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

In normothermic anesthetized cats cerebral blood flow was interrupted completely for one hour by arterial clamping and induced hypotension. The effect of ischemia on the ionic gradients of the cerebral cortex was assayed by determining total cortical electrolytes and by recording the activities of extracellular potassium ([K+i1e) and subarachnoid sodium ions ([Na+])s) with ion-sensitive electrodes. During ischemia [K+]e increased from 3.3+/-0.3 to 56+/-5.4 mEq per liter (means+/-SE) and [Na+]s decreased from 133+/-3.8 to 53+/-5.8 mEq per liter. When the brains were recirculated with blood after one hour's ischemia, [K+]e and [Na+]a gradually returned to normal within 45 minutes. The calculated intracellular uptake of sodium during ischemia amounted to 139 mEq per kilogram dry weight, whereas the intracellular release of potassium was only 64 mEq per kilogram. The increase in intracellular cation was accompanied by a movement of water from the extracellular into the intracellular compartment, causing a reversible shrinkage of the extracellular space from 18.9 to 8.5 vol %. The changes in ionic gradients were related to the development and resolution of ischemic brain swelling, and to the elctrophysiological events during and after ischemia.
Stroke
PMID:Cation activities in reversible ischemia of the cat brain. 83 60

Twelve male mongrel dogs were used for this study; six were untreated (control) and six were given intravenous furosemide (1 mg/kg) daily for seven consecutive days before each study. Each animal received intravenous KCl 0.8, 1.6 or 3.2 mMol/kg/hr for one hour, but only one dose for each study and at least seven days were allowed between studies. The animals were given thiopentone for tracheal intubation and mechanically ventilated, maintaining a PaCO2 of 4.0 to 4.5 kPa (30-35 torr) and anaesthetized with nitrous oxide-oxygen and halothane. Daily administration of furosemide reduced serum potassium from 4.48 to 4.09 mMol/1 with no significant change in serum sodium. A greater number of furosemide-pretreated animals (6 vs 3) developed cardiac dysrhythmias during non-lethal intravenous KCl at 0.8, 1.6 mMol/kg/hr. The furosemide-pretreated group tended to succumb at a lower serum potassium concentration (12.2 vs 13.8 mMol/I, P less than 0.05) and developed earlier onset (44 vs 54 min, P less than 0.05) of cardiac standstill or ventricular fibrillation following intravenous KCl at 3.2 mMol/kg/hr. Cardiac output, heart rate and mean arterial pressure were significantly elevated during serum concentrations of 6.9-9.1 mMol/1, while no statistically significant changes were observed for stroke volume and peripheral resistance. There were no significant differences of urinary potassium excretion between the untreated and treated groups when like doses of KCl were infused. These data suggest that acute infusion of KCl in furosemide-pretreated dogs may not be an effective means of treating hypokalaemia and could be hazardous.
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PMID:Acute intravenous administration of potassium chloride to furosemide pretreated dogs. 84 74

The author determined the phasic structure of the systole of the left ventricle by the method of polycardiography and hemodynamics in 20 patients suffering from hypothyrodism. Blood plasma and erythrocyte electrolytes were examined at the same time. Patients with hypothyroidism displayed a phasic syndrome of hypodynamia and a marked correlation between the phase of the synchronous contraction, the period of ejection, the strength of contraction of the left ventricle and the electrolyte content. Sodium and magnesium produced the greatest influence on the phasic structure of the systole; potassium and calcium had a lesser effect. The heart stroke volume diminished; as to the cardiac index, expenditure of the energy of cardiac contractions directed to the maintenance of movement of 1 litre of the minute blood volume; the external work, and the peripheral vascular resistance displayed no significant change.
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PMID:[Myocardial contractility and hemodynamics in hypothyroidism]. 84 74

To examine the influence of preexistent diabetes mellitus on left ventricular performance and coronary blood flow responses to acute ischemia, mild normoglycemic diabetes was induced in nine mongrel dogs after three doses of alloxan, (20 mg/kg, iv), at monthly intervals. Hemodynamic measurements and coronary blood flow (85Kr clearance) were obtained before and after the onset of ischemia. This was produced by occlusion of the proximal left anterior descending coronary artery via a balloon-type catheter in nine intact anesthetized diabetic dogs and 10 nondiabetic dogs. During the 1st hour of ischemia in the diabetic group, the end-diastolic pressure rose from 7 +/- 1.1 (mean +/- SE) mm Hg to 23.8 +/- 2.3 without a significant increase of end-diastolic volume. In controls end-diastolic pressure rose from 8.6 +/- 1.1 mm Hg to 15.3 +/- 1.4, and end-diastolic volume was significantly increased, so that the ratio of end-diastolic pressure and volume was significantly higher in the diabetic group (P less than 0.005). Although indices of contractility did not differ, stroke volume and work reductions were significantly greater in diabetics, despite the fact that coronary blood flow was reduced to a similar extent. Size of the ischemic areas appeared comparable as judged by distribution of dye injected distal to the occlusion. Since potassium loss and sodium gain in the inner and outer layers of ischemic tissue did not differ between the two groups, the intensity of ischemia seemed similar. Glycogenolysis was unimpaired in the diabetic ischemic muscle but triglyceride levels remained elevated. Morphologically the diabetic myocardium was characterized by a diffuse accumulation of periodic acid-Schiff-positive glycoprotein in the interstitium, which was thought to limit diastolic filling of the ischemic ventricle and to contribute to the substantial reduction of ventricular performance.
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PMID:Myocardial function and coronary blood flow response to acute ischemia in chronic canine diabetes. 87 Feb 38

Fluorescence-and electron-microscopic studies were performed on nerve terminals close to intracerebral blood vessels in the rat. For the electron microscope subdural perfusion fixation with potassium permanganate was used. In the rat cerebral cortex deprived of the bilateral superior cervical ganglion some aminergic terminal boutons containing large and small core vesicles were observed contiguous to blood vessels. These terminals abutted on the capillary basement membrane. Since these terminals are found in the rat after bilateral superior cervical ganglion exision, they probably originate from central catecholaminergic neurons in the brain stem. These findings suggest that central aminergic neurons might play some role in cerebral blood flow regulation. In addition to aminergic terminal boutons, non-aminergic nerve terminals containing non-core vesicles also ended in the capillaries. Cerebral capillaries also have central dual innervation, aminergic and cholinergic, and dual peripheral innervation by sympathetic and parasympathetic fibers.
Stroke
PMID:Central dual innervation of arterioles and capillaries in the brain. 87 Oct 25

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

Hemodynamic and inotropic effects of 200 mg and 400 mg Aldactone pro injectione (Canrenoate-Potassium, Aldadiene) were measured in three different series (n=60) during and after cardiac surgery in neuroleptanalgesia; results were compared to a control group (n=35). The first investigation was performed after sternotomy and pericardiotomy. During a measuring period of ten minutes no significant changes in inotropic parameter dp/dt max were found in comparison to individual control values. The second investigation during "steady state" extracorporeal circulation revealed a small decrease in arterial perfusion perfusion pressure after both dosages, which can be interpreted as an arteriolar vasodilatation. There was, however, no significant difference in comparison to the control group. Additional measurements were done after cardiac surgery in a total of 20 patients (200 mg and 400 mg Aldactone pro injectione) during an investigation period of 60 min. In comparison to a control group (n=15) no significant differences in arterial pressure, heart rate, cardiac index, stroke index and pulmonary arterial pressure were found. There were no acute and direct positive inotropic effects of Canrenoate-Potassium after administration of 200 mg and 400 mg respectively in cardiosurgical patients.
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PMID:[Cardiac and selective vascular effects of canrenoate-potassium (aldactone pro injectione) in cardiosurgical patients (author's transl)]. 91 81

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.
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PMID:Effect of sotalol on haemodynamics and renin-angiotensin-aldosterone system in hypertensive patients. 93 70

The effect of dopamine on hemodynamics (CO, AoPm, TPR, SV, SW, CVP, PAPm, PAEDP), microcirculation (MBF, PS-product) and renal function (VU, CKI, CNa, CK, Cosm, TcH2O) was studied in 8 patients with hypnotic drug poisoning. With increasing doses of dopamine, cardiac output and heart rate increased and the peripheral resistance decreased. An augmentation of stroke volume and left ventricular stroke work was observed in the low dose range only (200--400 mug/min). With increasing doses, central venous pressure as well as mean pulmonary artery pressure and enddiastolic pulmonary artery pressure decreased. No vasoconstriction was found in muscle tissue vessels even with large doses of dopamine. This is explained by the vasoplegic properties of hypnotic drugs. In circulatory shock associated with hypnotic drug poisoning, dopamine develops only minor pressure effects in contrast to its action in circulatory shock of cardiogenic or septic shock origin. High doses of dopamine result in a significant increase in heart rate, without concomitant increase in stroke volume and blood pressure. Therefore the dosage of dopamine should not exceed 400 mug/min in these cases. A combination with small doses of norepinephrine (10--20 mug/min) seems to be more effective. Renal function tests showed variable expansion of urine volume, glomerular filtration rate, and clearances of sodium, potassium and osmotic substances. Therapy with dopamine might increase the renal elimination rate of hypnotic drugs.
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PMID:[The influence of dopamine on hemodynamics, microcirculation and renal function in patients with hypnotic drug intoxication (author's transl)]. 94 Feb 91


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