Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental regional cerebral ischemia was produced in the middle cerebral artery (MCA) territory in primates (M. mulatta) by macrosphere embolization. Determinations of percentage tissue dry weight and tissue sodium and potassium concentrations were obtained in samples from the ischemic and non-ischemic hemispheres at various time from 12 to 48 hours after the onset of cerebral ischemia. Samples from the cortex normally supplied by the occluded MCA showed maximal accumulation of edema fluid with fluxes in sodium and potassium in reciprocal directions at 12 hours and similar edematous changes in putamen at 24 hours after embolization By 48 hours after MCA occlusion and despite the presence of infarction, partial reversal was observed in the redistribution of water and electrolytes in these gray matter structures. In contrast to cerebral cortex and putamen, the adjacent subcortical white matter showed progressive increases in water content from 12 to 48 hours and definite increases in tissue sodium with decreases in potassium were not observed until 48 hours after MCA occlusion. This late severe white matter edema associated with cerebral infarction appears to be a major factor responsible for the hemispheric swelling observed at this state.
 ...
PMID:Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 3: effects on brain water and electrolytes in the late phase of acute MCA stroke. 9 10

With a closed head primate stroke model, acute cerebral ischemia limited to the middle cerebral artery (MCA) territory was produced by macrosphere embolization of the internal carotid artery bifurcation. Measurements of the oxygen tension (PO2) at the cerebral cortical surface were obtained by continuous on-line mass spectrometry. Percentage of dry weight and tissue sodium, potassium, and chloride concentrations from ischemic and nonischemic hemispheres were determined at various times. With this preparation, we registered the precise onset of cortical surface PO2 depletion, which showed an exponential downward trend (fast component from 0 to 5 minutes, t 1/2 = 0.8 minute, rate of change = 89% per minute; slow component from 5 to 240 minutes, t 1/2 = 285 minutes, rate of change = 0.3% per minute). After the onset of cerebral ischemia, there was an immediate fall of the cortical surface PO2 with reductions of more than 45% at 5 minutes before definite hemiparesis and electroencephalographic abnormalities were recognized. During the secondary phase from 5 to 240 minutes the cortical surface PO2 fell by only an additional 23% of the steady state. Even so, when cortical surface PO2 was maintained at this critically low level, the earliest cerebral cortical edema was evident 180 minutes after MCA occlusion. Thereafter, progressive accumulation of edema fluid in the cortex (90 to 170.8 microliters per g of tissue) and in the white matter (19 to 46.2 microliter per g of tissue) was detected by the end of 240 minutes of cerebral ischemia.
 ...
PMID:Alterations in cortical oxygen tension during the development of ischemic cerebral edema in primates (Macaca mulatta). 11 Nov 52

Adult normothermic rhesus monkeys were submitted to one hour's complete cerebral ischemia, followed by periods of blood recirculation varying from 45 min to 24 h. The functional impact of ischemia and the subsequent recovery was monitored by electrophysiological recording and a distinction was made between animals with signs of functional recovery and animals without recovery. Prior to ischemia the water content of the gray matter was 81.1 plus or minus 0.3% (mean plus or minus S.D.) and of the white matter 68.9 plus or minus 0.8%. The sodium-potassium ratio in the gray matter was 0.43 plus or minus 0.02 and in the white matter 0.62 plus or minus 0.06. During one hour's ischemia brain water did not change significantly, but the differences in the sodium-potassium ratio in white and gray matter were reduced. Blood recirculation of the brain after ischemia caused a considerable increase in brain water content and a shift in the sodium-potassium ratio up to 1.0. Calculated brain swelling was maximal after 45 min when it reached 11.1% of the total brain volume in an animal with recovery and 12.2% in another one without recovery. In animals with signs of functional recovery brain swelling rapidly diminished, followed by a more gradual normalization of brain electrolytes within 24 h. In animals without functional recovery electrolyte shifts were irreversible or even progressed further. It is concluded that brain swelling and electrolyte derangements following one hour's cerebral ischemia are fully reversible when signs of functional recovery appear and brain metabolism returns.
 ...
PMID:Resuscitation of the monkey brain after one hour's complete ischemia. II. Brain water and electrolytes. 16 36

Acute regional cerebral ischemia was produced in the middle cerebral artery (MCA) territory in monkeys (Macaca mulatta) by selective embolization of the internal carotid (ICA) bifurcation with minimum surgical intervention in the neck under sedated conditions. Two of five hours after embolization, brain water (measurement of dry weight) and tissue concentration of sodium and potassium were determined in the tissues of the sylvian cortex, putamen and subcortical white matter in the affected MCA territory. As early as three hours, initial increase in brain water was detected in the samples of the putament without noticeable change in tissue electrolytes in two of three animals. Gross ischemic swelling of the gray matter, in both the sylvian cortex and putamen, became obvious in six of eight animals after four to five hours. This swollen gray matter showed marked increase in brain water (up to 36% swelling), increase in tissue sodium (up to 100% of the control value), and decrease in tissue potassium (down to 55%). On the other hand, edema in the white matter, if present at all, was minimal without detectable change in tissue electrolytes and was always accompanied by much greater ( greater than two to seven times) edema in the gray matter. Thus, the gray matter edema, in both the deep subcortical structures and the cortex, appeared to play the major role in the development of hemispheric swelling of the brain which may begin within hours of the onset of the MCA stroke in monkeys. Microscopically, the swollen gray matter which showed more than 10% swelling with a definite shift of tissue sodium and potassium content appeared to be dead tissue. However, early edema in the gray matter which showed less than 10% swelling without detectable change in electrolytes might be caused by simple diffusion of water through the dysfunctional capillary wall or cell membrane with or without a permeability gradient between the intravascular cerebrospinal fluid and cerebral tissue compartment and might possibly be reversible.
 ...
PMID:Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 2: Effects on brain water and electrolytes in the early phase of MCA stroke. 40 42

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
 ...
PMID:Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability. 50 96

Total cerebral ischaemia in rats caused a marked increase in the cisternal CSF potassium concentration but little change in CSF sodium or chloride concentration. The anaesthetic techniques studied (pentobarbitone, halothane/oxygen and nitrous oxide/oxygen/relaxant) did not effect the potassium increase following cerebral ischaemia. We conclude that the mechanism of barbiturate protection following cerebral ischaemia is different from that of hypothermia.
 ...
PMID:Effect of anaesthetic agents on the ionic composition of cerebrospinal fluid following total cerebral ischaemia. 62 2

In the course of our studies on cerebral blood flow in newborn infants, we have observed a striking depressing effect of sodium bicarbonate infusion on cerebral blood flow which in some cases may severely aggravate cerebral ischemia. We measured cerebral blood flow before and after the treatment with 1 to 8 meqs of sodium bicarbonate in seven distressed newborn infants. The 133 Xe clearance technique was used. The results showed in six of the seven cases a decrease in cerebral blood flow, which in most cases was reduced to 14 to 22 ml/100 g/min, which is about half the value prior to the bicarbonate infusion. In one case an extreme reduction occurred: cerebral blood flow was reduced to 3 ml/100 g/min, well below the level compatible with tissue survival. The results are discussed with regard to the optimal treatment of the acidotic newborn.
 ...
PMID:Decreased cerebral blood flow after administration of sodium bicarbonate in the distressed newborn infant. 66 45

Regional cerebral ischemia was produced in 18 Java monkeys by permanent middle cerebral artery (MCA) occlusion. All monkeys were thereafter paralyzed (pancuronium bromide, 0.05 mg/kg/hr) and sedated (diazepam, 0.1 mg/kg/hr) for a 48-hour period. Thirty minutes after MCA occlusion, pentobarbital sodium anesthesia was induced in nine of the monkeys (14 mg/kg) and maintained for 48 hours (7 mg/kg every two hours), with continuous supportive care. After 48 hours, all drugs were discontinued; the monkeys were observed for five days, and then killed. Seven of the control monkeys developed a cerebral infarction, three did not survive past the 48 hours of intensive care, and the other four had a notable neurologic deficit. All pentobarbital monkeys survived the seven days, but four had a cerebral infarction and two of these had a notable neurologic deficit. These differences were statistically significant.
 ...
PMID:Cerebral protection by barbiturate anesthesia. Use after middle cerebral artery occlusion in Java monkeys. 81 99

The authors have assessed the effects of subacute traumatic brain edema (BE) on cerebral circulation and metabolism, and on clinical outcome. Fifty-five severely injured, comatose, young patients who survived for more than 24 hours were studied on 78 occasions within 30 days of injury. After hematomas had been surgically evacuated, BE was diagnosed by radiological evidence of brain swelling, demonstrated by cerebral angiograms and ventriculograms. At identical levels of carbon dioxide pressure, intracranial pressure was significantly elevated in the Edema Group to twice the value in the No Edema Group (27.1 vs 14.1 torr). There were, however, no significant differences in cerebral perfusion pressure cerebral blood flow, resistance to blood flow, cerebral metabolic oxygen rate, ventricular cerebrospinal fluid acid-base, lactate, K+ or Na+ concentrations, or in clinical outcome. It is concluded that this type of subacute traumatic BE, which is significantly associated with surgical lesions, is not of major hemodynamic or clinical significance in intensively treated patients, and does not cause cerebral ischemia. Patient outcome is determined more by the severity of the initial diffuse cortical and subcortical injury than by the presence or absence of subacute BE.
 ...
PMID:Cerebral circulation after head injury. Part 2: The effects of traumatic brain edema. 94 15

Deliberate hypotension can reduce major blood loss and indelicate operations can produce a drier field increasing the ease of surgery and the likelihood of a good result. The techniques used to induce hypotension can also be used to avoid dangerous hypertension during and after surgery. These benefits must be weighed against the risks of inadequate perfusion: especially cerebral, myocardial, or renal. In previously normotensive patients these risks are minimal when the arterial pressure is held above 80 torr systolic, and may be acceptably small even at mean pressure of 50 to 60 torr. Previously hypertensive patients show signs of cerebral ischemia at higher pressures; they should probably not be subjected to deliberate hypotension, but they also can be harmed by severe hypertension which can be avioded by the proper use of hypotensive agents. For most situations a balanced technique is suitable: after a stable anesthetic level has been achieved using halothane or enflurane, hypotension can be induced with sodium nitroprusside or trimethaphan camsylate. Longer-acting agents such as pentolinium are sometimes desirable, but the shorter-acting agents are easier to control. Careful monitoring with observation of intra-arterial pressure, electroencephalogram, electrocardiogram, and determination arterial blood gas tensions is likely to make for safer conduct. Close postoperative observation is essential. With careful preparation and monitoring deliberate hypotension can be a safe technique for reducing blood loss or facilitating delicate procedures.
 ...
PMID:Deliberate hypotension. 110 15


1 2 3 4 5 6 7 8 9 10 Next >>