enalapril dose of 10 mg, maximal reduction of blood pressure (BP) occurred after 4 hours (mean 34/17 mmHg; p less than 0.001). No further reduction was found after higher doses. After the open period significant improvement was shown as judged by NYHA class (p less than 0.01), stroke volume (p less than 0.05), maximal working capacity (p less than 0.05), heart volume (p less than 0.01) and maximum rate pressure product (RPPmax) (p less than 0.001). Urinary aldosterone markedly decreased (p less than 0.01), whereas serum potassium and serum creatinine slightly increased (p less than 0.05). At the end of the blind period enalapril was superior to placebo concerning NYHA class (p less than 0.01), heart volume (p less than 0.05) and RPPmax (p less than 0.05). Other parameters, including aldosterone in urine, did not differ between the groups. Carry-over effects may have diminished the differences between enalapril and placebo. Diarrhoea (n = 5) and hypotension (n = 5) were the most common side-effects. Overall, enalapril was well tolerated and seems to be useful in single daily doses in the treatment of CHF.
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PMID:Once daily dosing of enalapril in congestive heart failure. 283 90


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