No abstract

Although COPD and asthma share common markers of systemic inflammation, serum levels of TGF-beta1 and alpha1-AT may reflect differences between the diseases.

It has been shown that centrally administered neuropeptide Y (NPY) delays gastric emptying. To determine the receptor subtypes of NPY mediating the inhibitory effects on gastric emptying, effects of intracerebroventricular injection of NPY, [Leu31,Pro34]NPY (a Y1 agonist) and NPY-(3-36) (a Y2 agonist) on solid gastric emptying and postprandial antropyloric motility were studied in conscious rats. Intracerebroventricular injection of NPY and NPY-(3-36), but not [Leu31,Pro34] NPY, delayed solid gastric emptying in a dose-dependent manner (0.03-3 nmol). After the feeding (40 min), contractions with low frequency and high amplitude of the antrum were frequently observed, and the peak contraction of the antrum occurred most often 3-6 s before the peak contraction of the pylorus. Intracerebroventricular injection of NPY and NPY-(3-36) (3 nmol), but not [Leu31,Pro34]NPY, significantly reduced antral contractions and the number of antropyloric coordination events. It is suggested that centrally administered NPY impairs postprandial antral contractions and antropyloric coordination via Y2 receptors, resulting in delayed gastric emptying.

Pyloric sphincter tone plays an important role in the regulation of gastric emptying. Non-adrenergic, noncholinergic (NANC) innervation to the pylorus is predominantly inhibitory and mediates relaxation of the sphincter (Anuras et al. 1974). A high density of NOSimmunopositive nerve cells and fibres has been demonstrated in the pylorus (Ekblad et al. 1994), and significant reduction of NOS activity of the pylorus has been demonstrated in infantile hypertrophic pyloric stenosis (Vanderwinden et al. 1992). It has been shown that transgenic mice with homozygous depletion of the nNOS gene develop grossly enlarged stomachs with hypertrophy of the pyloric sphincter (Huang et al. 1993). Thus, gastric outlet obstruction is associated with the lack of NO-generating neurons in the pylorus. Previous studies have shown that NO biosynthesis inhibitors delay Gastric distension-induced pyloric relaxation: central nervous system regulation and effects of acute hyperglycaemia in the rat 1. The pylorus plays an important role in the regulation of gastric emptying. In addition to the autonomic neuropathy associated with long-standing diabetes, acute hyperglycaemia per se has effects on gastric emptying. In this study, the role of the central nervous system in modulating the effects of hyperglycaemia on gastric distension-induced pyloric relaxation was investigated.2. Gastric distension-induced pyloric relaxation was significantly reduced by subdiaphragmatic vagotomy, hexamethonium (20 mg kg _1 ) and N G -nitro-L-arginine methyl ester (L-NAME; 10 mg kg _1 ), a nitric oxide synthase (NOS) biosynthesis inhibitor, in anaesthetized rats. In contrast, neither splanchnectomy nor guanethidine (5 mg kg _1 ) had an effect. 8. Taken together, these findings suggest that gastric distension-induced pyloric relaxation is mediated via a vago-vagal reflex and NO release. Acute hyperglycaemia stimulates hypothalamic NPY release, which, acting through the Y1 receptor, inhibits gastric distensioninduced pyloric relaxation in rats exposed to acute elevations in blood glucose concentrations.