Stiffness of cerebral arteries--its role in the pathogenesis of cerebral aneurysms.
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Biomedical subjects
Publications and source records attributed to K Moritake.
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The CT findings of 19 children under 16 years of age with primary brain tumors in the cerebral hemisphere were investigated with special reference to the existence of cerebral hemiatrophy ipsilateral to the side of the tumor. "Ipsilateral cerebral hemiatrophy" was observed in four of 19 cases (21%). These included two cases with germinoma in the basal ganglia and two with low-grade astrocytoma in the frontal and occipital cortex. This peculiar CT finding was not specific to the location or histology of the tumor. The four cases were characterized by slow progression, which contrasted with the rapid progression of tumors shown in seven cases with a mass effect on CT.
Hemodynamic changes were examined with an ultrasonic Doppler flowmeter and with a sound-spectrograph in 5 patients with internal carotid giant aneurysms or with recurrent laryngeal cancer undergoing gradual carotid occlusion. The ultrasonic Doppler technique was useful for preoperative assessment of intracranial cross-filling and as a practical guide for the graded reduction of blood flow in the carotid artery. The degree of flow increase in the contralateral carotid artery when the ipsilateral carotid artery was totally occluded was greater in postoperative gradual occlusion than in intraoperative rapid occlusion. In one patient with bilateral internal carotid artery giant aneurysms, whose left internal carotid artery had already been ligated at its origin, gradual occlusion of the right internal carotid artery was performed after the bilateral superficial temporal artery-middle cerebral artery (STA-MCA) anastomoses. Flow in the donor artery of the right STA-MCA anastomosis developed with increasing occlusion of the right internal carotid artery.
The elastic properties of the basilar artery were studied in control and treated dogs in which 3 ml of blood was injected intracisternally. Vascular specimens were resected transclivally as cylindrical segments and their external diameters were measured in vitro in the pressure range from 0 mm Hg to 250 mm Hg in the active condition of smooth muscle in Krebs-Ringer solution and in the passive condition in saline solution. The development of cerebral vasospasm was confirmed comparing the diameter difference between these two conditions. The experimental data indicated that vasospasm was most prominent on the 7th day after the treatment of blood injection. In the passive condition no significant dimensional change (i.e. radius and wall thickness) was observed between the control and the treated arteries at various pressure levels. These results imply that the luminal narrowing under vasospasm is not attributable to an irreversible organic change in the wall but to the constriction of vascular smooth muscle. The treated arteries are more distensible and have lower elastic moduli than the control arteries, possibly due to a change in the content of their connective tissues. These changes of the passive elastic properties of arterial walls after blood injection might be one of the factors affecting the development of cerebral vasospasm.
We studied the mechanical properties of canine basilar arteries subjected to experimental subarachnoid hemorrhage (SAH). Smooth muscle contractility was determined from pressure-diameter curves obtained after subjecting the basilar arteries to three different conditions: Krebs-Ringer solution (KRS), Krebs-Ringer solution containing serotonin (5HT), and saline solution. Pressure-diameter curves obtained in KRS and 5HT are biphasic and have sharp flexions that yield flexion points. The pressure level at the flexion point increases as vasospasm increases. Strong constriction is retained up to that pressure above which the constriction is released abruptly. These data suggest that increasing the intraluminal pressure dilates the spastic artery nonlinearly and that induced hypertension could relieve the cerebral ischemia caused by vasospasm if blood pressure were maintained above the flexion point. The contractile response of spastic arterial wall to serotonin remains unchanged after SAH although the spastic constriction increases progressively and becomes maximal seven days after SAH. The lesser the arterial wall stiffness, the more efficiently it constricts. This means that the diminution of arterial stiffness observed after SAH might be one of the factors promoting the development of vasospasm.