Early Operation of Ruptured Cerebral Aneurysms: The Role of Norepinephrine in Subarachnoid Hemorrhage and in Experimental Vasospasm

Shigeno, Taku; Mori, Kazuko; Saito, Isamu; Sano, Keiji; Brock, M.

doi:10.1007/978-3-642-67943-8_29

Cited by 1 publication

(2 citation statements)

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“…12,25 EEG and SEP were totally suppressed when the cerebral perfusion pressure showed critical reduction below about 20 mm Hg. During the subsequent decline of ICP, however, the recovery of electrical activities was still incomplete.…”

Section: Subsequent Course Of Parameters After Sahmentioning

confidence: 95%

“…This may support the mechanical in- fluence on perivascular adrenergic innervation, which has been suspected as a cause of cerebral vasospasm. 12 ' " When rCBF was greatly reduced in the cerebral hemisphere including thalamus and basal ganglia, brain stem circulation was relatively well preserved. Since the increase of ICP, or, in other words, the decrease of perfusion pressure is estimated to be equal between the supratentorial and infratentorial structure, it can be said that the brain stem is resistant to ischemic insult for maintenance of vegetative function of the brain.…”

Section: Pc Sc Pw Sw Pc Sc Pw Swmentioning

confidence: 99%

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Cerebral edema following experimental subarachnoid hemorrhage.

Shigeno¹,

Fritschka²,

Brock³

et al. 1982

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The development of cerebral edema after experimental subarachnoid hemorrhage (SAH) was studied in cats by determining regional brain tissue water content with the microgravimetric technique as well as the drying-weighing method. SAH was induced by withdrawing needles previously pierced into one or both infraclinoid internal carotid arteries through a unilateral transorbital approach. Serial determinations of regional cerebral blood flow (rCBF) by labelled microspheres, and monitorings of vital signs such as intracranial pressure (ICP), blood pressure and EEG were carried out up to 24 h after SAH. Animals could be classified into three grades according to the severity of SAH. In grade I, the increase of ICP was transient and minor. In grade II, ICP increased up to 200 mm Hg with a marked reduction of rCBF below 20% of control in cerebral hemispheres. Following subsequent reduction of ICP, rCBF increased over control, indicating reactive hyperemia. Thereafter, a great reduction of rCBF was again observed. In grade III, rCBF was sustained at essentially zero flow with the presence of continuously increased ICP above 100 mm Hg. Cerebral edema was observed particularly in the parasagittal water-shed areas of all grade II animals. It is concluded that cerebral edema complicating SAH is caused by the combination of an initially induced global cerebral ischemia and the subsequent recovery of cerebral circulation. Post SAH hypertension is another factor to exacerbate the development of cerebral edema.

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Section: Subsequent Course Of Parameters After Sahmentioning

confidence: 95%

Section: Pc Sc Pw Sw Pc Sc Pw Swmentioning

confidence: 99%