[A trend of surgical treatment for cerebrovascular disease].
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Biomedical subjects
Publications and source records attributed to M Takayasu.
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This report describes a rare case of primary intrasellar haematoma in a 66 year-old man with hypopituitarism. Computerized tomography (CT) and magnetic resonance imaging (MRI) showed an intrasellar cystic lesion with small suprasellar extension. Transsphenoidal surgery revealed that the lesion was a chronic haematoma, without evidence of a tumour or vascular anomaly. Pathological diagnosis confirmed this. This is the first report of a chronic intrasellar haematoma, which is probably primary.
We describe a pulsatile aneurysm in the skin of 16-year-old boy that was found to be a sign of a systemic vascular disease, that is, arterial fibromuscular dysplasia. The patient had aneurysms in the renal, cerebral, coronary, and other arteries; he developed renovascular hypertension and had a cerebrovascular accident and acute myocardial infarction at 17 years of age. This disease has not been previously reported in the dermatologic literature.
A 34-year-old woman with primary choroid plexus papilloma occurring in the suprasellar region is reported. No connection with the ventricular system was found during intraoperative observations. The findings of pathological examinations such as hematoxylin and eosin staining, transthyretin (prealbumin) immunoreactivity, and electron microscopy were consistent with choroid plexus papilloma. Radiologically, it was extremely difficult to differentiate from tuberculum sellae meningioma. To our knowledge, this is the first case of primary choroid plexus papilloma in this location reported in the literature.
The reactivity of rabbit basilar artery and penetrating arteriolar microvessels was studied in vitro using an isometric-tension measurement technique and an isolated perfused arteriole preparation, respectively. Comparisons were made between reactivities of normal vessels and those obtained from animals subjected to experimental subarachnoid hemorrhage (SAH) 3 days prior to examination. Subarachnoid hemorrhage produced significant increases in basilar artery contraction in response to increasing concentrations of serotonin (5-hydroxytryptamine) (10(-9) to 10(-5) M) and prostaglandin F2 alpha (10(-9) to 10(-5) M) when compared to normal arteries. In addition, SAH attenuated the relaxing effect of acetylcholine following serotonin-induced contraction and of adenosine triphosphate after KCl-induced basilar artery contractions. In contrast to the changes observed in large arteries, cerebral microvessels did not demonstrate significant differences in spontaneous tone or in reactivity to a number of vasoactive stimuli including application of calcium, serotonin, and acetylcholine. On the other hand, small but significant changes in arteriolar responsiveness to changes in extraluminal pH and to application of KCl were noted. Findings from this study suggest that intracerebral resistance vessels of the cerebral microcirculation are not greatly affected by the presence of subarachnoid clot, in contrast to the large arteries in the basal subarachnoid space. The small changes that do occur are qualitatively different from those observed for large arteries. These findings are consistent with the observation of significant therapeutic benefit with the use of calcium channel blockers without changes in angiographically visible vasospasm in large vessels. It is likely, therefore, that calcium antagonists may act to decrease total cerebrovascular resistance at the level of the relatively unaffected microcirculation after SAH without changing large vessel diameter.
The vasoactive properties of pentobarbital (PB) were studied in intracerebral arterioles and venules (diameter, 30-90 microns). These vessels mediate changes in cerebrovascular resistance and capacitance, respectively. Mean control vessel diameters of arterioles and venules at pH 7.3 were 53.9 +/- 2.8 microns and 78.4 +/- 4.3 microns, respectively. Both arterioles and venules dilated when the pH of the extraluminal solution was lowered to 6.8 and constricted when the pH was raised to 7.6. PB, 10(-6) to 10(-2) mol/L, dilated intracerebral arterioles in a dose-dependent manner at pH 7.3, reaching a maximal dilation of 129.7 +/- 3.1% of control diameter at a dose of 10(-3) mol/L. In contrast, PB at 10(-6) to 10(-2) mol/L failed to produce significant changes in the diameter of intracerebral venules. In addition, PB at 10(-3) mol/L significantly inhibited arteriolar constriction induced by KCl (120 mmol/L), but not venular constriction. The present study suggests that intracerebral venules are relatively less responsive to PB than cerebral arterioles and peripheral veins. In addition to its effect on cerebral metabolism. PB may act to redistribute venous blood volume from cerebral veins to more responsive peripheral veins, thereby decreasing intracranial blood volume and intracranial pressure.
The differential effects of intraluminal and extraluminal application of endothelin, the endothelium-derived constricting factor, were studied in isolated intracerebral arterioles that were cannulated and perfused in vitro. Extraluminal and intraluminal application of 10(-8) M endothelin constricted the arterioles to 38.2 +/- 6.7 and 75.1 +/- 5.7% of the control diameter, respectively. Constrictions induced by either the intraluminal or the extraluminal application of endothelin were inhibited in a Ca(2+)-free solution. Nimodipine attenuated, but did not completely abolish, the constriction induced by the extraluminal application of endothelin, but it did abolish the constriction induced by the intraluminal application. The duration of vasoconstriction also differed between intra- and extraluminal application. Vessel diameter quickly returned to the control value as soon as intraluminal perfusion of endothelin was terminated. In contrast, the constriction induced by extraluminal application of endothelin lasted much longer and was difficult to reverse. The differential effect of intraluminal and extraluminal endothelin application appears to reflect the important barrier-function of the cerebrovascular endothelium of intracerebral arterioles.
The effects of hypothermia and hyperthermia on the cerebral microcirculation were studied using isolated perfused intracerebral (parenchymal) arterioles obtained from rats. In a temperature-dependent manner, hypothermia (20.0 degrees to 35.0 degrees C) dilated the spontaneous tone developed by the arterioles and also diminished their contractile response to potassium and prostaglandin F2 alpha. In contrast, hyperthermia (40.0 degrees to 45.0 degrees C) induced a biphasic response consisting of initial vasoconstriction and secondary vasodilation. Exposure of the vessels to 45.0 degrees C for 30 minutes irreversibly abolished the spontaneous tone and responsiveness of the arterioles when the temperature of the preparation was returned to 37.5 degrees C. In calcium-free solutions, however, the arteriolar diameter was not affected within a temperature range of 20.0 degrees to 45 degrees C. Furthermore, arterioles that had been in a calcium-free solution during exposure to 45 degrees C temperature recovered their viability at 37.5 degrees C. These results suggest that changes in ambient temperature alter calcium-induced contraction in arteriolar smooth muscle, and that the irreversible effects of hyperthermia on the arterioles are dependent upon extracellular calcium. These studies indicate that alterations in brain temperature may affect the pathogenesis of cerebral ischemia by mechanisms that are in part independent of parenchymal metabolism.
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The effects of the new spasmolytic agent HA1077, which belongs to the calciumantagonists but acts by mechanisms different from those of conventional calcium channel blockers, on the cerebral microcirculation were studied in rats using isolated and cannulated intracerebral (parenchymal) arterioles of 50 microns average diameter. After the vessels had developed spontaneous tone, increasing concentrations of HA1077 were applied extraluminally. HA1077 induced vasodilation in a dose-dependent manner with a maximal increase of vessel diameter of 73.9 +/- 5.1% (mean +/- SEM, n = 5) at 10(-4) M and with half-maximal responses (ED50) of 1.00 x 10(-6) M. The extent of maximal vasodilation achieved by HA1077 was significantly greater than that induced by such conventional calcium channel blockers as diltiazem, verapamil, nifedipine and nimodipine (about 50% each in a previous report from our laboratory). Vasoconstriction induced by synthetic thromboxane A2 (10(-9) M to 10(-5) M) which is through to be highly dependent on intracellular calcium, was completely inhibited by 10(-4) M HA1077, whereas both verapamil and nimodipine at a concentration at maximal vasodilation effects (10(-5) M and 10(-7) M respectively) only partially inhibited such vasoconstriction. These results suggest that HA1077 may exert a more potent vasodilator effect on the cerebral microcirculation than do conventional calcium channel blockers.
Effects of STA-MCA anastomosis on two patients with neovascular glaucoma due to occlusion of the internal carotid artery are presented. Both patients improved in visual acuity and central retinal artery pressure as well as in signs of transient ischaemic attack. Postoperative angiography showed a marked decrease in collateral flow through the ophthalmic artery, which is reversed from the normal direction, with the development of blood flow through the anastomosis. Discussion is offered indicating that the lack of collateral flow through both the anterior and posterior communicating arteries is important in addition to occlusion of the internal carotid artery in order to produce full-blown ischaemic oculopathy such as venous stasis retinopathy, neovascular glaucoma or rubeosis iridis. It is stressed that EC-IC bypass surgery should be performed soon after the appearance of ischaemia and before the development of neovascular glaucoma or rubeosis iridis in order to obtain normal vision. In ischaemic oculopathy the results of EC-IC bypass can be evaluated objectively and quantitatively by many noninvasive neuroophthalmological tests which are important in discussing the efficacy of the bypass surgery.
Endothelin (ET) caused transient and sustained elevations of cytosolic free Ca2+ concentrations ([Ca2+]i) in cultured rat and rabbit vascular smooth muscle cells (VSMC). Specific platelet activating factor (PAF) antagonists (CV-6209 and WEB-2086) and arachidonic acid (AA) cascade blockers (chlorpromazine, indomethacin, CV-4151 and AA-2414) potently inhibited the ET-induced increase in [Ca2+]i. Additionally, these compounds inhibited the PAF-induced increase in [Ca2+]i. These results suggest that PAF and thromboxane A2 (TXA2) may be involved in the mechanism of ET-induced mobilization of Ca2+ in cultured rat and rabbit VSMC.
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The vasoactive properties of inhibitory (gamma-aminobutyric acid (GABA), glycine) and excitatory (glutamate, aspartate) amino acid neurotransmitters were studied in isolated rat cerebral parenchymal arterioles. None of these neurotransmitters had a significant effect on vessel diameter at concentrations between 10(-9) and 10(-3) M, except for 10(-3) M glycine. These amino acid neurotransmitters are unlikely to play a role in regulation or pathophysiology of the cerebral microcirculation by directly changing vascular diameter.
The purpose of our study was to determine in rats the dependence of constrictor responses of intracerebral (parenchymal) penetrating arterioles on extracellular calcium. Vessel diameter was monitored in vitro, after spontaneous tone had developed. When the organ bat solution was changed from a physiological solution to a Ca2+-free one containing 0.5 mM EGTA, these vessels showed rapid and marked vasodilation to a mean +/- SEM of 159.8 +/- 8.2% of control (p = 0.018). After 3 minutes of pretreatment with Ca2+-free solution, constrictor responses to solutions of 140 mM KCl, pH 8.0, or 10(-4) M prostaglandin F2 alpha, were completely abolished, except for small transient contractions with the latter (6.6 +/- 1.8%). When vasoconstrictors were applied simultaneously with the Ca2+-free solution, all vessels still dilated to 159.8 +/- 8.4% (KCl), 146.7 +/- 6.1% (pH 8.0), and 124.3 +/- 9.1% (prostaglandin 2 alpha) of control (p = 0.018). Our results suggest that both vasomotor tone and constrictor responses in intracerebral arterioles are highly dependent upon activation from an extracellular calcium source.
An isolated cerebral arteriole preparation was used to test the hypothesis that a temporary reduction in transmural pressure causes a subsequent vasodilation mediated by mechanisms intrinsic to the vessel wall. Thirty-five cerebral vessels of 44.7 +/- 1.4 microns (+/- standard error of the mean) mean diameter were cannulated in vitro and pressurized at a transmural pressure of 60 mm Hg: after an equilibration period the vessels developed spontaneous tone. When transmural pressure was decreased to 0 mm Hg for a period of 4 minutes then returned to 60 mm Hg, vessels dilated to 155.1% +/- 6.8% of control diameter before gradually redeveloping spontaneous tone in 5.5 +/- 0.7 minutes. Varying the duration of the period during which transmural pressure was at 0 mm Hg had no significant effect on the degree of vasodilation. Conversely, varying the level of decreased transmural pressure between 0 and 20 mm Hg significantly affected both the magnitude of vasodilation and the time course of spontaneous tone recovery. These findings indicate that a temporary period of decreased transmural pressure may result in a loss of spontaneous tone in the resistance vessels of the cerebral microcirculation. Mechanisms intrinsic to the vessel wall may play a significant role in the early stage of post-reperfusion hyperemia. Such mechanisms could also be implicated in other hyperemic phenomena affecting the cerebral circulation, such as the rapid increase in intracranial pressure after subarachnoid hemorrhage, the development of the normal perfusion pressure breakthrough phenomenon, and the initiation of intracranial pressure plateau waves.