Isamu Saito

The role of endothelin in the pathogenesis of vasospasm following subarachnoid haemorrhage

The purpose of the present study was to evaluate the vasocontractile activity of endothelin, a newly isolated endothelium-derived constrictor peptide, in canine basilar arteries in vitro and in vivo. Endothelin at concentrations of 10(-12) M approximately 3 X 10(-8) M elicited dose-dependent contractions of canine basilar arteries in vitro. The maximum tension was larger than that induced by 40 mM KCl. The EC50 value was 1.9 +/- 0.6 X 10(-9) M (mean +/- SEM). The endothelin-induced contraction was reversed by 10(-8) M nicardipine or 10(-5) M approximately 10(-4) M papaverine. An intracisternal injection of 0.6 approximately 1.2 X 10(-12) mol/kg of endothelin caused biphasic contraction of the basilar artery lasting for more than 24 h. The initial phase of the contraction accompanied remarkable changes in vital signs such as an acute rise of blood pressure, bradycardia and respiratory arrest. An intracisternal injection of 2.0 X 10(-12) mol/kg of endothelin also induced acute contraction of the basilar artery. However, all of the dogs which received an intracisternal injection of 2.0 X 10(-12) mol/kg of endothelin died from sustained respiratory insufficiency. The present results demonstrate that endothelin induces strong and long-lasting contractions of cerebral arteries. Therefore, endothelin may play an important role in the pathogenesis of vasospasm.

Indomethacin ameliorates ischemic neuronal damage in the gerbil hippocampal CA1 sector.

The purpose of our experiment was to examine whether the cyclooxygenase inhibitor indomethacin ameliorates neuronal injury in the gerbil hippocampal CA1 sector following 5 minutes of forebrain ischemia. Thirty minutes before bilateral carotid artery occlusion, Mongolian gerbils were injected intraperitoneally with 1 (n = 10), 2 (n = 10), 5 (n = 12), or 10 (n = 7) mg/kg of indomethacin. Seven days after occlusion, the gerbils were perfusion-fixed and neuronal density in the hippocampal CA1 sector was assessed. The mean +/- SEM neuronal density in nine unoperated normal gerbils was 307 +/- 9/mm, in 10 untreated ischemic gerbils 55 +/- 21/mm, and in seven vehicle-treated ischemic gerbils 15 +/- 9/mm. The mean +/- SEM neuronal density in ischemic gerbils treated with 1, 2, 5, or 10 mg/kg indomethacin was 132 +/- 28/mm, 154 +/- 29/mm, 176 +/- 30/mm, and 136 +/- 39/mm, respectively. Indomethacin at any dose significantly ameliorated ischemic neuronal damage in the gerbil hippocampal CA1 sector.

Effect of cyclooxygenase and lipoxygenase inhibitors on delayed neuronal death in the gerbil hippocampus.

The purpose of our study was to examine whether cyclooxygenase and lipoxygenase inhibitors ameliorate delayed neuronal death in the hippocampal CA1 sector in Mongolian gerbils after 5 minutes of forebrain ischemia. Gerbils were injected intraperitoneally with cyclooxygenase inhibitors piroxicam and flurbiprofen or with lipoxygenase inhibitors AA-861 and BW-755C. Seven days after ischemic insult, the animals were perfusion-fixed, and the neuronal density in the hippocampal CA1 sector was estimated. The average neuronal density in unoperated normal gerbils was 247 +/- 9/mm (mean +/- SEM). In ischemic gerbils with vehicle administration, the average neuronal densities were 13 +/- 2, 14 +/- 2, 13 +/- 2, and 13 +/- 1 for piroxicam, flurbiprofen, AA-861, and BW-755C, respectively. The average neuronal densities in ischemic gerbils treated with 1.5 and 10 mg/kg piroxicam and 1.5 and 10 mg/kg flurbiprofen were 13 +/- 2, 194 +/- 9, 19 +/- 5, and 143 +/- 12, respectively. In ischemic gerbils treated with 15 and 100 mg/kg AA-861 and 30 mg/kg BW-755C, the average neuronal densities were 12 +/- 1, 13 +/- 1, and 14 +/- 2, respectively. At their higher doses, both piroxicam and flurbiprofen significantly (p less than 0.01) ameliorated delayed neuronal death in the hippocampal CA1 sector. Our results suggest that cyclooxygenase products play an important role in the development of delayed neuronal injury after cerebral ischemia.

Intramedullary cavernous angioma with trigeminal neuralgia: a case report and review of the literature.

A case of intramedullary cavernous angioma of the upper cervical spinal cord, initially associated with trigeminal neuralgia, is reported. Magnetic resonance imaging precisely depicted the entire extent of the lesion. The angioma was totally removed and the operation was successful in relieving the patient of neuralgia. The previously reported 23 cases of intramedullary cavernous angiomas are reviewed, and the clinical symptoms, diagnosis, and treatment of this rare condition are discussed.

Subarachnoid hemorrhage in children.

45 cases of subarachnoid hemorrhage in children were surveyed. 73 percent of the causes were arteriovenous malformations and spontaneous intracerebral hematomata. Arteriovenous malformations in children may grow in size which may be due to the fact that besides the nidus demonstrated by angiography there are surrounding abnormal vascular groups, the reserved nidus. If one fails to extirpate this reserve nidus at the time of surgical excision of the arteriovenous malformation, it may become nidus several years later and may bleed again. The follow-up results of surgery in subarachnoid hemorrhage cases were fairly good.

Spatial Memory Disruption in Hydrocephalic Rats Assessed in the Radial Arm Maze

For the purpose of elucidating the pathophysiology of memory disturbance in hydrocephalus, the authors studied behavioral change in experimentally induced hydrocephalic rats by using a radial eight-arm maze which is known to be a useful experimental tool for assessing spatial memory in animals.

Timing and Risk Factors in Surgery of Ruptured Cerebral Aneurysms

The decision whether to operate or not in cases with ruptured cerebral aneurysms in the acute stage is still a controversial problem [1, 2, 5, 6]. Since the beginning of 1970, microsurgery has been utilized in our operations on cerebral aneurysms and we have actively performed early operations after rupture. In this paper, we will analyze 248 consecutive cases of ruptured cerebral aneurysms admitted within one week after subarachnoid hemmorhage (SAH) and detail the risk factors producing unfavorable surgical results.