SummaryLower limb compartment syndrome after a prolonged period in the lithotomy position develops as a result of an increase in the pressure within a closed muscle compartment that impedes arterial perfusion. It is associated with several diverse circumstances and risk factors. The resultant ischaemia may have permanent and disabling sequelae. It is therefore essential that the risk factors are promptly recognized and appropriate action taken to prevent the disastrous sequelae of compartment syndrome. Immediate decompression could be effective in preventing the limb dysfunction that results from an untreated compartment syndrome.
cancer tissue was determined by immunohistochemistry and Western blot analysis.
RESULTS5HT caused a dose-dependent increase in the proliferation of HT1376 cells. The maximum increase in cell proliferation (12%; 12 samples, P < 0.001) was at 10 − 8 M as compared to the control at 72 h. At 10 − 4 M , 5HT 1A antagonist and 5HT 1B antagonist (SB224289 hydrochloride) had a 10% (12 samples, P < 0.001) and 93% (12, P < 0.001) inhibitory effect on HT1376 cell growth, respectively, compared to the control at 72 h. There was immunostaining for 5HT 1A and 5HT 1B receptors in HT1376 cells and malignant bladder tissue, confirming the presence of these two receptor subtypes. Western blot analysis showed the presence of 5HT 1A and 5HT 1B receptor proteins with bands of 46 kDa and 43 kDa, respectively.
CONCLUSION5HT 1A and to a greater extent 5HT 1B antagonists significantly inhibit bladder cancer cell growth. This effect is probably mediated via the 5HT 1A and 5HT 1B receptors. These results highlight the potential use of 5HT 1A and 5HT 1B antagonists in the treatment of bladder cancer.
Objective To investigate the effect of superoxide dismutase (SOD, the enzyme that accelerates the breakdown of the superoxide anion, O 2 ± to H 2 O) on nitric oxide (NO)-mediated and electrical ®eld stimulated (EFS) relaxation in diabetic rabbit cavernosal smooth muscle. Materials and methods Diabetes was induced with alloxan (65 mg/kg) in six adult New Zealand White rabbits. After 6 months, cavernosal smooth muscle strips from age-matched controls and diabetic animals were mounted in organ baths. After precontraction with phenylephrine (10 mmol/L) in the presence of atropine (1 mmol/L), guanethidine (5 mmol/L) and indomethacin (10 mmol/L), relaxation responses to EFS (1±20 Hz), carbachol (10 x8 x10 x4 mol/L) and sodium nitroprusside (SNP, 10 x9 x10 x4 mol/L) were assessed in the presence and absence of SOD (100 IU/ mL). Results SNP-and carbachol-mediated (endotheliumindependent and -dependent, respectively) relaxations were impaired in the diabetic cavernosal smooth muscle strips compared with controls (concentration required for 50% inhibition, 1.4 mmol/L for diabetic and 0.75 mmol/L for control with SNP, and 44 mmol/L for diabetic and 0.4 mmol/L for control with carbachol). SOD signi®cantly enhanced both SNP-and carbachol-mediated diabetic cavernosal smooth muscle relaxations (both P<0.05). EFS-mediated relaxations were also signi®cantly (P<0.05) impaired in the diabetic cavernosal smooth muscle strips; these relaxations were also signi®cantly (P<0.05) enhanced by SOD. Conclusion NO-and EFS-mediated cavernosal smooth muscle relaxation is impaired in a rabbit model of diabetes but SOD signi®cantly reversed the impaired relaxation. Therefore, in diabetes, the generation of reactive oxygen species may play an important role in the development of erectile dysfunction.
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