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J A Rodríguez Montes

Publications and source records attributed to J A Rodríguez Montes.

At least 19 recordsLinked to original sources

[Pathophysiology of neuromuscular impairments in the critically ill patient].

OBJECTIVE: to analyze the causes and manifestations of muscle weakness that critically ill patients develop during their staying at the ICU, and literature review. DEVELOPMENT: in the early 1980s, a mixed axonal polyneuropathy was described in septic critically ill patients, which clinically manifested by muscle weakness of variable severity, leading to quadriplegia and/or ventilator dependency in its most severe presentation. Almost at the same time, an acute intensive care myopathy was described in asthmatic patients admitted to the ICU for asthma exacerbation. Later on, this myopathy was also observed in transplanted, septic, or burnt patients. Several authors consider acute intensive care myopathy as the main cause of muscle weakness in the ICU. CONCLUSIONS: in this article, we describe the clinical presentation, etiopathogenesis, diagnosis, and treatment of polyneuropathy of the critically ill patient and of acute intensive care myopathy. Both clinical pictures may be differentiated, with neurophysiological studies and eventually muscle biopsy being of great help. Although some authors rather include these conditions under the name of polyneuromyopathy, we propose the general denomination of Acute Neuromuscular Syndrome of the Critically Ill Patient, a more descriptive term no presupposing a single mechanism or etiology.

Critical Illness↗

Trophic effects of neurotensin in massive bowel resection in the rat.

The trophic effect of the administration of exogenous neurotensin on the intestinal mucosa was studied in rats following an 80% bowel resection. Villus length and mucosal DNA content were assessed in the jejunal and ileal mucosa of the remnant intestine 14 days after resection. The data obtained in an 80% resected control group (80% group) and an experimental group receiving an infusion of neurotensin (300 micrograms/kg/day) for 14 days subcutaneously (80% + NT group) were compared. The results indicate that the administration of exogenous neurotensin (80% + NT) increases villus length (jejunum: 920 +/- 77 vs 861 +/- 25 microns and ileum length: 975 +/- 23 vs 875 +/- 99 microns) to an extent greater than that observed in the 80% resected group not receiving exogenous neurotensin. The levels of mucosal DNA per milligram of protein increased significantly in both groups but was paradoxically less in the 80% + NT group than in the 80% resection group (jejunum: 8.12 +/- 0.56 vs 10.18 +/- 0.80; ileum: 8.63 +/- 0.43 vs 10.05 +/- 0.46). These data suggest that the administration of exogenous neurotensin to the rat potentiates the growth of intestinal villi and accelerates the intestinal trophic response seen following massive bowel resection. The increase in circulating enteroglucagon levels noted after neurotensin administration (80% + NT: 547 +/- 48 pg/ml vs 80%: 341 +/- 41 pg/ml) suggests that some of the trophic effects of neurotensin may be mediated, at least in part, by enteroglucagon. These data also suggest a potential role for the use of neurotensin in the initial treatment of individuals with short bowel syndrome.

Adaptation, Physiological↗

Plasma enteroglucagon levels in different models of intestinal resection in the rat.

To assess the influence of the different intestinal segments on the plasma enteroglucagon level, three models of intestinal resection in the rat were studied (jejunal, ileal, 90%). The basal values for this peptide and those obtained after an infusion of intraduodenal glucose were compared. The results obtained in basal/post-glucose infusion were: 50% proximal (jejunum): 220/728 pg/ml; 50% distal (ileum): 10/233 pg/ml; and the middle 90%: 108/297 pg/ml. The glucose infusion produced a maximal response, permitting a better evaluation of the differences among the three resection models. The highest levels corresponded to the group in which the entire ileum was conserved.

Adaptation, Physiological↗