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

Left ventricular (LV) function and dimensions were assessed with Doppler and M-mode echocardiography in 26 men and 17 women with newly diagnosed non-insulin-dependent diabetes mellitus, and in 13 healthy control men and 13 women. The diabetic men had lower peak filling rate normalized to mitral stroke volume than the control men (mean +/- standard error of the mean, 4.2 +/- 0.1 vs 4.9 +/- 0.3 stroke volume/s, p less than 0.01). The diabetic women had increased LV mass (102 +/- 12 vs 86 +/- 8 g/m2, p less than 0.01) and decreased fractional shortening (34 +/- 1 vs 38 +/- 1%, p less than 0.05) when compared with control women. At 3 and 15 months, 23 diabetic men and 15 women were reexamined. Concomitantly with decreasing blood glucose levels, fractional shortening improved mainly during the first 3 months and was significantly higher in both diabetic men (36 +/- 2 vs 30 +/- 2%, p less than 0.05) and women (38 +/- 1 vs 34 +/- 1%, p less than 0.05) at 15 months than at baseline. In the diabetic men, peak filling rate increased from 4.3 +/- 0.1 stroke volume/s at baseline to 4.8 +/- 0.2 stroke volume/s at 15 months (p less than 0.05). At 15 months, peak filling rate was correlated (r = 0.61, p less than or equal to 0.001) with autonomic nervous function assessed as heart rate variability during deep breathing test in diabetic men who also showed an inverse correlation between LV hypertrophy and heart rate variability throughout the follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular function and dimensions in newly diagnosed non-insulin-dependent diabetes mellitus. 163 6

Hypercholesterolemia is a major risk factor in coronary heart disease (CHD) and ischemic stroke. However, there is no general agreement on the usefulness of systematic screening of patients with hyperlipidemia by stress exercise electrocardiogram (ECG). The feasibility of this approach would depend on selecting patients with a high risk of CHD, since the sensitivity and specificity of the test depends on the prevalence of the disease. In view of the association of CHD and ischemic stroke, we undertook a study to determine whether the presence of atherosclerosis in the carotid arteries was predictive of a positive exercise ECG in a group of 778 asymptomatic patients referred to their hyperlipidemia. We a much higher percentage of positive exercise ECG in patients with carotid atherosclerosis in our ultrasonographic examinations. In a multiple regression analysis which included 13 parameters (age, sex, body mass index, arterial blood pressure, lipid parameters, serum level of glucose, smoking status and the severity of carotid lesions), the strongest predictors of a positive exercise ECG test were age (P = 0.014) and the degree of carotid atherosclerosis (P = 0.010). We therefore conclude that hyperlipidemic patients with atherosclerotic lesions on carotid arteries would benefit most from screening by the exercise ECG.
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PMID:Carotid stenosis is a powerful predictor of a positive exercise electrocardiogram in a large hyperlipidemic population. 163 43

A left to right shunt increases myocardial work and is often accompanied by increased catecholamine levels. Because both increased myocardial work and increased catecholamine levels may induce increased fatty acid utilization, which could increase resting myocardial oxygen consumption and therefore unfavorably affect coronary reserve, we studied myocardial uptake of glucose, pyruvate, lactate, beta-OH-butyrate, acetoacetate, FFA, and triglycerides in 12 7-wk-old lambs with aortopulmonary left to right shunts (58 +/- 2% of left ventricular output, mean +/- SEM) and in 10 control lambs 2 wk after surgery. Despite the shunt, systemic blood flow in the shunt lambs was maintained at the same level as in the control lambs. This was accomplished by an increased heart rate and stroke volume. Furthermore, the shunt was accompanied by an increased myocardial oxygen consumption in the shunt lambs (834 +/- 70 versus 528 +/- 43 mumol O2.min-1 x 100 g-1; p less than 0.05). There were no significant differences in arterial substrate concentrations between the two groups. The same was true for arteriovenous differences across the myocardium, with the exception of lactate, which was substantially higher in shunt than in control lambs (72 +/- 25 versus 18 +/- 23 mumol/L; p less than 0.05). As a consequence, myocardial lactate uptake in the shunt lambs was increased 15-fold (18 +/- 6 versus 1 +/- 2 mumol.min-1 x 100 g-1; p less than 0.02), whereas uptake of the other substrates merely paralleled the increased myocardial blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial carbohydrate, ketone, and fatty acid uptake in conscious lambs with aortopulmonary shunts. 163 42

The present study was conducted to assess the effect of chromium (Cr) administration on glucose tolerance in insulin-dependent diabetes that accompanies hypertension. Four rat groups were used: stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY) with and without streptozotocin (SZ, 40 mg/kg)-induced diabetes. Each group of rats was subdivided to the Cr-dose group and the control group. The Cr-dose group, which was intraperitoneally administered Cr solution (20 micrograms trivalent chromium/kg body weight/d for 4 weeks), and the control group (saline) were studied for plasma glucose and plasma insulin during intraperitoneal glucose tolerance test (IPGTT) and insulin action by isolated adipocytes. For diabetic SHRSP showing the highest plasma glucose and lowest plasma insulin among the four groups, Cr administration led to the greatest reduction in plasma glucose without a significant effect on plasma insulin during IPGTT. For each diabetic WKY and normal SHRSP and WKY, those given Cr showed lower levels of plasma glucose with lower levels of plasma insulin than the controls. For diabetic SHRSP, glucose uptake by isolated adipocytes in the Cr-dose group was higher than that in the control group. This effect of Cr administration involved enhancement of insulin responsiveness and sensitivity, attributed to enhanced affinity of the insulin receptor. A similar tendency was observed for diabetic WKY. However, for normal SHRSP and WKY, the increase in glucose uptake due to Cr administration coincided only with enhanced insulin responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of chromium administration on glucose tolerance in stroke-prone spontaneously hypertensive rats with streptozotocin-induced diabetes. 164 Aug 49

Evidence from animal stroke models suggests that the proximate cause of neuronal degeneration after ischemia is massive release of glutamate and activation of NMDA receptors. However, in the physiologic presence of oxygen and glucose in the rat hippocampal slice preparation, the neurotoxicity of glutamate, as measured by inhibition of protein synthesis, requires high concentrations and is not prevented by glutamate receptor antagonists. Thus, the NMDA receptor-mediated neurotoxic effects of extracellular glutamate accumulation during ischemia might depend on additional factors, such as neuronal depolarization. In the experiments reported here, slices were exposed to glutamate in a medium intended to mimic the ionic conditions found during ischemia, high potassium (128 mM) and low sodium (26 mM). This depolarizing medium itself inhibited protein synthesis in a manner which was partially mediated by NMDA receptor activation, since it was significantly reversed by the noncompetitive NMDA antagonist, MK-801. Furthermore, the effect of glutamate under depolarizing conditions was also significantly decreased by MK-801, suggesting that glutamate was acting at NMDA receptors. Thus, depolarization appears to enhance the sensitivity of neurons to toxic NMDA receptor activation by glutamate. Under conditions that mimic ischemia, hypoxia plus hypoglycemia, a similar protective effect of NMDA receptor antagonists was observed. Depolarization and ischemia both appeared to attenuate the neurotoxicity of non-NMDA receptor agonists. It appears that under conditions of normal glucose and oxygen, high concentrations of bath applied glutamate inhibit protein synthesis at sites other than the NMDA receptor. However, when the Na+ gradient is decreased, as occurs during ischemia, glutamate's NMDA effects predominate. These findings suggest that ionic shifts may play a central role in permitting NMDA receptor-mediated ischemic neuronal damage.
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PMID:Enhancement of NMDA receptor-mediated neurotoxicity in the hippocampal slice by depolarization and ischemia. 165 99

1. Splanchnic haemodynamic changes were studied in seven healthy subjects during hypoglycaemia induced by the intravenous infusion of insulin. Superior mesenteric artery blood flow and cardiac output were examined noninvasively by a Doppler ultrasound technique. 2. Blood glucose concentration fell from 4.5 (0.14) mmol/l basally to 1.5 (0.09) mmol/l [mean (SEM), P less than 0.003] at the hypoglycaemic reaction ('R') and recovered to baseline by 'R' + 60 min. There was an associated rise in plasma glucagon, adrenaline and noradrenaline levels. 3. Superior mesenteric artery blood flow rose at 'R' from a basal value of 532 (38) ml/min to a peak of 803 (73) ml/min at 'R' + 10 min [mean (SEM), P less than 0.005] and remained significantly elevated until 'R' + 40 min. Resistance in this vessel fell by 33% at 'R' + 10 min (P less than 0.005) and remained significantly low until 'R' + 40 min. 4. Cardiac output rose by 33% at 'R' (P less than 0.004) and returned to normal by 'R' + 20 min. This was associated with a 24% rise in pulse rate (P less than 0.03), but no change in stroke volume or mean arterial pressure. Total peripheral resistance fell by 21% at 'R' (P less than 0.005) and had returned to normal by 'R' + 20 min. 5. The sustained rise in splanchnic blood flow during hypoglycaemic recovery may be of homoeostatic importance by providing metabolic fuel to the liver for gluconeogenesis.
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PMID:Splanchnic haemodynamic changes during acute hypoglycaemia in man. 165 99

Antihypertensive treatment, by lowering blood pressure and correcting functional and/or structural abnormalities of the arterial wall, may prevent the arterial damage due to the accelerated ageing process. The objective of the present study was to determine, using a cross-sectional approach, whether arterial distensibility of patients whose blood pressure had been normalized for several months by antihypertensive treatment, was significantly higher than that of untreated hypertensive patients. The properties of the vessel wall of the common carotid artery (CCA) were studied non-invasively, using an original pulsed ultrasound echo-tracking system based on Doppler shift, during a study comparing 46 normotensive subjects and 81 age-matched hypertensive patients. The latter group included 25 patients well controlled by antihypertensive treatment for at least 3 months and 56 untreated hypertensives. The three groups did not differ with respect to age, total and high-density lipoprotein cholesterol, blood glucose and smoking. In each group, there were significant relationships between age and CCA dimensional and functional data, including end-diastolic diameter, absolute and relative stroke changes in diameter and Peterson modulus, indicating a widening of the CCA with advancing age and a decrease in its buffering function. When compared with untreated hypertensives, well controlled hypertensives had significantly lower blood pressure and Peterson elastic modulus according to age. However, although blood pressure of well controlled hypertensives was not significantly different from that of normotensive subjects, their arterial distensibility remained altered compared with that of normotensive subjects (significant increase in Peterson elastic modulus). These results suggest that long-term antihypertensive treatment may not fully reverse arterial lesions due to the hypertensive disease.
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PMID:Stiffness of the common carotid artery in treated hypertensive patients. 165 37

The objective of treating patients with hypertension is not simply to reduce blood pressure but rather to prevent the associated morbidity and mortality. Recent assessments of clinical trials have shown that while the risk of stroke is consistently lower with antihypertensive therapy, the same degree of success has not been demonstrated for coronary artery disease (CAD). Although there are many explanations of why we have not done as well in preventing CAD, one possibility is that the therapy used in clinical trials, primarily thiazide diuretics and beta-adrenoreceptor blockers, has increased the patient's risk of developing coronary atherosclerosis or lethal arrhythmias. Four classes of antihypertensive agents are recommended for initial therapy--thiazide diuretics, beta-adrenoreceptor blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium entry blockers. The metabolic effects of thiazide diuretics include electrolyte disturbances (hypokalemia, hypomagnesemia, and hyponatremia), dyslipidemia (increased triglycerides), abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance), and hyperuricemia. beta-Adrenoreceptor blockers have many of the same metabolic adverse reactions. beta-Adrenoreceptor blockers without intrinsic sympathomimetic activity (ISA) also cause dyslipidemias (lowered high-density lipoprotein cholesterol and increased triglycerides) and abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance). beta-Adrenoreceptor blockers with ISA and third-generation beta-blockers with selective partial agonist activity (celiprolol and dilevalol) do not cause dyslipidemia and to date do not appear to induce abnormalities in glucose metabolism. ACE inhibitors may decrease triglycerides and increase high-density lipoprotein cholesterol, and captopril may improve insulin sensitivity. Calcium entry blockers are metabolically neutral.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic considerations in the choice of therapy for the patient with hypertension. 167 Nov 90

This study was designed to test the hypothesis that intracoronary administration of esmolol can confer metabolic protection during coronary constriction or occlusion, without affecting hemodynamic parameters, in a canine model. Seventeen anesthetized open-chest dogs underwent direct cannulation of the left anterior descending coronary artery (LADa), its companion vein (LADv), and the distal circumflex vein (CFXv). LADa flow was measured with an electromagnetic flowmeter. Using a micrometer-driven snare around the LADa, flow was reduced by 50%, 75%, and 100% for 15 minutes, with 1 hour of normal flow before each constriction. In 7 dogs (group 1) chosen randomly, esmolol, 15 to 20 micrograms/kg/min, was infused continuously into the LADa; the rate was adjusted to maintain baseline hemodynamic values. The second group (10 dogs) was not treated with esmolol. Heart rate (HR), electrocardiogram (ECG), LADa flow, LV dP/dt, and aorta (Ao), pulmonary artery (PA), LADa, and left ventricular (LV) pressures were recorded continuously. Cardiac output (CO) (thermodilution) was measured and blood was sampled from all catheters before and after constrictions for analysis of glucose, lactate, sodium, potassium, and blood gases. Flow and pressure in the LADa in both groups decreased similarly during each corresponding constriction. Systolic LV pressure, LV dP/dt, and LV stroke work index were affected in both groups only during 100% constriction. HR, Ao, and PA pressures, and total and peripheral pulmonary resistances were affected similarly in both groups during each constriction. Myocardial lactate extraction and consumption were less negative (negative = net production and output) in the LAD perfusion bed during corresponding constrictions with esmolol than without it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased regional lactate production and output due to intracoronary continuous infusion of esmolol during acute coronary occlusion in dogs. 167 24

Oral contraceptives (OCs) were initially approved for unrestricted use in 1960 in the United States and have been used and studied extensively for 30 years. The initial formulations contained a fixed dose of estrogen and progestogen ingested for 21 days, with a seven-day pill-free interval. Subsequent formulations contained a sequential estrogen dose, a progestogen alone given daily, and variable doses of both progestogen and estrogen. Although the estrogen and progestogen doses employed in currently marketed OCs are markedly lower than those used in the OCs of the 1960s and 1970s, the excellent contraceptive efficacy of these compounds has not been compromised. The estrogen component produces a dose-related increase in serum globulin concentrations, triglycerides, and high-density lipoprotein (HDL) cholesterol, along with a decrease in low-density lipoprotein (LDL) cholesterol, while the progestogen component causes peripheral insulin resistance, a decrease in HDL cholesterol, an increase in LDL cholesterol, and various androgenic effects. The effect of nicotine on thromboxane release acts synergistically with the elevated serum clotting factors to increase the incidence of both arterial and venous thrombotic events, particularly in women smokers over 35 years of age. However, there is no evidence of increased risk of myocardial infarction or stroke in healthy, nonsmoking women of any age who use OCs containing less than 50 micrograms estrogen. Likewise, the lower-dose estrogen/progestogen formulations do not have a clinically significant effect on glucose metabolism and have a neutral effect on lipoprotein metabolism. In addition, the many noncontraceptive health benefits associated with OCs are maintained with the lower-dose formulations. Thus, the low-dose formulations should improve the overall health of healthy, nonsmoking women as well as effectively prevent unwanted pregnancy.
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PMID:Oral contraception: past, present, and future perspectives. 167 81


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