Artikel
Comparison of early pathophysiology of subarachnoid hemorrhage with/without intraventricular hemorrhage and intracerebral hemorrhage in a porcine hemorrhage model
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Veröffentlicht: | 4. Juni 2012 |
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Gliederung
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Objective: Unexpected subarachnoid hemorrhage (SAH) with intraventricular extension (IVH) may result in attempts to create intracerebral hemorrhage (ICH) in swine. We investigated early pathophysiological changes in experimental SAH/IVH and ICH using multiparametric neuromonitoring.
Methods: 12 male swine (30–35 kg) were divided in two groups, a SAB/IVH group (gr1, n = 5) and an ICH group (gr 2, n = 7). All animals were sedated, mechanically ventilated and 4 right parietal cerebral monitoring probes were inserted (ICP; CBF; PbrO2; microdialysis) into the supposed perihemorrhagic zone (PHZ) of a planned subcortical ICH. A volume of 3 ml was applied. Online monitoring of all relevant physiological parameters was permanently obtained up to 12 hours post hemorrhage. The clot formation was confirmed post mortem as subarachnoid with/ without intraventricular haemorrhage or ICH alone.
Results: In 19% of ICH inductions solid clot formation could not be reached, but SAH/IVH was present. In the gr1 hematoma induction resulted in an immediate increase of ICP. The ICP progressively increased and peaked at 10.7 ± -4.4 mmHg mean ICP, but remained under pathologic values. CBF was subsequently increased from 36.9 ± -13.1 to 39.2 ± -7.4 ml / 100 mg/min attempting to compensate CPP related decrease of PbrO2 from 28 ± 6.9 mmHg to 14.7 ± 2.5 mmHg. LP-ratio non-significantly increased from 28.9 ± 4.6 to 35.2 ± 12.2. In ICH animals CBF decreases from 36.5 ± 12.7 to 27.9 ± 10.9 ml / 100 mg/ml resulted in mild significant LP-ratio increase from 26.7 ± 13.4 to 46.1 ± 18.1 arguing for an ischemic perihemorrhagic zone.
Conclusions: In porcine SAH/IVH ICP increase leads to significant PbrO2 decreases and compensatory relative CBF increase in the early phase after SAH. Neurometabolic effects in this acute phase could not be detected in SAH. However, in ICH rCBF was clearly reduced which may be explained by local for toxic effects of the solid clot in the early phase. This model can serve as a basis for further research in experimental SAH and neuromonitoring.