Oxidative stress may play an important role in the regulation of MMP activity. Augmented MMP activity may be involved in the development of ventricular remodelling in patients with coronary artery disease.
Although a decrease in extravascular pH has been suggested to be involved in coronary flow regulations during hypoxia, ischemia, and increased metabolic demand of the heart, its vasomotor control mechanism has not been elucidated. To examine the effect of acidosis of vasomotor tone, porcine coronary arterioles (40 to 110 microns) were isolated, cannulated, and pressurized to 60 cm H2O intraluminal pressure without flow for in vitro study. Acidosis (pH 7.4 to 7.0) was produced by adding HCl to the extravascular solution. The involvement of potassium channels in the vasomotor response to acidosis was evaluated by using BaCl2 (100 mumol/L, nonspecific potassium channel inhibitor), glibenclamide (5 mumol/L, ATP-sensitive potassium channel inhibitor), and iberiotoxin (100 nmol/L, calcium-activated potassium channel inhibitor). To determine whether endothelial hyperpolarization contributes to the acidosis-induced dilation, the pH-diameter relation of the vessel was examined under a high intraluminal concentration of KCl (40 mmol/L). The involvement of nitric oxide and prostaglandins was assessed by using NG-monomethyl-L-arginine (L-NMMA, 10 mumol/L) and indomethacin (10 mumol/L), respectively. To evaluate the role of endothelium in the acidosis-induced dilation, the pH-diameter relation was studied after endothelial removal. All vessels developed a similar level of spontaneous tone (internal diameter, 75 +/- 4 microns [approximately 69 +/- 1% of maximum diameter) and dilated to HCl in dose-dependent manner. Glibenclamide completely abolished vasodilation to a mild level of acidosis (pH 7.2 to 7.3) and attenuated the vasodilation by 70% at pH 7.0. Acidosis-induced dilation was also inhibited by BaCl2 but not by iberiotoxin. L-NMMA, indomethacin, and intraluminal KCl did not alter the pH-diameter relation. Vasodilation to acidosis of the endothelium-denuded vessels was identical to that of the endothelium-intact vessels. In addition, glibenclamide attenuated the acidosis-induced arteriolar dilation of endothelium-denuded vessels. These results suggest that the opening of ATP-sensitive potassium channels in vascular smooth muscle mediates the coronary arteriolar dilation during acidosis.
The purpose of this study was to investigate the efficacy of chemical shift, fast low-angle shot (FLASH) imaging at 1.5 T to differentiate adrenal masses. The materials included patients with adrenocortical adenomas (n = 32), metastatic tumors (n = 17), and pheochromocytomas (n = 4). FLASH images were obtained with breath holding at 100/11 (repetition time msec/echo time msec) (out-of-phase images) and 100/13 (in-phase images) and a flip angle of 20 degrees to differentiate the lipid contents in the adrenal tumors. The signal-intensity (SI) indexes of adrenal masses ([SI on IP - SI on OP]/[SI on IP x 100]), where IP = in-phase image and OP = out-of-phase image, were calculated. All adenomas had SI indexes of more than 5%, while SI indexes of metastatic tumors and pheochromocytomas were less than 5%, with accuracy of 100% in the differentiation between adenoma and nonadenoma. Hyperfunctioning adenoma, however, could not be differentiated from nonhyperfunctioning adenoma. Chemical shift FLASH imaging was superior to the calculated T2 in the characterization of adrenal masses.
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