[Discussion: The role of nursing in medical services - expectation of nursing services].
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Biomedical subjects
Publications and source records attributed to M Matsuda.
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The effect of topical and intravenous administration of phenoxybenzamine, an alpha adrenergic blocking agent, on experimental vasospasm was studied in cats. Topical application of phenoxybenzamine prevented the occurence of vasospasm without noticeable systemic alpha adrenergic blocking effect. Intravenous use, however, was ineffective in the dosage with which total systemic alpha adrenergic blockade was obtained. Effects of intravenous administration in much larger dosage seemed to be largely due to the non-specific action of phenoxybenzamine on vascular smooth muscle.
Effects of a new synthetic vasodilator, YC-93, a derivative of 1. 4-dihydropyridine, on experimental cerebral vasospasm, were studies in cats. A topical administration of YC-93 solution was found to rapidly reverse the spasm of the basilar artery induced with a subarachnoi application of fresh blood, serotonin or porstaglandin F2 alpha. Pretreatment of the basilar artery with YC-93 prevented the development of experimental vasospasm with all these agents.
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In 29 consecutive patients, the epidural intracranial pressure (EDP) was continuously measured with a semiconductor strain film transducer, and with a telemetric monitoring system in two patients. Factors affecting the EDP during pre-, intra- and postoperative periods were analyzed and their significance in clinical practice stressed.
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Effects of topical and intravenous administration of phenoxybenzamine (PBZ) on the experimental vasospasm were studied in cats. Cerebral vasospasm was produced by a topical application of blood, prostaglandin (PG) E2 or PGF2alpha to be exposed basilar artery. Topical PBZ caused a significant dilatation of the basilar artery and the occurrence of vasospasm was completely prevented either with blood, PGE2 or PGF2alpha. Intravenous administration of PBZ in the dosage with which the pressor response to phenylephrine was completely blocked, or three times that dosage, failed to show any preventive effect on the vasospasm. From these experimental results, it seems that the antispasmogenic action of topically applied PBZ is due largely to the non-spacific vasodilator action of PBZ and not to its alpha adrenergic blocking action. It is also suggested that the role of alpha adrenergic mechanism in the genesis of vasospasm in this experimental design is not significant.
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A subdural abscess which is cinfined to the interhemispheric space alone, which does not extend over the convexity is rare. This is a specific form and is a complication of a common intracranial subdural abscess. It is of great practical importance to determins this uncommon location, and cerebral angiography is most useful. Multiple trephinations or craniotomy for exploration and evacuation must be performed near the midline. A 20 year old female was in a comatose state on admission. There was a flaccid paralysis of the right lower extremity and a dilated left pupil. Examination of the eyegrounds showed bilateral choked discs. Left cerebral angiography revealed the proximal pericallosal artery to be shifted to the right side and the callosomarginae artery was displaced from the midline parallel to the distal pericallosal artery. Although 20 ml of pus was evacuated through the parietal burr hole, which was located a bout 2.5 cm from the midline, she died. At autopsy, a subsural abscess was found in the interhemispheric space. It extended from the frontal pole to the occipital and had a thick membrane which adhered firmly to the falx medially. We could find no other subdural nor intracerebral pus collections. The left cerebral hemisphere was edematous. The superior sagittal sinus had a thick wall and was almost occluded. This dural sinus thrombophlebitis may have developed into the interhemispheric subdural abscess. It is emphasized that this uncommon location for subdural abscess poses a specific problem in clinical practice.
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