Biomedical subjects

D S Delbro

Publications and source records attributed to D S Delbro.

32 records · Page 2Linked to original sources

PubMed1995

Role of nitric oxide in motility and secretion of the feline hepatobiliary tract.

BACKGROUND: Nitric oxide (NO) mediates inhibition of gastrointestinal smooth-muscle cells via nonadrenergic, non-cholinergic (NANC) nervous pathways. The effect of NO on the absorption and secretion by the mucosa of the gastrointestinal and hepatobiliary tracts is less well known. The aim of this study was to evaluate the effects of a pharmacologic blockade of NO synthase on sphincter of Oddi activity, gallbladder function, and bile secretion and to demonstrate the presence of NO synthase-positive neurons in this region. METHODS: Experiments were conducted on anesthetized cats after blockage of noradrenergic and cholinergic neurotransmission. Flow resistance in the sphincter of Oddi, gallbladder fluid absorption and motility, bile outflow from the liver, and bile salt secretion were registered. RESULTS: Flow resistance exerted by the sphincter of Oddi increased dose-dependently in response to the NO synthase blocker NG-nitro-L-arginine. The increase in flow resistance was reversed stereospecifically by L-arginine, the substrate for NO synthesis. No significant effects on bile secretion, gallbladder fluid transport, or gallbladder motility were observed. NO synthase-positive neurons were identified close to the sphincter of Oddi and in the gallbladder mucosa. CONCLUSIONS: This tonically active inhibitory NANC innervation of the sphincter of Oddi may be important in the physiologic regulation of the bile duct pressure.

Animals↗

PubMed1994

Vagal influence on the motility of the feline jejunum.

1. The effects of electrical stimulation of the peripheral end of the cervical vagal nerve on jejunal motility were investigated in anaesthetized cats, pretreated with guanethidine, with sectioned splanchnic nerves and ligated adrenal vessels. Motility was monitored as volume changes of an intraluminal balloon. 2. Vagal stimulation elicited frequency-dependent hypermotility with a short latency. Relaxatory events were also observed, which could indicate the presence of a non-adrenergic inhibitory pathway. 3. After atropine treatment, contractions and relaxations could still be elicited. The former were compared to cholinergic contractions and showed a lower maximal amplitude and a longer latency to onset. Moreover, they were antagonized by 80-100% by the opioid receptor antagonist, naloxone. 4. Vagal stimulation after hemicholinium, given in order to deplete the preganglionic acetylcholine content, elicited naloxone-sensitive contractions. This suggests that a subpopulation of the vagal preganglionic fibres is non-cholinergic. 5. Isolation of the balloon-containing segment did not qualitatively alter the responses, indicating that the vagal fibres reach the small intestine via the paravascular mesenteric nerves. 6. It is concluded that cholinergic and non-adrenergic, non-cholinergic (NANC) contractions, as well as relaxations, could be elicited by efferent vagal stimulation. The NANC contractions seem to result from the activation of opioid receptors causing disinhibition of a tonic neurogenic restraint on the gut muscle.

Animals↗

PubMed1994

Neurogenic inhibition of duodenal and jejunal motility in the anaesthetized rat.

Duodenal or jejunal motility (monitored as pressure changes in a saline-perfused intraluminal catheter) was studied in anaesthetized rats, vagotomized and pretreated with adrenergic blocking agents. In the duodenum (but not the jejunum), atropine or the selective muscarinic M1 and M3 receptor antagonists, pirenzepine and 4-diphenyl-acetoxy-N-methylpiperidine (4-DAMP), respectively, augmented the spontaneous contractile activity. This effect could be abolished either by nicotinic ganglionic receptor antagonism with hexamethonium, or with morphine. Moreover, blockade of the synthesis of nitric oxide by N omega-nitro-L-arginine elicited hypermotility both in the duodenum and the jejunum, and also this response was abolished by hexamethonium. It is proposed from the present results that the rat small is controlled by non-adrenergic, non-cholinergic inhibitory as well as excitatory motor neurons. The latter motor neurons seem to be modulated by muscarinic, nitroxergic or opioidergic mechanisms.

Animals↗

PubMed1994

Loperamide improves anal sphincter function and continence after restorative proctocolectomy.

The physiological and clinical effects of loperamide treatment versus placebo were investigated in a randomized, double-blind, crossover study in patients operated with restorative proctocolectomy. Sixteen patients operated with endoanal mucosectomy and a handsewn ileal pouch-anal anastomosis and 14 patients operated with abdominal proctocolectomy and stapling of the pouch to the top of the anal canal were studied. While loperamide treatment increased resting anal pressure in both groups of patients by approximately 20% (P < 0.05), squeeze pressure was not affected. Loperamide did not affect pouch volume or contractility. Sensory thresholds and the recto/pouch-anal inhibitory reflex were not influenced by loperamide treatment. Clinical function was improved, with a reduced bowel frequency and an improved nighttime continence, with less soiling (P < 0.05) as well as need to wear a protective pad.

Adult↗

PubMed1994

Evans blue permeation of intestinal mucosa in the rat.

The azo dye Evans blue (EB; molecular weight, 960.83) is widely used as an indicator of increased capillary permeability. In the present study, however, rat gut absorption of EB was investigated after dye instillation in either the small or large intestine. During a brief period of ether anaesthesia, EB was injected either into jejunal loops with a challenge period of 30 or 60 min or into a proximal and a distal colon loop with a challenge period of 30, 60, or 120 min. After the rats had been killed the intestinal specimens were washed with 6 mM acetylcysteine dissolved in phosphate-buffered saline, which efficiently cleared the tissues of mucus, and thus of EB trapped in mucus. Only EB absorbed by the gut wall remained to be estimated, and this absorption was found to be both dose- and time-dependent in the jejunum and the colon. After instillation in the colon, but not in jejunum, EB could be detected in the blood. EB absorption from the jejunum remained unaffected by the addition of either ouabain (1 mM) or lidocaine (0.38 mM). Either of these compounds inhibited EB uptake in the proximal part of the colon, while enhancing it in the distal part. Fluorescence microscopy showed penetration into the intestinal wall to be a prerequisite for EB to become fluorescent, and EB fluorescence increased with time. It is proposed that EB is transported over the mucosa by the paracellular route and that the amount of absorbed EB reflects epithelial permeability differently in different parts of the gastrointestinal tract.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Motor effects of indomethacin, morphine or vagal nerve stimulation on the feline small intestine in vivo.

Some factors known to affect jejunal motility (recorded as volume changes of an intraluminal balloon) were investigated in anaesthetized cats (ether-chloralose) pretreated with guanethidine and atropine. Indomethacin, morphine (both compounds administered systemically) or vagal nerve stimulation elicited jejunal excitatory motor responses. The effect of indomethacin seemed to be independent of cyclooxygenase inhibition and probably did not involve opioid receptors. It is suggested that the spasmogenic stimuli caused jejunal hypermotility by inhibiting tonically active, inhibitory motor neurons that are intrinsic to the gut. Furthermore, when the jenunal tone had been raised by indomethacin or morphine spontaneous relaxations were observed, and these could be mimicked by vagal stimulation. Hexamethonium antagonized these relaxations but did not attenuate the drug-induced jejunal hypermotility.

Animals↗

PubMed1993