Our results indicate that hemodynamic changes related to aortic valve disease contribute to alterations in the resting phasic coronary blood flow and velocity profiles observed in these patients.
Background and Purpose-Potassium channels or nitric oxide or both are major mediators of acidosis-induced dilation in the cerebral circulation. However, these contributions depend on a variety of factors such as species and vessel location. The present study was designed to clarify whether potassium channels and endothelial nitric oxide are involved in acidosis-induced dilation of isolated rat cerebral arterioles. Methods-Cerebral arterioles were cannulated and monitored with an inverted microscope. Acidosis (pH 6.8 to 7.4) produced by adding hydrogen ions mediated dilation of the cerebral arterioles in a concentration-dependent manner. The role of nitric oxide and potassium channels in response to acidosis was examined with several specific inhibitors and endothelial damage. Results-The dilation was significantly inhibited by potassium chloride (30 mmol/L) and glibenclamide (3 mol/L; ATP-sensitive potassium channel inhibitor). We found that 30 mol/L BaCl 2 (concentration-dependent potassium channel inhibitor) also affected the dilation; however, an additional treatment of 3 mol/L glibenclamide did not produce further inhibition. Tetraethylammonium ion (1 mmol/L; calcium-activated potassium channel inhibitor) and 4-aminopyridine (100 mol/L; voltage-dependent potassium channel inhibitor) as well as ouabain (10 mol/L; Na-K ATPase inhibitor) and N-methylsulphonyl-6-(2-proparglyloxyphenyl) hexanamide (1 mol/L; cytochrome P450 epoxygenase inhibitor) did not alter acidotic dilation. N -Monomethyl-L-arginine (10 mol/L) and N -nitro-L-arginine (10 mol/L) as nitric oxide synthase inhibitor blunted the dilation. Furthermore, the dilation was significantly attenuated after the endothelial impairment. Additional treatment with glibenclamide (3 mol/L) further reduced the dilation in response to acidosis. Conclusions-Endothelial nitric oxide and smooth muscle ATP-sensitive potassium channels contribute to acidosisinduced dilation of rat cerebral arterioles. Endothelial damage caused by pathological conditions such as subarachnoid hemorrhage or traumatic brain injury may contribute to reduced blood flow despite injury-induced cerebral acidosis.
The findings in asymptomatic individuals in this study will help in deciding which findings observed on MR images may cause symptoms. In addition, the authors describe the variations of normal anatomy in older individuals. Knowledge of the normal anatomy helps to hone the diagnostic practices for microvascular decompression, which may increase the feasible results on such surgery.
No signs of recurrence have been observed for 7 years after surgery without adjuvant therapy. Histologically, the tumor resembled pleomorphic xanthoastrocytoma or pleomorphic granular cell astrocytoma, but the immunohistochemical findings were not completely compatible with either diagnosis. This benign astrocytoma in the pineal gland with unique features is the first such case reported.
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