ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Many investigators have analyzed the effectiveness of the cardiac care unit (as a model of a disability oriented, specially staffed, geographically isolated unit) in altering outcome following acute myocardial infarction. Little data are available, however, on the efficacy of caring for patients with stroke on specially staffed disability oriented units. Of 667 patients with stroke recently discharged from the Burke Rehabilitation Center, 589 were admitted to the stroke unit (SU group) and 78 were admitted to other units (NSU group). Statistical analysis showed that the SU patients were significantly weaker, had longer onset-admission intervals, and exhibited more concurrent medical problems and neurologic deficits. There were no statistically significant intergroup differences in age, sex, and distribution of weakness. Both groups had similar treatment programs provided by staff who had rotated through the stroke unit. Ability to perform activities of daily living (dressing, feeding, hygiene, bowel and bladder routines) and length of hospitalization were similar for both groups. SU patients walked better and went home more frequently than NSU patients. These data indicate that even in a rehabilitation center specializing in treating functional disabilities, patients with stroke are more likely to improve if placed on a disability oriented unit than if they are admitted to mixed disability units which are scattered throughout the hospital.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The effect of pentobarbital and hypothermia on the development of ischemic brain edema was studied in 23 rhesus monkeys undergoing transorbital middle cerebral artery occlusion. Fifteen additional animals served as undipped controls. Regional cortical cerebral blood flow (rCBF), arteriovenous oxygen content difference (AVDOa), and regional cortical metabolic rate of O2 (rCMROa) were measured hourly until sacrifice 11 hours postocclusion, at which time ischemic cerebral edema was measured. In 8 animals no treatment followed the occlusion, and these developed significant edema. In 7 animals pentobarbital 14 mg/kg was administered intravenously 30 min after occlusion and 7 mg/kg every 2 hours thereafter. In this group ischemic brain edema was negligible. In 8 animals, hypothermia to 25.9 ± 0.5°C was started 30 min after occlusion and maintained until sacrifice; ischemic brain edema was not significantly altered from untreated-clipped animals. On the basis that both pentobarbital and hypothermia produced similar changes in rCBF, AVDOj, and rCMRO2, but only pentobarbital prevented edema, it is postulated that the mode of action of barbiturates in preventing ischemic brain edema is not entirely related to their known effect on blood flow and metabolism.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

EEG activity and regional cerebral blood flow were monitored during S hour survival following cardiac arrest in 32 pentobarbital anesthetized mongrel dogs. The animals were mechanically ventilated and blood gases were maintained at physiologic levels. Regional cerebral blood flow and cardiac output were measured using 15 n microspheres. EEG was recorded from 6 epidural electrodes using bipolar techniques. The animals were divided into 3 groups. The animals in Group I had an arrest of 8-11 minutes and those in Group II and III had an arrest of 12-16 minutes. Group II animals received no treatment. Group III animals were given 1 g/kg of dextran 40 at a concentration of 10% in normal saline following the arrest and maintained with 10 mg/kg/min during the 5 hours of recovery. In Groups I and III there was shorter duration of a flat EEG and 5 hours after the arrest the EEG activity was closer to normal than in Group II. After 5 hours the EEG scores of Group III were significantly greater than Group II (p < 0.03). The cortical grey matter and hippocampus had the greatest reduction of blood flow following cardiac arrest. The mean cortical grey matter blood flow in Group II was less than in Groups I and III at 3 hours. After 5 hours the grey matter blood flow was greater in Group III than in Group II (p < 0.09). The findings of this study are consistent with the hypothesis that after cardiac arrest perfusion abnormalities persist or develop after return of blood pressure and that these can be corrected or prevented with improved functional survival by treatment with dextran 40 after the arrest.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The effect of hypoxia (reduction of arterial Po2 to 26-28 mm Hg) on cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) was studied in paralyzed and artificially ventilated rats, using a CBF technique of improved accuracy at high flow rates. Results obtained on animals maintained on 70% N2O unexpectedly showed that hypoxia of this severity is accompanied by an increase in CMRO2, and they indicated that 2 different mechanisms are involved, both related to catecholamine metabolism. In one breed of Wistar rats studied, hypoxia was accompanied by a 6-fold increase in CBF and by an increase in CMRO2 to 180% of control. Prior removal of the adrenal glands curtailed the increase in CBF (400% of control) and CMRO2 (125% of control). The excessive increase in CMRO2 (to 180% of control) did not occur in another breed of Wistar rats. However, since infusion of adrenaline in normoxic animals gave rise to a doubling of CMRO2 it is concluded that, at least under some circumstances, circulating catecholamines can increase oxygen consumption in the hypoxic brain. In the second breed of rats studied, hypoxia was consistently accompanied by a 20-30% increase in CMRO2 which was unaffected by prior adrenalectomy. Since the increase was prevented by sedative and anesthetic doses of diazepam, it is tentatively concluded that the increase was elicited by increased activity in cerebral catecholaminergic pathways. The conclusion is supported by parallel studies showing that a similar increase in CMR02 occurs in hypercapnia, which is blocked both by diazepam and propranolol.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Cerebral arteriospasm is a common complication of subarachnoid hemorrhage and is responsible for much of the brain damage which accompanies it. No pharmacologic agent has been found which regularly alleviates arteriospasm. We have evaluated the effect of continuous intravenous nitroglycerin infusion on the diameter of the basilar artery in dogs with cerebral vasospasm experimentally induced by subarachnoid blood injection. In 6 consecutive dogs, 10 minutes after beginning intravenous nitroglycerin at 100 ^ig/min and at other times during 120 minutes of infusion, the diameter of the basilar artery had increased from 75 ± 2% of control value to 114 ± 2% of control value (p < 0.001). In all 6 dogs, the basilar artery diameter during infusion was greater than the control value prior to creating subarachnoid hemorrhage. Intravenous nitroglycerin caused only a moderate (8%) decrease in blood pressure. Further investigation of the effects of nitroglycerin on cerebral vasospasm is warranted.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Described is a modified method of measuring organ blood flow which combines the serial injection of a standard dose of microspheres and the external counting of their gamma activity when they are distributed to the tissues. The method produces similar results to measurements of grey matter blood flow by the clearance of "'xenon.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Cerebral microemboli were formed in rats by injecting 4,000 carbonized microspheres, 50 ± 10 ix in diameter, labelled with 85Sr, into the internal carotid artery. The use of radioactive microspheres as embolic agents enabled the number of microspheres to be determined in each cerebral hemisphere. The microspheres were mainly distributed in the cerebral hemisphere on the side of the injection. In 61 rats this hemisphere contained 582 ± 20 microspheres against 99 ± 9 in the contralateral hemisphere. Brain edema was assessed by measuring brain content of water, sodium and potassium. Blood-brain barrier (BBB) permeability was determined by brain accumulation of 125I-albumin. In the ipsilateral hemisphere brain edema and an increase in BBB permeability appeared 6 hours after embolization and progressed up to 48 hours. Twenty-four hours after embolization, significant correlations were observed between the microsphere content of the cerebral hemispheres and 1) the increases in water and sodium levels, 2) the decrease in potassium level, 3) the increase in BBB permeability. The study of these correlations should make it possible to ignore the poor reproducibility of embolizations and to analyze with'increased accuracy the results of various experiments.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

The pathophysiology of post-cardiac arrest brain damage is not well understood. Many of the model systems presently used to study global ischemia have serious limitations. A new model system for total cerebral ischemia (TCI), using aortic and inferior vena caval occlusion balloons, is described. This model system produces verifiable TCI and avoids surgical invasion of the thorax or the use of vasoactive drugs. It does not impede cerebral venous return and protects the cardiopulmonary system from damage. This model system can be used to study the efficacy of various therapeutic interventions following a standardized CNS global ischemic insult.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

We measured brain tissue Po2 in the frontal and occipital cortices, mid-brain and basal ganglia in monkeys for up to 5 hours after 16 min global brain ischemia to gain some insight into those factors responsible for the selective vulnerability of the brain to ischemic anoxia. Brain tissue Po2 measurements were made with gold microelectrodes with tip diameters of 5 to 10 nm. Reoxygenation of the different brain regions occurred at different "apparent" cerebral perfusion pressures and times postischemia. Areas of low susceptibility to ischemic brain damage, such as the frontal cortex, were not consistently reoxygenated at lower perfusion pressures or earlier postischemia than were areas of high susceptibility such as the occipital cortex, basal ganglia and midbrain. These findings support earlier observations that perfusion defects and brain histologic changes are multifocal in nature after global brain ischemia. We suggest that the selective vulnerability of the brain to ischemia is attributable to the development of regional edema and a local increase in tissue pressure during ischemia thereby decreasing cerebral perfusion pressure and leading to local perfusion defects after restoration of circulation. Also, that the selective vulnerability of the brain is attributable to variable degrees of neuronal-glial edema and regional shifts in brain water during ischemia leading to the development of local perfusion defects and the expansion of lesions from areas of high to low vulnerability.

ISSN:0039-2499    

出版商:OVID    

年代:1979

数据来源: OVID