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The purpose of the study was to determine the effect β₂-adrenergic receptor agonist-clenbuterol on tibiae mineralization of female rats with established osteopenia. The experiments were conducted on 30 female 3-months-of-age Wistar rats with an initial body weight of about 250 g. The sham-operation - SHO (n=10) and bilateral ovariectomy - OVX (n=20) were performed. After 60 days of osteopenia induction the ovariectomized rats were divided into a group fed a standard diet (n=10) and a group that received a diet supplied with clenbuterol at a dose of 5 mg/kg. After 14 days of the experiment the tibiae was isolated and tested using a DEXA densitometer, peripheral quantitative computer tomography (pQCT) and three-point bending test. The obtained results proved that a 14 day period of clenbuterol treatment significantly increased mechanical properties content and mineral density, both planar (BMD) and volumetric (vTotBMD) of the tibiae of ovariectomized rats.
The present study was designed to determine the involvement of nitric oxide (NO) and prostaglandins (PG) in the stimulatory action of clenbuterol, a selective ß2-adrenergic receptor agonist on hypothalamic-pituitary-adrenal (HPA) axis under basal and social crowding stress conditions. Clenbuterol given i.c.v. (10 µg) or i.p. (0.2 mg/kg) considerably increased ACTH and corticosterone secretion. A selective ß2-receptor antagonist compound ICI 118551 and non-selective ß-receptor antagonist propranolol given by either route reduced the stimulatory action of clenbuterol. Crowding stress (21 rats in a cage for 7) for 3-7 days significantly reduced the i.c.v. clenbuterol-induced ACTH and corticosterone secretion and i.p. clenbuterol-elicited ACTH secretion. L-NAME, mainly endothelial nitric oxide synthase (NOS) blocker, stronger than L-NNA, a neuronal NOS blocker, reduced the clenbuterol-evoked ACTH and corticosterone secretion in control rats but did not significantly alter this secretion already reduced by crowding stress. Piroxicam, predominantly constitutive cyclooxygenase (COX-1) inhibitor, given i.p. significantly diminished the i.p. clenbuterol-induced ACTH and corticosterone secretion in control rats and tended to reverse the reduction of ACTH secretion by crowding stress. These results indicate that clenbuterol, a selective ß2-adrenoceptor agonist, is much stronger stimulator of the HPA axis than isoprenaline, a non-selective ß-receptor agonist. Social crowding stress reduces to a larger extent the HPA response to ß2-receptor stimulation. Likewise, in the HPA axis stimulation via ß2-adrenoceptors endogenous NO and prostaglandins are significantly involved. Beta2-adrenoceptor is a dominant functional subtype of ß-receptor in the stimulatory and modulatory signals regulating the HPA axis activity under basal and social stress conditions.
Modification of the composition of the carcass, especially reduction of the fat depot and enlargement of the musculature mass have been recognized as a main feature of the action of beta-2-adrenergic agonist clenbuterol. As a result of a dietery treatment with clenbuterol significant decreases of chylomicrons, VLDL and LDL2 in the plasma of chickens were observed. There was a tendency for a diminishing of saturated fatty acids (palmitic and stearic acids). Simultaneously, an increase in the content of unsaturated fatty acids (linoleic, linolenic and arachidonic acids) was observed. Compared to control chickens, those fed 5 mg clenbuterol/kg had decreased total content of fatty acids in fatty tissue from 686.99 to 563.50 mg/g, respectively. The ratio of insaturated to saturated fatty acids in plasma and adipocytes increased in the treated groups. On the basis of histochemical differentiation of fibre types it was established that type II В fibres were most pronounced in clenbuterol treated groups.
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