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Biomedical subjects

A Salas

Publications and source records attributed to A Salas.

At least 109 records · Page 6Linked to original sources
PubMed1994

Phosphatidylcholines as mediators of adaptive cytoprotection of the rat duodenum.

BACKGROUND/AIMS: Surfactant phospholipids impede diffusion of acid through the gastric mucus, but their relevance in the defense of the duodenum against luminal acid is not known. METHODS: Duodenal resistance to acid was tested in anesthetized rats by instillation of HCl using a tube implanted in the proximal duodenum. The effects of a detergent (Brij 35; Sigma, St. Louis, MO) and a lipid mixture flushed through the luminal surface on duodenal resistance to acid were studied. The lipid content in the mucus and the effects of acid, prostaglandins, and indomethacin on the lipid layer were also analyzed. RESULTS: Instillation of 100 mumol HCl or 5 micrograms/kg 16,16-dimethyl prostaglandin E2 increased resistance to acid, preventing duodenal lesions induced by 500 mumol HCl. However, 100 mumol HCl or 16,16-dimethyl prostaglandin E2 did not prevent lesions induced by 500 mumol HCl in rats undergoing perfusions with 5% Brij 35. Indomethacin suppressed acid-induced protection. A mixture of tripalmitin and dipalmitoyl-phosphatidylcholine protected against 500 mumol HCl, and the effect was also observed in rats receiving indomethacin. Finally, 100 mumol HCl increased the phosphatidylcholine content in the duodenal mucus but not in rats receiving 5% Brij 35 or indomethacin. CONCLUSIONS: Surface-active phospholipids are critical for adaptive cytoprotection to acid in the rat duodenum.

16,16-Dimethylprostaglandin E2↗
PubMed1994

Localized fibrous tumor of the pleura: immunohistochemical and flow-cytometric DNA study.

This report describes three cases of localized fibrous tumor of the pleura (LFTP) with clinical and pathological differences. Case 1 presented with symptoms; the tumor size was 6.5 cm and it was attached to the lung and chest wall; histologically it was composed of spindle cells with pleomorphism, mitoses, hemorrhage and necrosis. Cases 2 and 3 were casual findings and consisted of well-circumscribed tumors of 3 and 8.5 cm, respectively; histologically both showed hypocellularity. All cases exhibited positive stains for vimentin and negative for keratin. These results, added to histological features, suggested a mesenchymal origin. Flow cytometry quantitation of DNA disclosed a diploid pattern in all three cases with a small "near diploid" cell population additionally in Case 1; the S-phase fraction was low in all cases. These findings, that could be considered favourable prognostic signs, and the complete tumoral resection performed in the three tumors, could explain the absence of recurrences after 32, 27 and 19 months, respectively.

Aged↗
PubMed1994

Abnormal leukotriene C4 released by unaffected jejunal mucosa in patients with inactive Crohn's disease.

The mucosal release of inflammatory mediators is enhanced in active inflammatory bowel disease. This study examines whether leukotriene C4 production occurs in apparently unaffected segments of the gut. The intraluminal release of leukotriene C4 was determined by jejunal perfusion in seven healthy controls, in nine patients with chronic ulcerative colitis, and in 13 patients with Crohn's disease (six with ileal disease, and seven with only colonic). All patients were in clinical remission and none of them had evidence of jejunal involvement. Mild intraluminal irritation with a 2.5 mmol/l deoxycholic acid solution was induced to stimulate local inflammatory mechanisms. The release of DNA (a marker of mucosal desquamation) and prostaglandin E2 (PGE2) was simultaneously measured. Jejunal release of DNA was higher in Crohn's disease patients than in ulcerative colitis or healthy controls. Basal release of PGE2 was similar in the three groups of patients. Basal release of leukotriene C4 was considerably enhanced, however, in Crohn's disease patients compared with healthy controls. In ulcerative colitis patients, basal leukotriene C4 release was non-significantly different from controls. Bile acid perfusion stimulated PGE2, leukotriene C4, and DNA release in all groups studied, but leukotriene C4 release was significantly higher in Crohn's disease patients. It is concluded that in inactive Crohn's disease there is an enhanced intraluminal release of leukotriene C4 in apparently unaffected segments of proximal small bowel, which may reflect fundamental changes in the function of the gut mucosal barrier.

Adult↗
PubMed1994

Role of intestinal microflora in chronic inflammation and ulceration of the rat colon.

Bacteria and their products stimulate inflammatory responses. The effects of different antimicrobial regimens (amoxicillin/clavulanic acid, tobramycin, imipenem, vancomycin, metronidazole) were investigated on the course of experimental colitis induced by trinitrobenzenesulphonic acid (TNB) in the rat. On day 7 and 21 after the induction of colitis, matched groups of control and antibiotic treated rats were subjected to colonic dialysis to measure eicosanoid release, and killed for morphological assessment of the colonic lesions (macro and microscopic scores). Stool samples were cultured. Selective antibiotic treatment against Gram positive, Gram negative or anaerobic bacteria had no effect on colonic lesion scores. By contrast, certain broad spectrum antibiotics (amoxicillin/clavulanic acid or the association of imipenem plus vancomycin) significantly reduced macro and microscopic scores. Rats receiving these antibiotics did not develop chronic colitis as shown by the virtual absence of colonic strictures, adhesions, fibrosis, and granulomas. On day 21 after TNB, the intracolonic release of prostaglandin E2, thromboxane B2, and leukotriene B4 was significantly higher in control than in antibiotic treated rats. Control stool cultures showed abundant colony forming units of both aerobic and anaerobic bacteria. Amoxicillin/clavulanic acid and imipenem plus vancomycin induced appreciable reductions in luminal bacteria. In conclusion, certain broad spectrum antibiotics prevent chronic colitis. The normal colonic flora seems to play an important pathogenetic part in the progression of inflammatory colonic lesions to chronicity.

Animals↗
PubMed1994

[Nitric oxide and Hirschsprung's disease: a causal relation biochemically, immunohistochemically and functionally demonstrated].

UNLABELLED: Hirschsprung's disease may be due to impaired nonadrenergic-noncholinergic inhibitory input in the aganglionic segment of the colon. It has been suggested that nitric oxide (NO) might be the lacking neurotransmitter. Thus, our specific aims were to determine in ganglionic and aganglionic segments: 1. The activity of the NO synthetase (NO-S); 2. The location of this enzyme; and 3. The "in vitro" basal motor activity of the muscle strips and their responses to an NO donor and to an NO antagonist. METHODS: NO synthetase activity was quantified in samples of tissue from both aganglionic and ganglionic segments obtained during surgery in 6 patients with Hirschsprung's disease by the transformation of 14C-L-arginine into 14C-L-citrulline in tissue homogenates. Immunohistochemical staining of the tissues was performed using a polyclonal antibody raised against a peptide sequence of rat brain NO synthetase. Furthermore, in 2 patients we measured "in vitro" the tonic response of muscle strips to an exogenous NO donor (sodium nitroprusside) and to an NO antagonist (L-NAME). RESULTS: NOS activity was undetectable in every aganglionic segment whereas it was present in all ganglionic segments (0.49 +/- 0.09 pmol citrulina/mg.min; mean +/- SE). Immunohistochemically, NO-S was absent in the myenteric plexus of aganglionic segments and it was present in ganglionic segments. "In vitro" basal motor activity of ganglionic segments was normal, with presence of low-frequency contractions (LFC) and summation contraction (SC); in aganglionic segments SC were absent. Sodium nitroprusside induced a marked relaxation (90% from basal) in muscle strips, both aganglionic and ganglionic, precontracted with bethanocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Arginine↗
PubMed1994

[The control of arterial hypertension in primary care: the evaluation of a program of self-care].

OBJECTIVE: To evaluate the efficacy of a self-care hypertension programme within primary care. DESIGN: Two models of intervention by means of self-care were compared, both using individual education and family support, with one of them using group education. SETTING AND PATIENTS: All those attending 10 health centres in Andalucía and who had a recent diagnosis of light or moderate Hypertension or with their hypertension not monitored over the preceding 6 months, were included. MEASUREMENTS AND MAIN RESULTS: These 160 people were assigned at random to the intervention group (group education) or the control group (individual education). Data analysis provided the results for the 95 people who completed the study. Both systolic and diastolic arterial pressure (SAP and DAP) diminished significantly during the study period, both in the sample as a whole and in the intervention group. However, the lessening of systolic pressure only reached statistically significant differences in the control group. Over the study period, the lessening of SAP was 6.2 in the intervention group and 8.0 in the control group; whereas the lessening of DAP was 7.0 in the intervention group and 2.3 in the control group. CONCLUSIONS: Arterial hypertension can be controlled in primary care by health education for self-care. On the basis of this study's findings, it is not valid to conclude that group is more efficacious than individual education.

Adult↗
PubMed1994

[Considerations regarding the treatment of non-aganglionic congenital intestinal neuropathies].

Hyperganglionosis or neuronal intestinal dysplasias (NID) and hypoganglionosis (HO) are intestinal diseases of difficult diagnosis and treatment and diverse evolution, despite identical histologic findings. The aim of this study was to discuss the therapeutic problems derived from the patients differing clinical course. Retrospective review of 14 patients with regard to diagnosis, manometry and histology (hematoxylin-eosin, acetylcholinesterase activity, immunohistochemistry and Smith's silver stain) was done. Six patients presented intestinal occlusion or sub-occlusion from the first months of life with impeded oral feeding. Ileostomy was performed in 5 and total colectomy with anastomosis in 1. All patients required parenteral nutrition; cisapride was added in 2. Three died from sepsis (3 NID). Of the 3 survivors, 2 have ileostomies (2 NID) and the other ileo-rectal anastomosis (NID). Of the remaining patients, two presented aganglionism and the finding of proximal hyperganglionism occurred post-surgery. Surgery was repeated in one patient. The remaining 6 (1 HO, 5 NID) were diagnosed between 3 and 10 years of age because of constipation. Four are under treatment with cisapride and 2 required partial colic resection. No relationship can be established between histologic findings and clinical manifestations. In chronic clinical courses, treatment with cisapride and cleaning enemas should be tried first. Acute clinical pictures (occlusion-sub occlusion) should be treated by decompressive ileostomy. Partial colic resection may lead to new intestinal failure.

Anastomosis, Surgical↗
PubMed1993

[Extrabronchial small-cell carcinoma: apropos 6 cases].

Extrabronchial small cell carcinoma (ESCC) is an infrequent tumor with controversial histogenesis, clinical evolution and therapeutic strategy. The aim of this study was to know the immunohistochemical features and the clinical evolution of patients diagnosed of ESCC during a 10 year period. All the diagnoses of small cell carcinoma (bronchial and extrabronchial) carried out by the Unit of Pathology between 1980-1989 were reviewed. In all the ESCC an immunohistochemical study was performed with three neuroendocrine markers, chromogranin, neurospecific enolase and synaptophysin. The clinical evolution of the patients is described. The 6 patients with ESCC represented 4.7% of all the small cell carcinomas. The primary localization was: parotid, urinary bladder, the skin, maxillary sinus and esophagus (2 patients). In five cases positivity was observed for one or more of the neuroendocrine markers. In two cases the ESCC was associated with differentiated cell populations (squamous carcinoma). The diagnosis of ESCC logically obliges the bronchial origin and the presence of ectopic hormonal secretion syndromes to be discarded. The administration of chemotherapy regimes used in small cell lung carcinoma is advised.

Aged↗
PubMed1993

Polyostotic coexisting fibrous dysplasia and aneurysmal bone cyst of the chest wall.

A case of a 39-year-old woman with a palpable mass in the right hemithorax is presented. The mass had been growing during the last 16 years. Radiographs and computed tomography showed two lesions in the right thoracic wall: the greater was in the anterior and lateral portion of the 7th rib, the minor lesion in the 6th rib costovertebral joint. Both lesions were surgically removed. Histological examination demonstrated the association of fibrous dysplasia and aneurysmal bone cyst in the two lesions. The coexistence of these two lesions supports the theory that aneurysmal bone cyst may represent a secondary change due to haemodynamic alterations of the vascular bed caused by fibrous dysplasia.

Adult↗
PubMed1993

Patients with achalasia lack nitric oxide synthase in the gastro-oesophageal junction.

The abnormal function of the lower oesophageal sphincter in achalasia is likely to be due to impaired nonadrenergic, noncholinergic (NANC) inhibitory input. Since recent studies in animals suggest that nitric oxide (NO) is implicated physiologically in the inhibitory responses of the lower oesophageal sphincter, we have investigated whether the synthesis of NO is altered in the gastro-oesophageal junction of patients with achalasia. NO synthase activity was investigated in samples of tissue from the gastro-oesophageal junction obtained during surgery in eight patients with typical achalasia and six non-achalasic controls who underwent oesophagectomy for reasons other than sphincter dysfunction. The NO synthase activity was determined by the transformation of 14C-L-arginine into 14C-L-citrulline in tissue homogenates. In addition, immunohistochemical staining of the tissues was performed using a polyclonal antibody raised against a peptide sequence of rat brain NO synthase. Furthermore, the relaxant response to an exogenous NO donor (sodium nitroprusside, SNP) was measured in vitro in muscle strips obtained from two patients with achalasia and in two non-achalasic controls. NO synthase activity was detected in each of the samples obtained from six control patients (0.59 +/- 0.21 pmol mg-1 min-1; mean +/- SE). By contrast, none of the samples obtained from the eight patients with achalasia had any detectable NO synthase activity. Immunohistochemical studies confirmed the presence of NO synthase in the myenteric plexus of the gastro-oesophageal junction of control patients and its absence in achalasia. SNP relaxed muscle strips precontracted with bethanechol in both control samples and those from patients with achalasia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Influence of dietary fat on duodenal resistance to acid.

Three experimental diets were prepared from a standard formula plus pure oleic, linoleic, or eicosapentaenoic acid (2% by weight). Mucosal resistance to acid was tested in anaesthetised rats fed the experimental diets for at least four weeks (60 rats per diet) by duodenal infusion of HCl (200 to 700 mumol) 30 minutes after pretreatment with either saline or 100 mumol HCl (used as a mild irritant). Rats were killed one hour after the test and the duodenal damage was assessed 'blindly' using a combined macroscopic and histological score. Differences were tested by analysis of covariance of the dose-response curves. Mucosal resistance was similar in the three groups when the acid challenge was given after saline pretreatment. Resistance to acid in all three groups was significantly increased by previous exposure to 100 mumol HCl (p < 0.01). Interestingly, rats fed a linoleic or eicosapentaenoic supplemented diet after pretreatment with HCl developed significantly higher resistance to acid than those fed the diet with oleic acid (p < 0.05). Pretreatment with indomethacin suppressed the difference between diets. In conclusion, dietary polyunsaturated fatty acids enhance duodenal resistance to acid by potentiation of adaptive cytoprotection.

Animals↗
PubMed1993

Adaptive cytoprotection of the rat duodenum is not dependent on nitric oxide-induced changes in blood flow.

Mild irritation of the rat duodenum enhances mucosal resistance to acid via a prostaglandin-mediated mechanism. Prostaglandins increase mucosal blood flow, but it is not known whether such changes in blood flow significantly contribute to adaptive cytoprotection. We induced blood flow changes by manipulating the arginine-nitric oxide pathway, which is independent from prostaglandin synthesis, and determined the resulting effects on the cytoprotective response. In anesthetized rats, we tested the effects of intraduodenal infusion of mild acid on duodenal blood flow and on the prevention of mucosal damage by subsequent strong acid in control, indomethacin-pretreated, and NG-nitro-L-arginine-pretreated rats (NG-nitro-L-arginine inhibits the nitric oxide synthase). Additional experiments tested the effects of the prostaglandin analogue 16,16-dimethyl-prostaglandin (PG) E2 or sodium nitroprusside (nitric oxide donor) on duodenal blood flow and on mucosal protection against acid. Exposure of the duodenal mucosa to mild acid increased duodenal blood flow and mucosal resistance to acid. Instillation of 16,16-dimethyl-PGE2 also increased blood flow and mucosal resistance to acid. However, sodium nitroprusside increased blood flow without increasing mucosal resistance to acid, and NG-nitro-L-arginine inhibited the change in blood flow induced by acid while preserving the adaptive cytoprotection phenomenon intact. In conclusion, adaptive cytoprotection of the duodenal mucosa appears to be independent of changes in blood flow.

16,16-Dimethylprostaglandin E2↗
PubMed1993

[Transesophageal echocardiography in the diagnosis of aortic dissection].

INTRODUCTION AND OBJECTIVE: Eighty-two patients with suspected aortic dissection were studied to assess the usefulness of transesophageal echocardiography in the diagnosis of this entity. METHODS: All patients underwent transesophageal echocardiogram. The diagnosis of aortic dissection was established in 46 patients by other diagnostic procedures including angiography and computed tomography, surgery and necropsy. RESULTS: The sensitivity and specificity of transesophageal echocardiography were 98% and 97%, respectively. By computed tomography, sensitivity was 92% and specificity 88%. By angiography, sensitivity and specificity were 97% and 93%, respectively. In the diagnosis of the dissection type, transesophageal echocardiography classified correctly in 98%, computed tomography in 89% and angiography 97% of cases. Transesophageal echocardiography visualized the tear in 82% of cases, and angiography in 53%. CONCLUSIONS: Transesophageal echocardiography provides rapid, accurate diagnosis of aortic dissection and permits the initiation of appropriate treatment. Angiography is indicated in non-conclusive cases or those which supra-aortic involvement clinically suspected.

Acute Disease↗
PubMed1992

[Intestinal dysmotility-pseudo-obstruction].

Chronic intestinal pseudo-obstruction is defined as a syndrome related to any process which affects intestinal regulation and propulsion. Its origin may be muscular, neurogenic or hormonal, excluding Hirschsprung's disease or any known mechanical obstruction. Between 1989 and 1991, 11 patients with intestinal pseudo-obstruction were studied at our centre, and included nine hyperganglionisms B, and two hypoganglionisms) and two visceral myopathies (Berdon's syndrome). Diagnosis was established in all cases by histologic study. The techniques of haematoxylin-eosin, acetylcholinesterase, enolase, protein S-100 and Smith were used in neuropathies and haematoxylin-eosin and Masson's trichromic in myopathies. Intestinal motility was studied by ano-rectal and gastrointestinal manometry in seven and three cases respectively. Gastrointestinal manometry and radiology permitted differentiation of localized and diffuse forms of involvement. Medical treatment consisted of total parenteral nutrition when oral feeding was impossible, and in five cases, cisapride was given, with good results in four. Derivative surgery was performed in cases of diffuse involvement, and resection with anastomosis in those of localized forms. We conclude that: 1. Diagnosis is established according to histologic criteria. 2. Complementary examinations should be directed towards distinguishing localized from diffuse involvement. 3. Cisapride was effective in the treatment of neuropathies in the majority of cases.

Female↗
PubMed1992

Duodenal mucosal resistance to intraluminal acid in the rat: role of adaptive cytoprotection.

The duodenal mucosa is normally challenged by intermittent exposure to acid because of periodic gastric emptying. We studied the mechanisms of duodenal adaptation to acid in anesthetized rats. A polyvinyl chloride tube passing through a ligated pylorus was used for duodenal pulse instillations of 1 mL of saline or acid (100 or 400 mumols HCl) at 30-minute intervals. Duodenal lesions were blindly assessed using a combined macroscopic and histological score. Mucosal damage after exposure to saline or 100 mumols HCl was negligible in intact, vagotomized, and indomethacin-pretreated rats, whereas 400 mumols induced noticeable macroscopic and microscopic lesions. Interestingly, in intact and vagotomized rats, previous exposure to a 100-mumols HCl bolus significantly prevented mucosal damage by a subsequent 400-mumols bolus. This effect was not observed in indomethacin-pretreated rats. In these rats, however, intraduodenal instillation of exogenous 16,16-dimethyl prostaglandin E2 (16,16-dm-PGE2) prevented the damage induced by 400 mumols of HCl. A second protocol investigated the luminal release of bicarbonate and PGE2 in response to intraduodenal perfusion with 100 mumols of HCl. Duodenal bicarbonate release was stimulated by acid in all groups, whereas the release of PGE2 increased in intact and vagotomized rats but not in the indomethacin-pretreated group. In summary, these data suggest that adaptive cytoprotection plays a significant role in protecting the duodenal mucosa from acid. Vagal innervation and bicarbonate release do not appear to be as critical as cyclo-oxygenase activity for this mechanism.

16,16-Dimethylprostaglandin E2↗