Transjugular intrahepatic portosystemic shunt improves liver function in veno-occlusive disease.
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Adult↗
Biomedical subjects
Y M Van Maercke
Publications and source records attributed to Y M Van Maercke.
Involvement of nitric oxide in the inhibitory innervation of the human isolated colon.
BACKGROUND: The exact nature of the inhibitory nonadrenergic noncholinergic (NANC) neurotransmitter in the human colon is still unknown. METHODS: The present study was designed to investigate the role of nitric oxide (NO) and adenosine 5'-triphosphate (ATP) in circular muscle strips of the human isolated colon. RESULTS: NO and ATP induced tetrodoloxin-resistant relaxations that mimicked those evoked by nerve stimulation. Apamin inhibited the response to ATP, had a variable effect on the relaxations to transmural stimulation, and had no effect on those to NO or nitroglycerin. NG-nitro-L-arginine (L-NNA) concentration dependently reduced the NANC nerve-mediated relaxations, but had no effect on those to ATP, NO, or nitroglycerin; the L-NNA resistant part of the NANC relaxation to nerve stimulation was further reduced by apamin. The inhibitory effect of L-NNA or the combination of L-NNA and apamin was prevented by L-arginine but not by D-arginine. CONCLUSIONS: These results suggest that NO and another substance, perhaps ATP, are involved in the inhibitory NANC neurotransmission in the circular muscle of the human colon.
Adenosine Triphosphate↗
Alpha 2-adrenoceptor-mediated modulation of the nitrergic innervation of the canine isolated ileocolonic junction.
1. The effects of specific alpha-adrenoceptor agonists and antagonists on electrically-evoked non-adrenergic non-cholinergic (NANC) relaxations, previously demonstrated as nitrergic, were investigated in isolated circular muscle strips of the canine ileocolonic junction. 2. During a substance P-induced contraction and in the presence of atropine and guanethidine, the specific alpha 1-adrenoceptor agonist, phenylephrine and antagonist, prazosin, as well as the specific alpha 2-adrenoceptor antagonist, yohimbine, had no effect on the NANC relaxations evoked by electrical field stimulation. In contrast, clonidine and the more specific alpha 2-adrenoceptor agonist, UK-14,304, significantly reduced the electrically-induced relaxations, preferentially those in response to low frequency stimulation. The inhibitory effect of UK-14,304 on these relaxations was antagonized by yohimbine. 3. During a noradrenaline-induced contraction, clonidine, but not UK-14,304 significantly augmented the relaxations to electrical stimulation. 4. The adrenoceptor agonists and antagonists used had no effect on concentration-response curves to NO or on the relaxation induced by nitroglycerin. 5. These results indicate that stimulation of prejunctional alpha 2-adrenoceptors inhibits the nitrergic NANC relaxations induced by field stimulation and thus suggest prejunctional regulation of nitric oxide release via alpha 2-adrenoceptors in the canine ileocolonic junction.
Adrenergic alpha-Agonists↗
Prejunctional modulation of the nitrergic innervation of the canine ileocolonic junction via potassium channels.
1. The effects of different K+ channel blockers were studied on nitric oxide (NO)-mediated non-adrenergic non-cholinergic (NANC) relaxations in the canine ileocolonic junction. 2. The non-selective blockers of K+ channels, 4-aminopyridine (4-AP) and tetraethylammonium (TEA) and the blocker of large conductance Ca(2+)-activated K+ channels, charybdotoxin, potently enhanced the NANC relaxations induced by low frequency stimulation. The blocker of small conductance Ca(2+)-activated K+ channels, apamin, had no effect on electrically-induced NANC relaxations. 3. NANC nerve-mediated relaxations induced by adenosine 5'-triphosphate (ATP), acetylcholine (ACh) and gamma-aminobutyric acid (GABA) were significantly enhanced by 4-AP and charybdotoxin but not by apamin. TEA significantly enhanced the NANC relaxations in response to GABA and ATP while that in response to ACh was abolished. 4. None of the K+ channel blockers had an effect on the dose-response curve to NO, on the noradrenaline-induced contraction or on the relaxation to nitroglycerine (GTN). 5. From these results we conclude that inhibition of prejunctional K+ channels increases the nitrergic relaxations induced by electrical and chemical receptor stimulation of NANC nerves and thus suggests a regulatory role for these prejunctional K+ channels in the release of NO from NANC nerves in the canine ileocolonic junction.
Acetylcholine↗
Ca2+ dependency of the release of nitric oxide from non-adrenergic non-cholinergic nerves.
1. The role of Ca2+ in nitrergic neurotransmission was studied in the canine ileocolonic junction. 2. The specific N-type voltage-sensitive Ca2+ channel blocker omega-conotoxin GVIA (CTX, 10-100 nM) significantly reduced the electrically-evoked (2-16 Hz, 1-2 ms pulse width) non-adrenergic non-cholinergic (NANC) relaxations, preferentially affecting those to low frequency stimulation, in circular muscle strips of the ileocolonic junction. In contrast, the nerve-mediated NANC-relaxations in response to acetylcholine (30 microM), gamma-aminobutyric acid (100 microM) and adenosine 5'-triphosphate (100 microM), as well as the relaxations to nitric oxide (NO) (3-10 microM) and nitroglycerin (1 microM), remained unaffected. 3. A NO-related substance (NO-R), released from the ileocolonic junction in response to NANC nerve stimulation (4 and 16 Hz, 2 ms pulse width), was assayed with a superfusion bioassay cascade. CTX (50 nM) reduced the release of NO-R induced by electrical impulses (4 Hz: from 18 +/- 4% to 6 +/- 4%; 16 Hz: from 33 +/- 2% to 14 +/- 4%, n = 5), but not that in response to the nicotinic receptor agonist, 1,1-dimethyl-4-phenylpiperazinium (DMPP, 0.3 mM). In Ca(2+)-free medium, the release of NO-R evoked by electrical impulses or DMPP was inhibited. The L-type Ca2+ channel blockers verapamil (1-3 microM) and nifedipine (1 microM) had no effect. 4. From these results we conclude that the release of NO-R in response to NANC nerve stimulation is Ca(2+)-dependent. The electrically-evoked release of NO-R results from Ca2+ entry through CTX-sensitive N-type voltage-sensitive Ca2+ channels, whereas that induced by nicotinic receptor activation involves CTX-insensitive Ca2+ channels, different from the L- or N-type.
Animals↗
Transrectal ultrasound study of the pathogenesis of solitary rectal ulcer syndrome.
Transrectal ultrasonography is of clinical value in anorectal carcinoma and in inflammatory diseases of the anorectum. In this study a rigid linear endorectal probe was used to examine 15 patients with endoscopically and biopsy proved diagnosis of solitary rectal ulcer syndrome. In 13 of the 15 patients the rectal wall was thicker (mean (SEM) 5.7 (0.4) mm; normal values: 2.8 (0.1) mm) near the rectal ulcer. In all these cases the muscularis propria layer exceeded the maximum normal diameter of 2 mm. In nine of the 15 patients the normal rectal wall echo-structure, with five distinct layers, was disturbed and there was fading of the borders between the mucosa and the muscularis propria. Poor relaxation of the puborectalis muscle during straining was seen on ultrasound in 11 patients, as was intussusception of the rectal wall. The obvious enlargement of the muscularis propria points to a chronic mechanical load on the rectal wall. The ulcerative lesions are formed in this area of overloaded rectal wall. The direct visualisation of the puborectalis muscle during dynamic transrectal ultrasonography indicates that the fact that it does not relax is an important element in the pathogenesis of solitary rectal ulcer syndrome.
Adult↗
Vitamin A abuse: development of cirrhosis despite cessation of vitamin A. A six-year clinical and histopathologic follow-up.
We report the case of a 35-year-old man who contracted vitamin A-induced liver cirrhosis. Five years before, he had been investigated for vitamin A-induced non-cirrhotic portal hypertension. In this case, the clinical and histopathologic evolution from non-cirrhotic portal hypertension to cirrhosis was documented. In spite of the cessation of pharmaceutical vitamin A intake, the disease progressed. Therapy with colchicine and phenobarbital apparently did not influence evolution to cirrhosis. This suggests that vitamin A can trigger largely unknown mechanisms of liver fibrosis which seem to be self-perpetuating.
Adult↗
Hepatoportal sclerosis demonstrated by abdominal ultrasonography.
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Adult↗
The role of nitric oxide in serotonin-induced relaxations in the canine terminal ileum and ileocolonic junction.
The role of nitric oxide (NO) in 5-HT-induced non-adrenergic non-cholinergic (NANC) relaxations was studied on circular muscle strips of the canine ileocolonic junction (ICJ) and terminal ileum. During an acetylcholine-induced contraction, NO (10(-5) M) evoked a transient relaxation, whereas 5-HT (10(-4) M) caused an initial NANC relaxation followed by a contraction. This initial relaxation to 5-HT, but not the relaxation to NO, was significantly inhibited by the stereospecific inhibitors of the NO biosynthesis NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (L-NNA). L-arginine, but not D-arginine, prevented the inhibitory effect of L-NMMA and L-NNA. The enantiomer of L-NMMA, D-NMMA, had no effect. Hemoglobin abolished the NO-induced relaxations and significantly inhibited the relaxation to 5-HT. From these experiments it is concluded that the 5-HT-induced NANC relaxation is mediated by NO or a NO releasing substance.
Acetylcholine↗
Polypoid hamartoma of the jejunum.
The authors report an unusual case of jejunal mesenchymal hamartoma which presented as a bleeding pedunculated polyp in a 67-year-old woman. The lesion was detected by enteroclysis and resected after localization by intraoperative endoscopy.
Aged↗
A rare cause of colitis--Brucella melitensis. Report of a case.
Documentation of gastrointestinal lesions in Brucella infections is sparse. A case of Brucella melitensis type 3 infection accompanied by erosive lesions of the colon, observed by endoscopy and histopathologic examination, is reported. Such gastrointestinal lesions have not been described since 1934. Before 1934 only postmortem observations are recorded.
Adult↗
Value of transrectal ultrasonography in Crohn's disease.
Anorectal lesions are common and can develop silently in patients with Crohn's disease. Transrectal ultrasound examinations were performed to study 40 healthy individuals and 40 patients with Crohn's disease. A rigid linear endorectal probe was used to examine the rectal wall, the perirectal tissues, and the anal sphincter. In healthy individuals, the rectal wall showed five layers with a total diameter of maximum 4 mm. The anal sphincter was clearly visualized as an echo-poor and sharply delineated structure. No pathological lesions were detected perirectally. In Crohn's disease, an enlargement of the rectal wall was seen in 16 patients and heterogeneity of the anal sphincter in 19 patients. This technique detected lesions missed with the routine proctological examinations: four pararectal abscesses, two pararectal fistulas, two para-anal abscesses, and one para-anal fistula. In all examined subjects, the anal sphincter increased in breadth during squeezing and in length during straining. It is concluded that transrectal ultrasonography sharply delineates the rectal wall and the anal sphincter at rest and under dynamic conditions and detects unknown abscesses and fistulas in the pararectal and para-anal tissues in patients with Crohn's disease.
Abscess↗
Bioassay of nitric oxide released upon stimulation of non-adrenergic non-cholinergic nerves in the canine ileocolonic junction.
1. The release and the nature of the inhibitory non-adrenergic non-cholinergic (NANC) neurotransmitter was studied in the canine ileocolonic junction. A circular muscle strip of the canine ileocolonic junction served as donor tissue in a superfusion bioassay in which rings of rabbit aorta with the endothelium removed served as detector tissue. 2. The ileocolonic junction released a labile factor with vasodilator activity upon stimulation of non-adrenergic non-cholinergic (NANC) nerves in response to electrical impulses and the nicotinic receptor agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP). This release was respectively frequency- and concentration-dependent. 3. The release was reduced by the blocker of neuronal conductance, tetrodotoxin, and by the inhibitor of the nitric oxide (NO) biosynthesis NG-nitro-L-arginine. The biological activity was enhanced by superoxide dismutase and eliminated by haemoglobin. Hexamethonium abolished only the release in response to DMPP. 4. Injection of adenosine 5'-triphosphate (ATP) or vasoactive intestinal polypeptide (VIP) onto the cascade induced relaxations of the rabbit aorta but they were different from those induced by NO or the transferable factor. 5. Based on organ bath experiments in which the reactivity of different parts of the circular smooth muscle layer of the ileocolonic junction was investigated, a muscle strip of superficial circular muscle with submucosa was chosen as the detector strip in the bioassay cascade. 6. The ileocolonic junction dose-dependently relaxed in response to nitroglycerin and NO. NO was much more potent in the rabbit aorta than in the canine ileocolonic junction. 7. In conclusion, our results demonstrate the release of a transferable vasorelaxant factor in response to NANC nerve stimulation which behaves pharmacologically like NO but not like ATP or VIP. Therefore, we suggest that NO or a NO releasing substance is the inhibitory NANC neurotransmitter in the canine ileocolonic junction.
Animals↗
The role of nitric oxide in inhibitory non-adrenergic non-cholinergic neurotransmission in the canine lower oesophageal sphincter.
1. The role of nitric oxide (NO) in non-adrenergic non-cholinergic (NANC) neurotransmission was studied on circular muscle strips of the canine lower oesophageal sphincter (LOS). Electrical field stimulation evoked frequency-dependent relaxations, which were resistant to adrenergic and cholinergic blockade and abolished by tetrodotoxin. 2. Exogenous administration of NO induced concentration-dependent and tetrodotoxin-resistant relaxations which mimicked those in response to electrical stimulation. 3. NG-nitro-L-arginine (L-NNA), a stereospecific inhibitor of NO-biosynthesis, inhibited the relaxations induced by electrical stimulation but not those by exogenous NO or vasoactive intestinal polypeptide (VIP). 4. The effect of L-NNA was prevented by L-arginine, the precursor of the NO biosynthesis but not by its enantiomer D-arginine. 5. Haemoglobin abolished the NO-induced responses and reduced those evoked by electrical stimulation. 6. Cumulative administration of VIP induced concentration-dependent relaxations, which were slow in onset and sustained. A complete relaxation to VIP was not achieved and the relaxations were not affected by L-NNA. 7. In conclusion, our results provide evidence that NANC relaxations are mediated by NO, suggesting NO or a NO releasing substance as the final inhibitory NANC neurotransmitter in the canine LOS.
Animals↗
Release of nitric oxide upon stimulation of nonadrenergic noncholinergic nerves in the rat gastric fundus.
The possible role of nitric oxide (NO) as inhibitory nonadrenergic noncholinergic (NANC) neurotransmitter was studied in the rat gastric fundus. NO induced tetrodotoxin-resistant NANC relaxations in longitudinal muscle strips similar to those induced by electrical stimulation. Incubation with the stereospecific inhibitors of the NO biosynthesis NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (L-NNA) resulted in an increase of the basal tension which was reversed partly by L-arginine, but not by D-arginine. L-NMMA and L-NNA inhibited the relaxations to electrical stimulation, but not those induced by ATP, vasoactive intestinal polypeptide (VIP), norepinephrine or NO. This inhibitory effect was prevented by L-arginine, but not by D-arginine. In a second series of experiments, the gastric fundus served as donor tissue in a superfusion bioassay with de-endothelialized rings of rabbit aorta as detector tissue. The fundus released a labile factor with vasodilator activity upon electrical stimulation. This release was inhibited by tetrodotoxin and L-NNA, whereas it was increased by L-arginine. The biological activity was enhanced by superoxide dismutase and eliminated by hemoglobin. Our results indicate that NO is formed and released upon brief stimulation of the NANC nerves in the rat gastric fundus which is essential for the transient relaxations in this preparation. Therefore, we suggest NO or a NO releasing substance as inhibitory NANC transmitter in the rat gastric fundus.
Adenosine Triphosphate↗
Portal and pulmonary vessel thrombosis associated with systemic lupus erythematosus and anticardiolipin antibodies.
We describe a 26-year-old patient with systemic lupus erythematosus and pulmonary and portal hypertension associated with the presence of anticardiolipin antibodies. Postmortem histological examination revealed the presence of recent thromboses of pulmonary and portal vessels. Our findings further support the concept of pulmonary hypertension being part of the antiphospholipid syndrome and suggest that portal hypertension due to intrahepatic portal vein thrombosis might be another manifestation of this syndrome.
Adult↗
Non-adrenergic non-cholinergic relaxation mediated by nitric oxide in the canine ileocolonic junction.
The nature of the inhibitory non-adrenergic non-cholinergic (NANC) neurotransmitter was studied in circular muscle strips of the canine terminal ileum and ileocolonic junction. Nitric oxide (NO) induced tetrodotoxin-resistant NANC relaxation, similar to that induced by electrical stimulation or acetylcholine (ACh). Incubation with the stereospecific inhibitors of NO biosynthesis, NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (L-NNA), resulted in an increase of basal tension in the ileocolonic junction which was partly reversed by L-arginine but not by D-arginine. Moreover, L-NMMA and L-NNA, but not D-NMMA, concentration dependently inhibited the NANC relaxation in response to electrical stimulation and ACh, but not that in response to NO or nitroglycerin. This inhibitory effect was reversed by L-arginine but not by D-arginine. Hemoglobin reduced the NANC relaxation in response to electrical stimulation, ACh and nitroglycerin, and abolished the responses to NO. Our results suggest that NO or a NO releasing substance mediates the NANC relaxation in the canine terminal ileum and ileocolonic junction.
Animals↗
Nitric oxide as an inhibitory non-adrenergic non-cholinergic neurotransmitter.
Inhibitory non-adrenergic non-cholinergic (NANC) nerves are thought to be important in the autonomic innervation of the gastrointestinal tract and other organ systems. The nature of their neurotransmitter is still debated. Speculation that nitric oxide (NO), formed from L-arginine in neuronal structures and other cells, could act as a neurotransmitter, is not yet supported by demonstration of its release upon nerve stimulation. Using a superfusion bioassay, we report the release of a vasorelaxant factor upon stimulation of the NANC nerves in the canine ileocolonic junction. Several pieces of evidence, including the selectivity of the bioassay tissues, chemical instability, inactivation by superoxide anion and haemoglobin, inhibition by NG-nitro-L-arginine (L-NNA) and potentiation by L-arginine all indicated that NO accounted for the biological activity of this transferable NANC factor.
Animals↗