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

The systemic hemodynamic effects of deep hypotension (MAP: 38 +/- 6 mm Hg) induced by sodium nitroprusside (S.N.) were studied in 20 patients who underwent surgery for cerebral aneurysm. The hemodynamic measurements were performed four times.: (1) during the preoperative period, (2) during stable anesthesia just before hypotension, (3) during stable hypotension, (4) 20 minutes after stopping nitroprusside. All patients were mechanically ventilated with a constant tidal volume and rate. Parameters for acid-base balance and Pa O2 were also recorded. Nitroprusside produces arterial and venous dilatation which results in a decrease of afterload and preload. The mean dosage of S. N. was 18 mcg/kg/mn. Systemic vascular resistances decreased by 62 p. cent. Mean arterial pressure decreased by 53 p. cent; it reached 40 mm Hg. Fall in preload resulted in a decrease in pulmonary wedge pressure by 28 p. cent. This fall in preload produced a decrease in stroke index according to Frank-Starling's mechanisms. However tachycardia allowed a rise in cardiac index by 20 p. cent. Increase of pulmonary wedge pressure at 8-10 mm Hg by blood volume expansion maintains stroke index at control level. Under these conditions the elevation of cardiac index is due to tachycardia. Cardiac rhythm disorders (wandering pace-maker, nodal rhythm) are observed in 5 patients after having stopped nitroprusside.
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PMID:[Deep hypotension induced by sodium nitroprusside in neurosurgery. I.--Systemic hemodynamic effects (author's transl)]. 48 87

Forty dogs were studied during MAC-1 halothane anesthesia with a chronically implanted electromagnetic flow probe on the ascending aorta. Cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure and total peripheral resistance were determined in addition to Pao2, pH, Paco2 and base deficit. Acupuncture moxibustion with electrocautery at Jen Chung (Go-26) produced a significant (five per cent level) increase in the cardiac output, stroke volume, heart rate, mean arterial pressure and pulse pressure and a significant decrease in total peripheral resistance during a 120-minute period of observation in dogs under halothane anaesthesia. Acupuncture moxibustion at Go-26 following pretreatment with the narcotic antagonist naloxone (1 mg.kg-1) produced a significant increase in cardiac output, heart rate, mean arterial pressure. It is concluded that naloxone, which inhibits the analgesic effects of acupuncture, does not inhibit the symphathomimetic effect of acupuncture or moxibustion at Jen Chung (Go-26) in dogs under light MAC-1 halothane anaesthesia.
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PMID:Can naloxone inhibit the cardiovascular effect of acupuncture? 48 36

To determine the effects of a chronic pressure load on cardiac function and morphology, spontaneously hypertensive rats (SHR) and two normotensive strains of Wistar rats (WKY and NWR) were studied under ether anesthesia at 13, 25, 52, and 90 wk of age. Although resting cardiac index of the SHR was comparable to that of WKY and NWR at all ages, the peak cardiac output and peak stroke volume per gram of left ventricle determined during a rapid intravenous infusion of Tyrode solution was markedly reduced in the SHR only at 90 wk of age. Autonomic inhibition did not alter the peak stroke volume attained, but reduced peak cardiac output at all ages in each of the strains. Absolute left ventricular dimensions in the SHR increased out of proportion to body growth, consistent with concentric hypertrophy. As peak pumping ability markedly declined from 52 to 90 wk of age in the SHR, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged. At this time the right ventricle also hypertrophied. This disproportionate thickening of the walls of the left ventricle and the hypertrophy of the right ventricle were reflected in measurements of their fiber diameters. These alterations in ventricular architecture may contribute to the decrease in pumping ability observed in long-standing hypertension.
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PMID:Cardiac function and morphology with aging in the spontaneously hypertensive rat. 49 31

Previous clinical studies establishing the efficacy of midazolam maleate (RO 21-3981), a new water-soluble benzodiazepine for induction of anesthesia, have not critically evaluated the effects of this agent on the cardiovascular system. The present study compares the cardiovascular effects of midazolam maleate and diazepam in conscious dogs. Systemic arterial, pulmonary arterial and central venous pressures, cardiac output, LVmax dP/dt, heart rate and regional coronary blood flow were measured 3 min following intravenous administration of diazepam (0.5, 1.0, and 2.5 mg/kg) or midazolam maleate (0.25, 1.0, and 10.0 mg/kg). Midazolam maleate increased heart rate 10--20 per cent with all three doses and decreased mean arterial blood pressure approximately 10--20 per cent at 1.0 and 10 mg/kg. Cardiac output was increased 10--12 per cent with all three doses of midazolam maleate, and LVmax dP/dt was decreased 13--16 per cent at the two higher doses. Diazepam at all three doses did not alter heart rate or mean arterial blood pressure. Diazepam, 1.0 and 2.5 mg/kg, produced significant (17 per cent) decreases in LVmax dP/dt, and 2.5 mg/kg produced a significant (10 per cent) increase in cardiac output. Neither drug in any dosage altered regional coronary blood flow, systemic or coronary vascular resistance, stroke volume, or stroke work. Maximum alterations in cardiovascular variables occurred with doses of midazolam maleate that are 10--15 times the recommended clinical induction dosage. It is concluded that in concentrations necessary for induction of anesthesia midazolam maleate has minimal effects on cardiovascular function.
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PMID:Cardiovascular responses to diazepam and midazolam maleate in the dog. 49 58

The responses to hypocapnia and to hypercapnia of both the systemic and the coronary circulations have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia. In the absence of significant variations of myocardial contractility, the reduction of cardiac output, because of hypocapnia, was determined by the increase of systemic vascular resistance, while the increase of cardiac output because of hypercapnia was determined by an increase of heart rate without change of stroke volume. The alterations of coronary blood flow (reduction following hypocapnia, augmentation following hypercapnia) were considerably larger than the changes of cardiac output and of myocardial oxygen consumption. Such disparity between oxygen supply and demand, together with the effect of pH and PCO2 on the oxyhaemoglobin dissociation curve led to a marked reduction of coronary sinus PO2 in response to hypocapnia and a marked increase of coronary sinus PO2 in response to hypercapnia. The data suggests that PCO2 (or respiratory alterations of pH) may have a direct effect on the regulation of coronary blood flow. The low coronary sinus PO2 observed at hypocapnia may suggest the risk of myocardial ischaemia.
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PMID:Effect of CO2 on the systemic and coronary circulations and on coronary sinus blood gas tensions. 49 91

The experiments in this report were designed to evaluate the effect of superficial temporal-middle cerebral artery (STA-MCA) anastomosis on the course of middle cerebral artery (MCA) occlusion by emboli while avoiding a vessel clipping technique as well as the use of long-acting barbiturate anesthesia. Dogs were divided into 3 general groups: A) embolus placement 1 h following anastomosis; B) embolus placement 5 h prior to anastomosis; C) control group without anastomosis. Anastomosis prior to MCA occlusion has a favorable clinical effect and reduces the size of an infarction. Anastomosis 5 h after embolus placement is deleterious unless other therapeutic modalities can be shown to delay the course of infarction.
Stroke
PMID:Effect of STA-MCA anastomosis on the course of experimental acute MCA embolic occlusion. 50 74

This paper concerns the management of stroke coming on in the early postoperative period after successful carotid endarterectomy. Our experience in effectively reversing hemiplegia in three such consecutive patients forms the basis of this report. The value of instant reoperation is emphasized, and several factors that facilitate urgent reoperation have been identified. These include omission of preoperative angiography, immediate reexploration under local anesthesia, and rapid restoration of cerebral flow by insertion of a shunt. Our experience would indicate that reversal of neurological deficit in such patients can be accomplished if reoperation is carried out within one hour of onset of stroke. All three patients managed by these criteria recovered and were neurologically intact eight to twelve months later. These results are in contrast to the failure to reverse stroke noted by us and others when the above measures were not followed.
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PMID:Successful management of early stroke after carotid endarterectomy. 50 78

The efficacy of pentobarbital in the treatment of ischemic cerebral edema was evaluated in 160 gerbils. Animals underwent carotid ligation under ether or pentobarbital (50 mg/kg) anesthesia. The pentobarbital anesthetized group received an additional dose of 30 mg/kg 4 h after ligation. Animals were evaluated for neurologic deficit at 4 and 8 h post-ligation, then sacrificed. Water content of each hemisphere and swelling percentage were calculated from the wet and dry weights of the hemispheres. Swelling percentage in animals anesthetized with ether was 6.374 +/- 0.89 SE, whereas gerbils who underwent sham carotid ligation showed a negligible (0.491 +/- 0.15) swelling percentage (p less than 0.01). Pentobarbital animals had a swelling percentage of 3.359 +/- 0.68. This represents a significant edema reduction compared to ether-anesthetized animals (p less than 0.01). Neurologic deficit was decreased by 56.7% (17/60 vs 30/60) in pentobarbital animals compared with ether animals (p less than 0.025). Mortality at 8 hours was reduced by 75% (2/60 vs 8/60) in pentobarbital animals (p less than 0.05).
Stroke
PMID:Attenuation of ischemic brain edema by pentobarbital after carotid ligation in the gerbil. 52 3

The effects of induction of anaesthesia by ketamine 2 mg.kg-1 were studied in six patients with valvular heart disease before tracheal intubation and operation. Cardiac index was unaffected because a mean decrease in stroke index was compensated for a mean increase in heart rate. A significant increase was found in mean arterial pressure, pulmonary arterial mean pressure, pulmonary capillary wedge pressure and central venous pressure. Systemic vascular resistance increased, but not significantly, whereas pulmonary vascular resistance increased significantly by more than 150 per cent. Right ventricular minute work index increased in all patients, and the increase was as much as 400 per cent. Left ventricular minute work index increased in four of the six patients, but the magnitude of the increase was not so marked. It is therefore concluded that ketamine causes pronounced pulmonary vasoconstriction and an undesirable strain on the myocardium. Such effects could prove deleterious in patients with limited functional reserve of the right ventricle.
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PMID:The cardiovascular effects of ketamine used for induction of anaesthesia in patients with valvular heart disease. 52 69

The haemodynamic effects of the induction of anaesthesia with Althesin 0.1 ml.kg-1 were studied in eight patients with valvular heart disease before tracheal intubation and surgery. A 20 per cent reduction in stroke index was compensated for by an increase in heart rate of similar magnitude. Cardiac index, mean arterial, pulmonary arterial, central venous and pulmonary capillary wedge pressures and systemic vascular resistance were unaffected. Pulmonary vascular resistance declined by nearly 30 per cent. It is therefore conclude that Althesin causes only minimal cardiovascular depression in patients with valvular heart disease.
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PMID:Cardiovascular haemodynamics after induction of anaesthesia with althesin in patients with valvular heart disease. 52 70


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