Cerebral blood flow and metabolism following subarachnoid haemorrhage: effect of subarachnoid blood

Jakobsen, Mogens; Skjødt, T; Enevoldsen, E.

doi:10.1111/j.1600-0404.1991.tb04687.x

Cited by 41 publications

(25 citation statements)

References 32 publications

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“…These findings indicated a primary reduction in CRMO2 with a secondary reduction in CBF due to the reduced metabolism. Similarly, Jakobsen et al [26,27], reported that aneurysmal bleeding is associated with a reduction in CMRQ from the early stage of SAH.…”

Section: Pathophysiological Mechanisms Of Sahinduced Hypometabolismmentioning

confidence: 93%

Brain energy metabolism in the acute stage of experimental subarachnoid haemorrhage: Local changes in cerebral glucose utilization

et al. 1996

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An experimental model was used to investigate acute alterations of cerebral metabolic activity in rats subjected to subarachnoid haemorrhage (SAH). Haemorrhages were produced in anaesthetized animals by injecting 0.3 ml of autologous, arterial nonheparinized blood into the cisterna magna. Control rats received subarachnoid injections of mock-cerebrospinal fluid to study the effect of sudden raised intracranial pressure, or underwent sham operation. Three hours after SAH rats were given an intravenous injection of [14C]-2-deoxyglucose. Experiments were terminated by decapitation, and the brains were removed and frozen. Regional brain metabolic activity was studied by quantitative autoradiography. In comparison with sham-operated controls, cerebral metabolic activity was diffusely decreased after SAH. Statistically significant decreases in metabolic rate were observed in 23 of 27 brain regions studied. Subarachnoid injections of mock-cerebrospinal fluid also produced depression of cerebral metabolic activity, but quantitatively these changes were not as pronounced and diffuse as in SAH rats. The present study shows that a widespread depression of brain metabolism occurs in the acute stage after experimental SAH and is probably secondary to the subarachnoid presence of blood itself and/or blood products.

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Section: Pathophysiological Mechanisms Of Sahinduced Hypometabolismmentioning

confidence: 93%

Brain energy metabolism in the acute stage of experimental subarachnoid haemorrhage: Local changes in cerebral glucose utilization

et al. 1996

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“…[7][8][9][10][42][43][44] Although this occurs even in patients in the best clinical condition, these reductions are greatest in patients with depressed levels of consciousness (Hunt-Hess grades III to V). [7][8][9][10][11][12][13][14][15] The primary cause of this phenomenon is thought to be a toxic effect of SAH on cerebral metabolism, 7,10,44 although hydrocephalus, cerebral edema, and increased intracranial pressure may also contribute.…”

Section: Lennihan Et Almentioning

confidence: 99%

Effect of Hypervolemic Therapy on Cerebral Blood Flow After Subarachnoid Hemorrhage

Lennihan

Mayer

Fink

et al. 2000

Stroke

394

220

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Background and Purpose-Cerebral blood flow (CBF) is reduced after subarachnoid hemorrhage (SAH), and symptomatic vasospasm is a major cause of morbidity and mortality. Volume expansion has been reported to increase CBF after SAH, but CBF values in hypervolemic (HV) and normovolemic (NV) subjects have never been directly compared. Methods-On the day after aneurysm clipping, we randomly assigned 82 patients to receive HV or NV fluid management until SAH day 14. In addition to 80 mL/h of isotonic crystalloid, 250 mL of 5% albumin solution was given every 2 hours to maintain normal (NV group, nϭ41) or elevated (HV group, nϭ41) cardiac filling pressures. CBF ( 133 xenon clearance) was measured before randomization and approximately every 3 days thereafter (mean, 4.5 studies per patient). Results-HV patients received significantly more fluid and had higher pulmonary artery diastolic and central venous pressures than NV patients, but there was no effect on net fluid balance or on blood volume measured on the third postoperative day. There was no difference in mean global CBF during the treatment period between HV and NV patients (Pϭ0.55, random-effects model). Symptomatic vasospasm occurred in 20% of patients in each group and was associated with reduced minimum regional CBF values (Pϭ0.04). However, there was also no difference in minimum regional CBF between the 2 treatment groups. Conclusions-HV therapy resulted in increased cardiac filling pressures and fluid intake but did not increase CBF or blood volume compared with NV therapy. Although careful fluid management to avoid hypovolemia may reduce the risk of delayed cerebral ischemia after SAH, prophylactic HV therapy is unlikely to confer an additional benefit. (Stroke. 2000;31:383-391.)

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“…Although the extent of this phenomenon positively correlated with the patients' clinical state and the amount of subarachnoid blood, it has been observed in patients of all clinical grades and with more or less subarachnoid blood (Jakobsen et al, 1991;Carpenter et al, 1991). Whether there is a relationship between cerebral vasospasm and the depression of oxygen metabolism is discussed with controversy.…”

Section: Introductionmentioning

confidence: 99%

Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

Westermaier

Jauss

Eriskat

et al. 2009

J Cereb Blood Flow Metab

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Present knowledge about hemodynamic and metabolic changes after subarachnoid hemorrhage (SAH) originates from neuromonitoring usually starting with aneurysm surgery and animal studies that have been focusing on the first 1 to 3 h after SAH. Most patients, however, are referred to treatment several hours after the insult. We examined the course of hemodynamic parameters, cerebral blood flow, and tissue oxygenation (ptiO 2 ) in the first 6 h after experimental SAH. Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (n = 8). Bilateral local cortical blood flow, intracranial pressure, cerebral perfusion pressure, and ptiO 2 were followed for 6 h after SAH. After induction of SAH, local cortical blood flow rapidly declined to 22% of baseline and returned to 80% after 6 h. The decline of local cortical blood flow markedly exceeded the decline of cerebral perfusion pressure. ptiO 2 declined to 57%, recovered after 2 h, and reached Z140% of baseline after 6 h. Acute vasoconstriction after SAH is indicated by the marked discrepancy of cerebral perfusion pressure and local cortical blood flow. The excess tissue oxygenation several hours after SAH suggests disturbed oxygen utilization and cerebral metabolic depression. Aside from the sudden increase of intracranial pressure at the time of hemorrhage and delayed cerebral vasospasm, the occurrence of acute vasoconstriction and disturbed oxygen utilization may be additional factors contributing to secondary brain damage after SAH.

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Cerebral blood flow and metabolism following subarachnoid haemorrhage: effect of subarachnoid blood

Cited by 41 publications

References 32 publications

Brain energy metabolism in the acute stage of experimental subarachnoid haemorrhage: Local changes in cerebral glucose utilization

Brain energy metabolism in the acute stage of experimental subarachnoid haemorrhage: Local changes in cerebral glucose utilization

Effect of Hypervolemic Therapy on Cerebral Blood Flow After Subarachnoid Hemorrhage

Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

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