Acta neurochirurgica
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Acta neurochirurgica · Jan 1999
Assessment of critical closing pressure in the cerebral circulation as a measure of cerebrovascular tone.
Critical closing pressure (CCP) calculated from the blood flow velocity (FV) and arterial blood pressure (ABP) waveforms has been previously reported to be useful in the assessment of the dynamics of cerebral circulation. We investigated the relationship between CCP and intracranial pressure (ICP) and cerebrovascular tone in a model of intracranial hypertension in 22 anaesthetised New Zealand White rabbits during manipulations of arterial CO2, ABP and vasodilatation caused by hypoxia. Recordings were made of FV in the basilar artery, ABP and ICP during subarachnoid infusion of saline. ⋯ Generally, CCP decreased significantly (p<0.05) with hypercarbia, arterial hypotension and after and post-hypoxia and the difference: CCP-ICP decreased consistently after each vasodilatatory manoeuvre studied. Our data confirmed the linear relationship between CCP and ICP, and between the difference: CCP-ICP and cerebrovascular tone. However, because the magnitude of increase in ICP was not correlated to magnitude of change in CCP, CCP cannot be use for detection of increasing ICP quantitatively.
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This study tested the hypothesis that colloidal blood volume expansion could improve the cerebral circulation during high intracranial pressure. We studied cerebrovascular haemodynamic variables during high intracranial pressure with and without colloidal blood volume expansion in 12 pigs, whereas five pigs served as controls with intracranial pressure increase twice without colloidal blood volume expansion. Cerebral blood flow was measured with ultrasonic flowmetry on the internal carotid artery, and cerebral microcirculation with laser Doppler flowmetry. ⋯ Cerebral micro-circulation tended to increase, but this was not statistically significant (P = 0.07). Augmentation of the intravascular blood volume during high intracranial pressure increased the arterial inflow to the brain and possibly the cerebral microcirculation by increasing the cerebral perfusion pressure. Our results tend to support that the effect of colloidal blood volume expansion is beneficial for the cerebral circulation during high intracranial pressure.
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Acta neurochirurgica · Jan 1999
Brain death and organ donation in Germany: analysis of procurement in a neurosurgical unit and review of press reports.
A prospective study was undertaken to determine the number of potential organ donors in a neurosurgical intensive care unit and to record the actual number of organ donations. The reasons for refusal of organ donations were analysed with respect to the controversial public discussion of the brain death concept and the transplantation law in Germany. ⋯ In Germany, the relatives refusal rate in organ donation is continuously high, presumable due to a depressing 39% of press reports rejecting the brain death concept, and resulting in a very low number of organ donations. There is hope that the transplantation law which has finally passed German parliament in 1997, confirming the brain death concept as well as the legal principle of prior consent by the donor or consent by the relatives will eventually result in an increase of organ donation especially when supported by an educational campaign which is embodied in the transplantation law.
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Acta neurochirurgica · Jan 1999
Disturbance of cerebral blood flow autoregulation in hypertension is attributable to ischaemia following subarachnoid haemorrhage in rats: A PET study.
The effects of subarachnoid haemorrhage (SAH) on cerebral blood flow (CBF) autoregulation during induced hypertension were studied by positron emission tomography (PET) during chronic vasospasm in anaesthetized Sprague-Dawley rats. SAH was induced by intracisternal injection of autologous blood. In the control animals saline was injected instead. ⋯ AI (%/10-mmHg) was 13.5+/-2.4 in the control group (n=24). In the SAH group, AI decreased (p<0.05) to 4.5+/-2.5 in non-ischaemic areas (n=15), while in the ischaemic areas (n=5) AI increased (p<0.05) to 25.2+/-4.1. Since the spastic artery is intrinsically resistant to hypertension, the marked increase in CBF during hypertension can be attributable to ischaemia following SAH.