CMS-Na was safely administered to healthy volunteers but resulted in transient increase of urinary N-acetyl-β-D-glucosaminidase (NAG) and protein. Based on this study, the highest recommended dose of CMS-Na had sufficient bacteriostatic effect.
The left ventricular hypertrophy (LVH) in response to pressure overload is an important risk factor in cardiac morbidity and mortality. To investigate the time course of histopathological alterations in the LVH in response to pressure overload, histopathological and immunohistochemical examination was performed using the aortic banding-induced mouse LVH model. Five-week-old male CD-1 mice were subjected to the inter-renal aortic banding. Major organs were sampled on 3, 10, 14, 21, 28 or 42 days after banding. Haematoxylin and eosin (H&E) staining, Masson's trichrome staining and immunohistochemistry for proliferating cell nuclear antigen (PCNA), alpha-smooth muscle actin (aSMA), ICAM-1, type I collagen and CD31 was performed and microscopically examined. Three days after aortic banding, acute inflammatory changes, such as macrophages/neutrophil infiltration and vascular wall injury were observed on/around the coronary arteries/arterioles of both ventricles. Intense ICAM-1 immunostaining was observed on the endothelium of the coronary arteries/arterioles. After day 10, vascular wall thickening and perivascular fibrosis was induced on the coronary arteries/arterioles. Immunohistochemistry for aSMA and PCNA demonstrated the proliferation of vascular smooth muscle cells in the media. After day 28, minimal cardiomyocyte hypertrophy was observed at the light microscope level. In the inter-renal aortic banding LVH model, histopathological alterations in early phase were mainly observed on coronary arteries/arterioles. These early phase alterations were thought to be hypertension-related changes in the coronary vasculatures. The cardiomyocyte hypertrophy observed in later phase was minimal at the light microscope level. These evidences would facilitate the understanding of pathophysiology of pressure overload LVH.
Abstract. We examined the effect of aspirin on urodynamic parameters in normal and cyclophosphamide-induced cystitic rats and compared them in rats with or without sensory denervation. Cystometry was performed under urethane anesthesia; and volume threshold for micturition (VT), micturition frequency (MF), micturition pressure (MP), and micturition volume (MV) were determined. Cystitis was induced by pretreatment with cyclophosphamide and sensory denervation was performed by pretreating animals with a large dose of capsaicin. PGE 2 and 6-keto-PGF 1a contents in the bladder were determined by ELISA. Sensory intact, cystitic rats showed decrement of VT and increment of MF. Aspirin increased VT and decreased MF in the cystitic condition. Both PGE 2 and 6-keto-PGF 1a contents in the bladder were significantly increased in cystitic rats, but such increases were completely inhibited by aspirin. In sensory denervated rats, aspirin showed a marginal tendency of increment of VT. Cystitic rats showed overflow micturition in the sensory denervated condition, but VT was the same as that of normal rats. Furthermore, following capsaicin pretreatment, aspirin had no effect on the cystometrogram in cystitic rats. From these findings, it is concluded that suppression of sensory C-fiber via inhibition of PGs synthesis in the bladder is involved in the pharmacological action of aspirin in the detrusor hyperactivity.
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