Search PubMed⌕ Search

Biomedical subjects

T Brinker

Publications and source records attributed to T Brinker.

42 records · Page 3Linked to original sources
PubMed1992

Cerebral blood flow and intracranial pressure during experimental subarachnoid haemorrhage.

The relationships of intracranial pressure (ICP), systemic blood pressure (SBP) and cerebral blood flow (CBF) during experimental subarachnoid haemorrhage were investigated in cats. Continuous monitoring of regional cerebral blood flow (rCBF) was done by a thermal diffusion method using a Peltier stack. During haemorrhage ICP rose within 5.4 +/- 0.97 minutes from 10.5 +/- 4.9 to 176.1 +/- 27.8 mmHg. This strong increase of ICP resulted in a temporary arrest of cerebral circulation. The Cushing response during the haemorrhage could not improve the cerebral circulation, but in contrast caused a further increase of ICP. After the haemorrhage the cerebral blood flow normalised within minutes. It is concluded, that the Cushing response during a subarachnoid haemorrhage should be regarded as a deleterious rather than a beneficial mechanism.

Animals↗
PubMed1992

Subacute hydrocephalus after experimental subarachnoid hemorrhage: its prevention by intrathecal fibrinolysis with recombinant tissue plasminogen activator.

It is investigated whether intrathecal fibrinolysis may prevent subacute hydrocephalus after subarachnoid hemorrhage (SAH). In 19 cats, SAH was induced by the intracisternal infusion of 1 ml/kg body weight of fresh autologous blood at a rate of 0.6 ml/min. Eleven of those animals were treated by intrathecal fibrinolysis performed 24 hours after experimental SAH by intracisternal infusion of 3 mg of recombinant tissue plasminogen activator. Included were eight animals suffering from experimental SAH and four healthy animals retained for control. A computed tomographic scan performed 24 hours after the SAH displayed an acute hydrocephalus from the experimental procedure. Cerebrospinal fluid outflow resistance was 71 +/- 5.0 mm Hg/ml/min in the healthy animals, 265 +/- 19.8 mm Hg/ml/min in the nontreated animals 7 days after SAH, and 151 +/- 6.4 mm Hg/ml/min in the recombinant tissue plasminogen activator-treated animals 7 days after SAH (mean +/- standard deviation; changes significant with P less than 0.01). Postmortem planimetry of both lateral ventricles gives a mean of 3.7 +/- 2.7 mm2 in the healthy animals, 11.1 +/- 3.9 mm2 in the nontreated group after SAH (P less than 0.01), and 3.5 +/- 1.1 mm2 in the animals treated with recombinant tissue plasminogen activator. Intracranial pressure monitoring demonstrated marked intracranial pressure waves only in the nontreated animals after SAH. It is concluded that intrathecal fibrinolysis may prevent subacute hydrocephalus after experimental SAH.

Animals↗
PubMed1991

Effect of intrathecal fibrinolysis on cerebrospinal fluid absorption after experimental subarachnoid hemorrhage.

The effect of intrathecal fibrinolysis on cerebrospinal fluid (CSF) absorption was investigated after experimental subarachnoid hemorrhage (SAH). In 11 cats, SAH was induced by intracisternal application of 1 to 4 ml of fresh autologous blood. Thirty minutes after the experimental SAH, the CSF outflow resistance was found to be elevated from a median of 77 mm Hg/ml/min (range 41.3 to 109 mm Hg/ml/min) to a median of 580 mm Hg/ml/min (range 104 to 7000 mm Hg/ml/min). A logarithmic relationship could be demonstrated between the volume of subarachnoid blood and the elevation of the CSF outflow resistance. The intrathecal application of 2 mg of recombinant tissue plasminogen activator (rt-PA), which is a fibrinolytic substance suitable for lysis of subarachnoid blood clots in man, resulted in an almost total restoration of CSF absorption after experimental SAH. The CSF outflow resistance after SAH was lowered by application of rt-PA from a median of 1028.05 mm Hg/ml/min (range 394 to 7000 mm Hg/ml/min) to 79 mm Hg/ml/min (range 56.7 to 223 mm Hg/ml/min). It is concluded that the impairment of CSF absorption after SAH may play an important role in the pathogenesis of post-hemorrhagic vasospasm.

Animals↗
PubMed1990

Acute changes in the dynamics of the cerebrospinal fluid system during experimental subarachnoid hemorrhage.

Early changes in intracranial pressure (ICP), ICP volume index, and resistance to absorption of cerebrospinal fluid induced by experimental subarachnoid hemorrhage were studied in cats. After SAH, the ICP was slightly elevated, and there was a decrease in the buffering capacity of the intracranial space and a sharp rise in outflow resistance. During infusion of blood into the cisterna magna with a constant infusion rate, an extensive increase in ICP could be demonstrated in contrast to the infusion of saline, which caused only slight elevation of ICP. Furthermore, during blood infusion, the ICP level did not reach a plateau phase of pressure, as was demonstrated during infusion of saline. It is suggested that the marked increase in ICP during blood infusion into the subarachnoid space is caused by intracranial volume loading and the simultaneous increase in cerebrospinal fluid outflow resistance. It is concluded that the reported relationship between increased cerebrospinal fluid outflow resistance and increased ICP supports the hypothesis of a strong increase in ICP during subarachnoid hemorrhage in human subjects.

Animals↗
PubMed1990

[Cerebrospinal fluid dynamics in experimental subarachnoid hemorrhage].

To investigate the acute effects on intracerebral pressure, intracranial reserve capacity and CSF absorption resistance, a subarachnoidal haemorrhage was induced experimentally in a cat by bolus injection or continuous infusion of autologous blood into the cisterna magna. Intracisternal bolus injection resulted in a brief steep increase in intracranial pressure. 30 or 60 minutes after the haemorrhage the median intracranial pressure is slightly increased, the reserve capacity markedly reduced and the CSF absorption resistance considerably enhanced. During intracisternal blood infusion there is a continuous intracerebral pressure rise that persists to the end of the infusion and decrease again within a short time. This intracranial pressure behaviour is due to the simultaneous reduction of intracranial reserve capacity and the increase in CSF absorption resistance during the blood infusion.

Animals↗