Nilce Mitiko Matsuda

The chronic gastrointestinal manifestations of Chagas disease

Chagas disease is an infectious disease caused by the protozoan Trypanosoma cruzi. The disease mainly affects the nervous system, digestive system and heart. The objective of this review is to revise the literature and summarize the main chronic gastrointestinal manifestations of Chagas disease. The chronic gastrointestinal manifestations of Chagas disease are mainly a result of enteric nervous system impairment caused by T. cruzi infection. The anatomical locations most commonly described to be affected by Chagas disease are salivary glands, esophagus, lower esophageal sphincter, stomach, small intestine, colon, gallbladder and biliary tree. Chagas disease has also been studied in association with Helicobacter pylori infection, interstitial cells of Cajal and the incidence of gastrointestinal cancer.

An AC biosusceptometer to study gastric emptying

A simple AC susceptometer was developed to study the gastric emptying when test meals labeled with 10% of a harmless magnetic tracer were ingested. The instrument allows the determination of T 1/2 of the stomach emptying with good precision compared to measurements with gamma camera and 99m Tc in the test meal.

Non-adrenergic non-cholinergic inhibition of gastrointestinal smooth muscle and its intracellular mechanism(s).

Relaxation of gastrointestinal smooth muscle caused by release of non‐adrenergic non‐cholinergic (NANC) transmitters from enteric nerves occurs in several physiologic digestive reflexes. Likely candidate NANC inhibitory agents include nitric oxide (NO), adenosine triphosphate (ATP), vasoactive intestinal peptide (VIP), pituitary adenylate cyclase‐activating peptide (PACAP), carbon monoxide (CO), protease‐activated receptors (PARs), hydrogen sulfide (H2S), neurotensin (NT) and beta‐nicotinamide adenine dinucleotide (β‐NAD). Multiple NANC transmitters work in concert, are pharmacologically coupled and are closely coordinated. Individual contribution varies regionally in the gastrointestinal tract and between species. NANC inhibition of gastrointestinal smooth muscle involves several intracellular mechanisms, including increase of cyclic guanosine monophosphate (cGMP), increase of cyclic adenosine monophosphate (cAMP) and hyperpolarization of the cell membrane via direct or indirect activation of potassium ion (K+) channels.

Budd-Chiari syndrome in a 25-year-old woman with Behçet's disease: a case report and review of the literature

IntroductionThe risk that patients with Behçets disease will develop thrombotic complications has been previously described. Although it is distributed worldwide, Behçets disease is rare in the Americas and Europe. Even though the pathogenic mechanisms of vascular complications of Budd-Chiari syndrome in patients with Behçets disease are unknown, severe vascular complications of Budd-Chiari syndrome associated with Behçets disease seem to affect mainly young men.The risk that patients with Behçets disease will develop thrombotic complications has been previously described. Although it is distributed worldwide, Behçets disease is rare in the Americas and Europe. Even though the pathogenic mechanisms of vascular complications of Budd-Chiari syndrome in patients with Behçets disease are unknown, severe vascular complications of Budd-Chiari syndrome associated with Behçets disease seem to affect mainly young men.Case presentationWe report a case of Budd-Chiari syndrome, a severe vascular complication that developed in a 25-year-old Afro-Brazilian woman with Behçets disease.ConclusionSevere vascular complications of Budd-Chiari syndrome in patients with Behçets disease are much more common in young adult male patients; we present a rare case of Budd-Chiari syndrome in a young Afro-Brazilian woman with Behçets disease.

Histoplasmosis in the nasal septum without pulmonary involvement in a patient with acquired immunodeficiency syndrome: case report and literature review

CONTEXT Histoplasmosis is a fungal disease caused by inhaling spores of the fungus Histoplasma capsulatum. The spores can be found in soil contaminated with bird, bat or chicken feces. Histoplasmosis occurs worldwide and is one of the most common pulmonary and systemic mycoses. CASE REPORT We report here the case of a 37-year-old man with acquired immune deficiency syndrome and histoplasmosis in the nasal septum, without pulmonary involvement, that evolved rapidly to disseminated infection, multiple organ failure and death.

Budd-Chiari syndrome in association with Behçet's disease: review of the literature

The risk that patients with Behçets disease may develop various thrombotic complications has been previously described. Although vascular complications from Budd-Chiari syndrome associated with Behçets disease have been described, the pathogenic mechanisms are still unknown. Severe vascular complications present in Budd-Chiari syndrome associated with Behçets disease are very common among young male adults. The objective of this study was to review the literature and present the association of Budd-Chiari syndrome with Behçets disease.

The effect of guanylate cyclase inhibitors on non-adrenergic and non-cholinergic neurogenic relaxations of the South American opossum lower esophageal sphincter

South American (SA) opossum lower esophageal sphincter (LES) circular smooth muscle relaxes by activation of enteric nerves elicited by EFS (electrical field stimulation, 0.5 ms, 48 V, 0.5–8 Hz for 10 s). The identity of the mediator released and the cellular mechanism, however, remain to be fully elucidated. The purpose of this study was to determine the effect of the enzyme soluble guanylate cyclase (cGC) inhibitors, cystamine (100 μm), methylene blue (30 μm), LY 83583 (6‐anilino‐5,8 quinoledione, 10 μm) and ODQ (H‐[1,2,4]oxadiazolo[4,3]quinoxalin‐1‐one, 1 μm) on the relaxations induced by EFS and by exogenous NO (nitric oxide, 0.5 mm) or NO‐donors on SA opossum LES smooth muscle strips. EFS caused frequency‐dependent relaxations, which were inhibited by NO‐synthase inhibitors and abolished by tetrodotoxin. Cystamine did not affect relaxations caused by EFS and NO or NO‐donor. Methylene blue also failed to affect EFS‐caused relaxations, although it was capable of inhibiting relaxation induced by NO. LY 83583 inhibited relaxations induced by NO, but did not affect those induced by EFS or by SNAP and HXA. ODQ abolished relaxations caused by EFS at lower frequencies and by HXA (hydroxylamine, 10 μm) and SNAP (S‐nitroso‐N‐acetyl penicillamine, 10 μm). Relaxations at higher frequencies of EFS and induced by SNP (sodium nitroprusside, 30 μm) and NO were only reduced by ODQ. These findings indicate that activation of the cGC can be involved in relaxations induced by EFS at lower frequencies, but other mechanisms can be involved at higher frequencies of EFS and caused by SNP or NO.

Heme-oxygenase-2 immunolabelling in pig jejunum

Heme-oxygenase-2 generates carbon monoxide in the enteric nervous system and in interstitial cells of Cajal in the canine, mouse and human jejunum. Carbon monoxide is considered a non-adrenergic and non-cholinergic inhibitory neurotransmitter and it establishes and maintains the resting membrane potential in the stomach and small intestine. The aim of this study was to determine the distribution of heme-oxygenase-2 in the enteric nervous system of the pig jejunum. Heme-oxygenase-2 immunoreactivity was found in neurons of myenteric ganglia and in nerve fibers in the circular and longitudinal muscle layers. These results suggest that carbon monoxide is produced in the enteric nervous system of the pig jejunum and might mediate inhibitory neural activity in myenteric ganglia and inhibitory neural input to smooth muscle cells in the circular and longitudinal muscle layers.

Effect of the effluent released from the canine internal mammary artery after intraluminal and extraluminal perfusion of acetylcholine and adenosine diphosphate

Segments of the canine internal mammary artery (35 mm in length) were suspended in vitro in an organ chamber containing physiological salt solution (95% O2/5% CO2, pH = 7.4, 37°C). Segments were individually cannulated and perfused at 5 ml/minute using a roller pump. Vasorelaxant activity of the effluent from the perfused internal mammary arteries was bioassayed by measuring the decrease in tension induced by the effluent of the coronary artery endothelium-free ring which had been contracted with prostaglandin F2α (2 × 10-6 M). Intraluminal perfusion of adenosine diphosphate (10-5 M) induced significant increase in relaxant activity in the effluent from the perfused blood vessel. However, when adenosine diphosphate (10-5 M) was added extraluminally to the internal mammary artery, no change in relaxant activity in the effluent was noted. In contrast, acetylcholine produced significant increase in the relaxant activity on the effluent of the perfused internal mammary artery with both intraluminal and extraluminal perfusion. The intraluminal and extraluminal release of endothelium-derived relaxing factor (EDRF) by acetylcholine (10-5 M) can be inhibited by site-specific administration of atropine (10-5 M). These experiments indicate that certain agonists can induce the release of EDRF only by binding to intravascular receptors while other agonists can induce endothelium-dependent vasodilatation by acting on neural side receptors.