Efficacy of stellate ganglion block in cholinergic urticaria with acquired generalized hypohidrosis.

Cholinergic urticaria with acquired generalized hypohidrosis, and its pathophysiology is not well known. Autoimmunity to sweat glands or to acetylcholine receptors on sweat glands has been mentioned as one of the possible etiologies. Systemic steroid therapy, antihistamines, anticholinergics, and avoidance of the stimulatory situations are recommended for treatment. We experienced a case of cholinergic urticaria with acquired generalized hypohidrosis in a patient who had no other associated disease, and the symptoms eased after repeated bilateral stellate ganglion block. Stellate ganglion block normalized the elevated sympathetic tone and may relieve symptoms in patients with this condition.

Udenafil enhances the recovery of erectile function and ameliorates the pathophysiological consequences of cavernous nerve resection.

INTRODUCTION: Radical prostatectomy is the treatment of choice for prostate cancer patients. Despite the introduction of nerve-sparing surgical techniques, its success is not entirely guaranteed and the majority of patients report compromised erectile function following surgical procedures. AIM: This study was performed to investigate the effect of repeated dosing of udenafil, a novel phosphodiesterase type 5 inhibitor, on penile hypoxia and fibrosis induced by bilateral cavernous nerve resection (BCNR) in rats. METHODS: Thirty male Sprague-Dawley rats (300-320 g) were used in this study. The animals were divided into three groups; group I consisted of sham-operated animals (N = 10), animals in group II underwent BCNR alone (N = 10), and animals in group III were orally treated with 10 mg/kg udenafil b.i.d. for 8 weeks following BCNR (N = 10). MAIN OUTCOME MEASURES: The expression of transforming growth factor-beta1, hypoxia-inducible factor-1 alpha, endothelial nitric oxide synthase, neuronal nitric oxide synthase, and endothelin B receptor in penile tissue was examined at gene level. Additionally, erectile function, measured by intracavernous pressure (ICP), and pathological changes in the corpus cavernosum were examined. RESULTS: While fibrosis, apoptosis, and the expression of TGF-beta1, HIF-1 alpha, and ET(B) were significantly increased, and the expression of eNOS and nNOS were significantly decreased in group II, compared with the sham-operated animals, repeated dosing of udenafil significantly ameliorated these changes. Erectile function was profoundly impaired in animals that underwent BCNR alone, and udenafil treatment significantly attenuated this impairment as measured by ICP. CONCLUSIONS: These results demonstrate that long-term administration of udenafil ameliorates penile hypoxia and fibrosis induced by cavernous nerve resection. This study also suggests the potential beneficial role of repeated dosing of udenafil in the recovery of erectile function in patients with neuronal erectile dysfunction.

Pulmonary thromboembolism after tourniquet inflation under spinal anesthesia -A case report-.

Pulmonary thromboembolism is one of the most important causes of morbidity and mortality in patients undergoing lower extremity orthopedic surgery. Early diagnosis and appropriate management are important clinical challenges. In this case, massive pulmonary embolism causing sudden cardiac arrest was attributed to use of tourniquet inflation during lower extremity orthopedic surgery. Resuscitation procedures were initiated and transesophageal echocardiography revealed pulmonary thromboembolism. Patients with high suspicion for the presence of deep vein thrombus must be monitored thoroughly during limb exsanguinations.

Effect of udenafil on portal venous pressure and hepatic fibrosis in rats. A novel therapeutic option for portal hypertension.

The purpose of this study was to investigate the therapeutic efficacy of udenafil (CAS 268203-93-6), a phosphodiesterase type 5 (PDE5) inhibitor, on bile duct ligation (BDL)-induced portal hypertension. Udenafil was given orally to rats at dose levels of 1, 5 or 25 mg/kg/day for 3 weeks in order to examine the chronic effect on portal venous pressure (PVP). Udenafil was also given orally to investigate the sequential change of PVP in BDL animals. The effect of udenafil on hepatic stellate cell activation and fibrotic change-related protein mRNA expression were examined. In a pharmacokinetic study, the pharmacokinetic parameters in sham-operated rats and BDL rats were compared. Three-week udenafil treatment decreased PVP by approximately 30% compared to the vehicle group. In a single oral administration study, the PVP of the udenafil treated group was lower than that of the control group throughout the experimental period. Compared to control, udenafil suppressed the expression of procollagen type I and alpha-smooth muscle actin mRNA. In the pharmacokinetic study, the AUC of udenafil in BDL rats was approximately 5 times higher than that in sham-operated rats. The results of this study suggest that udenafil has beneficial effects on portal hypertension and the effect may well be attributed to its anti-fibrogenic activity.

Gastroprotective effects of DA-6034, a new flavonoid derivative, in various gastric mucosal damage models.

This study evaluated the gastroprotective activity of DA-6034 against various ulcerogens including ethanol, aspirin, indomethacin, stress, and acetic acid. The basic mechanisms of DA-6034 as a defensive factor such as mucus secretion and endogenous prostaglandin E(2) synthesis were determined. Rats with gastric lesions induced by ethanol-HCl, aspirin, indomethacin, and stress that had been pretreated with DA-6034 orally showed a statistically significant decrease or decreasing tendency of the gastric lesion. In acetic acid-induced gastric lesions, repeated oral administration of DA-6034 exhibited a U-shape activity in ulcer healing, with the maximum and minimum inhibition being observed at 30 and 10 mg/kg/day, respectively. DA-6034 also increased the mucus content in the gel layer as well as endogenous prostaglandin E(2) synthesis. These results suggest that DA-6034 prevents gastric mucosal injury, and these gastroprotective activities appear to be due to the increase in the gastric defensive systems.

Microarray analysis of gene expression profile in the corpus cavernosum of hypercholesterolemic rats after chronic treatment with PDE5 inhibitor.

Gene expression changes in the corpus cavernosum of hypercholesterolemic rats were not fully assessed, which were not previously known to be associated with hypercholesterolemia-related erectile dysfunction (ED). To provide molecular insight into pathophysiology of hypercholesterolemia-related ED and to investigate the effects of Udenafil, a phosphodiesterase type 5 (PDE5) inhibitor, on gene expression, we performed microarray gene expression analysis via gene discovery methods using GenoCheck platinum cDNA chip (Ansan, S. Korea). Sixteen male Sprague-Dawley rats were fed 2% cholesterol diet for 5 months. Half of them were orally treated with Udenafil (20 mg/kg/day) simultaneously. Eight age-matched rats fed normal diet were served as normal control. RNA was extracted from corpus cavernosum and microarray analysis was performed. Decreased erectile responses and hypercholesterolemia were observed in hypercholesterolemic control group. In microarray analysis, 122 candidate genes were noted to be altered based on the magnitude of expression changes, which includes 44 down-regulated and 78 up-regulated genes compared with the age-matched normal controls. These changes were, however, significantly attenuated by treatment with Udenafil. Out of the 78 up-regulated genes, 8 genes were significantly decreased by the chronic treatment with Udenafil. The altered genes were cytochrome oxidase biogenesis protein OXA1, skeletal muscle myosin heavy chain, lipophilin, fast skeletal muscle isoforms beta/alpha, myosin light chain 3, cytochrome c oxidase, adipocyte fatty acid binding protein and one EST gene. In contrast, among the 44 down-regulated genes, Kruppel-like factor 5 and cyclin D1 genes were increased after the Udenafil treatment. These results provide the molecular basis for understanding the pathogenesis of hypercholesterolemia-related ED and offer clues on determining the underlying action mechanism of a PDE5 inhibitor.