Kaichi Tokiwa

Draining vein pressure increases and hemorrhage in patients with arteriovenous malformation.

BACKGROUND Recent radiological studies have shown that arteriovenous malformations with impaired venous drainage may be susceptible to hemorrhage. To evaluate this hypothesis using a hemodynamic approach, we measured intravascular pressure during surgery in three patients with arteriovenous malformation. SUMMARY OF REPORT In three patients we measured intravascular pressures in the draining venous system and the feeding arteries simultaneously before removal of arteriovenous malformations with marked segmental stenotic or occlusive draining veins and evidence of hemorrhage. The draining vein pressures at prestenotic (or preocclusive) sites in the three patients were 38, 25, and 40 mm Hg, respectively, all significantly above the normal cortical venous pressure, whereas pressure measurements in poststenotic sites and the sagittal sinus pressure in the venous drainage system approached normal values. The feeding artery pressures in the patients were lower than normal cortical artery pressure because of the arteriovenous shunt. CONCLUSIONS Intraoperative vascular pressure measurements support the hypothesis that arteriovenous malformations with impaired venous drainage may be associated with a local increase in venous pressure and thus may be susceptible to hemorrhage.

Correlation between intravascular pressure and risk of hemorrhage due to arteriovenous malformations

The correlation between intraoperative pressure levels measured in the feeding arteries and in the draining veins, and the risk of hemorrhage from arteriovenous malformations (AVMs) is discussed. Feeding artery pressure (FAP) was significantly higher in AVMs with hemorrhage (57 +/- 11 mmHg) than in AVMs without hemorrhage (38 +/- 4), and draining vein pressure (DVP) in the former (24 +/- 5) was significantly higher than that in the latter (13 +/- 5). FAP and DVP were inversely related to the number of draining veins and size of the AVMs. The present study suggests that a high FAP and a high DVP may contribute to the development of hemorrhage from AVMs, and supports previous reports that small AVMs and AVMs with only one draining vein are susceptible to hemorrhage.

Impaired Autoregulation in an Experimental Model of Chronic Cerebral Hypoperfusion in Rats

BACKGROUND AND PURPOSE To verify the hypothesis that impaired autoregulation may contribute to cerebral swelling or hemorrhage after a sudden recovery of perfusion pressure, we studied the chronic effects of cerebral hypoperfusion on the autoregulatory responses of the pial arterioles in situ. METHODS Eight to 12 weeks after a carotid-jugular fistula was created in rats, experiments were performed under alpha-chloralose and urethane anesthesia. Regional cerebral blood flow (rCBF) was determined by the hydrogen clearance method, and carotid pressure was measured. Using a closed cranial window, we determined the autoregulatory responses of the arterioles (30 to 50 microns) to both hypertension induced by norepinephrine and sudden fistula closure at various mean arterial pressures (MAPs). RESULTS rCBF on the fistula side was reduced by 27%. Carotid pressure was significantly lower than normal but was immediately increased by fistula closure. The pial arterioles showed marked elongation and enlargement. During induced hypertension, the arterioles in the fistula group started to dilate at an MAP lower than that of the control group (130 versus 180 mm Hg, respectively). The arterioles constricted when the fistula was occluded at normal MAP. However, when the fistula was occluded at an MAP higher than 130 mm Hg, the vessels dilated. CONCLUSIONS It was demonstrated that (1) chronic hypoperfusion induced impairment of the upper limit of autoregulation and (2) sudden fistula closure under hypertensive conditions caused vasodilation of the arterioles. These findings suggest that rapid restoration of perfusion pressure is possibly followed by a pressure breakthrough phenomenon in a chronically hypoperfused cerebrovasculature.

The effects of a carotid-jugular fistula on cerebral blood flow in the cat: An experimental study in the chronic period

The purpose of the present study was to investigate the effects of feline carotid-jugular fistula (Spetzlers model) on cerebral blood flow at 8 weeks after creation of the fistula. Using laser-Doppler flowmetry, cortical cerebral blood flow (CBF) on the fistula side was measured in 10 cats, Occlusion of the fistula showed no cortical CBF changes in 6 animals, but transient increases in 4. CO2 reactivity in the closed fistula was preserved. No neurological or histological abnormalities were recognized. These findings suggested that cerebral hemodynamic changes due to Spetzlers CJ fistula model are minimal even in the chronic period after fistulization. Therefore, creation of another experimental arterio-venous fistula model is mandatory for the investigation of hemodynamic changes following resection of a cerebral arteriovenous malformation.

The effects of a carotid-jugular fistula on cerebral blood flow in the cat: An experimental study in the acute period

The purpose of the present study is to investigate the effects of feline carotid-jugular (CJ) fistula (Spetzlers model) on cerebral blood flow (CBF) in the acute period after creation of the fistula. Using laser-Doppler flowmetry, cortical CBF was measured on the fistula side of 11 cats. Temporary occlusion and opening of the fistula led to an immediate increase and decrease, respectively, in cortical CBF. However, CBF returned to baseline within 1 minute, on average. CO2 reactivity in the closed fistula was preserved. It is suggested that cerebral hemodynamic changes due to Spetzlers CJ fistula model are minimal in the acute period after fistulization.

Measurement and Significance of Plasma Antidiuretic Hormone in Subarachnoid Hemorrhage

The authors already reported that the incidence of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after subarachnoid hemorrhage (SAH) was significantly higher in patients with Grade III and IV of Hunt and Hess, severe vasospasm and marked hydrocephalus than in patients without these factors. In order to clarify why the patients with these factors were susceptible to develop SIADH after SAH the plasma ADH level (PADH) in 25 control subjects and in 56 patients with SAH mainly due to cerebral aneurysms were measured using radioimmunoassay. PADH measurements, repeated 111 times, were made preoperatively within 4 weeks after SAH. PADH in 13 cases with SIADH was significantly higher than those of the control and were inappropriate for the corresponding serum osmolarities. The differences in PADH, according to clinical grades, vasospasm, hydrocephalus and aneurysmal locations were studied in 43 cases without SIADH. The results were as follows: 1) PADH in patients with Grade III and IV, specially measured within 14 days after SAH, was significantly higher than that in patients with Grade I and II. 2) Patients with mild or severe vasospasm had significantly higher PADH than patients without vasospasm. 3) In patients with hydrocephalus, the PADH was significantly higher than that without hydrocephalus. 4) The differences in PADH according to aneurysmal locations were not significant. Hematological and urinary studies showed that the excessive release of ADH recognized in the present study was a non-physiological (inappropriate) release of ADH, caused by non-osmotic factors, except blood volume depletion. These results suggest that the patients with Grade III and IV, vasospasm, and hydrocephalus in the acute stage after SAH are unable to suppress ADH release and to excrete the water load normally, even if they are under normoosmotic conditions. The present study supports the previous report by the authors that the patients with Grade III and IV, severe vasospasm, and marked hydrocephalus are susceptible to SIADH.

Treatment of Unruptured Cerebral Aneurysms Associated with Intracranial Arteriovenous Malformations

In this paper, the authors report on 9 cases of unruptured cerebral aneurysms associated with intracranial arteriovenous malformations (AVMs), and discuss therapeutic problems of unruptured aneurysms. The following are our conclusions: 1) The rate of combinations of AVMs and aneurysms is not small . Therefore, precise preoperative neuroradiological examinations should be made to confirm the presence or absence of aneurysms in all patients with cerebral AVMs. 2) We were unable to conclude whether or not unruptured aneurysms associated with AVMs should be operated on. However, no decrease in size of aneurysms following excision of AVMs is one important indication for considering a radical operation for aneurysms. 3) The authors reported one case who suffered retrograde thrombosis of the feeding artery , and developed neurological deficits after radical operation for on unruptured aneurysm of the feeding artery. Timing of radical operation for aneurysms following the excision of AVMs must be carefully considered. When surgical treatment of an aneurysm is intended, special attention should be paid to cerebral circulation following excision of AVMs. When an angiographical finding of stagnant arterial flow of feeding arteries is observed, radical operation for aneurysms should be avoided.