Cerebral blood flow and cerebral metabolism in acute increase of intracranial pressure

Hamer, J.; Hoyer, Siegfried; Stoeckel, H.; Alberti, E.; Weinhardt, F.

doi:10.1007/bf01405406

Cited by 27 publications

(6 citation statements)

References 43 publications

(20 reference statements)

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“…In the presence of either haematoma or ventricular bleeding the intra cranial pressure may rise, reducing the CBF to below metabolic demand. The high ICP, with decrease in CBF, is compensated by an increase in AVDO, (31), as we have observed in 8 of 48 patients. The CBF level will be influenced by these two antagonistic effects, and this could explain the wide distribution of CBF values.…”

Section: Discussionsupporting

confidence: 77%

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

Jakobsen

Skjødt

Enevoldsen

1991

Acta Neurologica Scandinavica

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The amount of effused blood following a subarachnoid haemorrhage (SAH) was estimated in 48 patients by cerebral computerized tomographic scanning. The cerebral oxygen consumption (CMRO2) was calculated as arteriovenous difference for oxygen multiplied by mean cerebral blood flow measured by the 133-Xe inhalation technique. A significant negative correlation was observed between CMRO2 and amount of subarachnoid blood, with additional reduction in CMRO2 in case of ventricular bleeding. Cerebral blood flow on admission, opposed to CMRO2, showed no correlation to amount of blood on CT scan. A correlation was observed for blood flow measured at day 5 and further on, indicating a restored coupling between flow and metabolism. The clinical (Hunt) grade on admission and the outcome correlated to the amount of blood. These observations suggest that the acute reduction in CMRO2 following a SAH is mainly determined by the amount of blood escaping during the aneurysm rupture, and that the cerebral blood flow level a few days after SAH mainly is determined by the initial reduction in oxygen uptake.

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Section: Discussionsupporting

confidence: 77%

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

Jakobsen

Skjødt

Enevoldsen

1991

Acta Neurologica Scandinavica

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“…An increase of lactate in brain parenchyma has been observed experimentally as a result of hypotension, ischaemia or hypoxia [11,14,41]. As known from animal studies, severe head injury frequently results in shortlasting apnea immediately after trauma.…”

Section: Discussionmentioning

confidence: 98%

Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury

Murr

Stummer²,

Schürer

et al. 1996

Acta neurochir

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Severe head injury is frequently associated with focal or global disturbances of cerebral blood flow and metabolism. Routine monitoring of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in these patients does not provide information about critically reduced local or global cerebral blood flow. Measurements of cerebral lactate difference, Lactate-Oxygen-Index (LOI) and cerebral oxygen extraction were evaluated for advanced monitoring by comparing these parameters with ICP, cranial computed tomography (CCT) findings, and outcome in a group of severely head-injured patients. In 21 patients with severe brain trauma (GCS < or = 8), arterial as well as jugular venous lactate levels and oxygen saturation were measured in vitro every 6 h after admission of patients to the intensive care unit (ICU) throughout the acute course of treatment. Arterial blood pressure, blood gases, and ICP were assessed by standard monitoring measurements. CCT was performed initially after admission of the patients to the hospital, during the acute period in the ICU, if indicated, and 10 to 14 days after trauma. Outcome was classified according to the Glasgow outcome scale (GOS) at six months after injury. Data were averaged in each patient for every day after trauma and over the entire monitoring period. Resulting values were tested for correlation by regression analysis. Additionally, the data of the group of patients with normal to minimally elevated mean ICP (ICP < 20 mmHg, n = 12) were compared to those of the patients with increased mean ICP (ICP > 20 mmHg, n = 9). The cerebral lactate difference in all patients on the day of trauma was significantly increased as compared to the later period (0.20 vs. 0.11-0.07 mmol/l, p < 0.05), but was not different with high or normal to minimally elevated ICP. In patients with intracranial hypertension, the cerebral lactate difference remained significantly increased from the first to the fifth day after injury, whereas it normalized in this period in the group with normal to minimally elevated ICP. Averaged over the acute course, patients with increased ICP had significantly higher mean lactate differences (0.18 +/- 0.16 vs. 0.067 +/- 0.025 mmol/l, p = 0.001) and higher mean LOIs (0.072 +/- 0.071 vs. 0.028 +/- 0.013, p = 0.011). There was a significant correlation of increased mean cerebral lactate difference to poor outcome (r = 0.46, p = 0.035). Cerebral oxygen extraction in all patients tended to increase on the day of trauma (36.7% vs. 29.2% to 31.5% during the subsequent course), but this difference was not significant. The initial degree of brain swelling, classified by CCT according to Marshall et al. (1991), showed no correlation with cerebral lactate differences, ICP, O2-extraction, or outcome. Neither was there a correlation of cerebral oxygen extraction to ICP nor to outcome. In conclusion, the severity of brain trauma and outcome of patients was reflected by increased cerebral lactate production. Unchanged values of global cerebral oxygen extraction suggest that the re...

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“…Acute survival, mean arterial blood pressure (MAP), blood gas levels, blood pH, body temperature, and changes in cortical blood flow (CBF) were assessed in weight-matched adult male and female rats following closed head injury. CBF was examined because subnormal CBF (hypoperfusion) is an exacerbating factor in the secondary injury cascade that follows brain injury and a significant decrease in CBF can cause substantial ischémie injury or even death (Golding et al, 1999;Hamer et al, 1973;Kelly et al, 1997;Mendelow and Teasdale, 1983;Robertson et al, 1992). CBF may be reduced after brain trauma as a response to lowered blood pressure, increased intracranial pressure, or loss of microvascular autoregulation (Golding et al, 1999;Mendelow and Teasdale, 1983).…”

Section: Introductionmentioning

confidence: 99%

Estrogen-Related Gender Difference in Survival Rate and Cortical Blood Flow After Impact-Acceleration Head Injury in Rats

Roof

Hall²

2000

Journal of Neurotrauma

214

122

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While a number of laboratories have begun to examine gender differences in outcome following experimental stroke, little is known about the relative response of male and female brains to traumatic injury. In the following series of experiments, we used the Marmarou impact-acceleration head injury model (with a 500-g, 1.5-m weight drop) to compare the pathophysiological responses of male and female rats to closed-head injury. Cortical blood flow (CBF; laser-doppler flowmetry), mean arterial blood pressure (MAP), blood gas levels, blood pH, and body temperature were measured preinjury and at regular intervals postinjury. Acute survival was assessed 1 h after injury. The role of estrogen in the observed gender differences was assessed by examining these physiological measures after injury in ovariectomized females, with or without 17beta-estradiol replacement, and in intact males, with or without exogenous 17beta-estradiol administration. In the first experiment, significantly more females (100%) survived the acute injury period (60 min) after injury than did males (72%). Survival appeared related to the magnitude and persistence of the posttraumatic drop in MAP. In a second experiment, females showed a less dramatic reduction in and better recovery of CBF than males. The gender difference in CBF was paralleled to some degree by differences in the pattern of MAP changes after injury. Differences in body weight, blood gas levels, or blood pH did not account for the gender difference in CBF. Postinjury CBF was higher in female and male rats given 2 weeks of daily 17beta-estradiol injections prior to injury compared to those given the vehicle only. However, 17beta-estradiol administration did not alter MAP, suggesting that the gender difference in CBF was not strictly due to MAP changes. Our findings suggest that estrogen plays a role in maintaining adequate cerebral perfusion in the acute period following closed-head injury. This protective mechanism may underlie the gender difference in acute survival observed in this study, and may help explain observations of better outcome in females than in males after brain injury. We conclude that CBF preservation is one mechanism by which estrogen is neuroprotective following traumatic brain injury. We hypothesize, based upon known effects of estrogen, that the beneficial microvascular effects of estrogen most likely involve a combination of endothelial nitric oxide synthase induction and an antioxidant effect.

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Cerebral blood flow and cerebral metabolism in acute increase of intracranial pressure

Cited by 27 publications

References 43 publications

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

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

Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury

Estrogen-Related Gender Difference in Survival Rate and Cortical Blood Flow After Impact-Acceleration Head Injury in Rats

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