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Purpose: We investigated the effects of ischemia/reperfusion in the intestine (I/R-i) on purine receptor P2X2-immunoreactive (IR) neurons of the rat ileum.Methods: The superior mesenteric artery was occluded for 45 min with an atraumatic vascular clamp and animals were sacrificed 4 h later. Neurons of the myenteric and submucosal plexuses were evaluated for immunoreactivity against the P2X2 receptor, nitric oxide synthase (NOS), choline acetyl transferase (ChAT), calbindin, and calretinin.Results: Following I/R-i, we observed a decrease in P2X2 receptor immunoreactivity in the cytoplasm and surface membranes of neurons of the myenteric and submucosal plexuses. These studies also revealed an absence of calbindin-positive neurons in the I/R-i group. In addition, the colocalization of the P2X2 receptor with NOS, ChAT, and calretinin immunoreactivity in the myenteric plexus was decreased following I/R-i. Likewise, the colocalization between P2X2 and calretinin in neurons of the submucosal plexus was also reduced. In the I/R-i group, there was a 55.8% decrease in the density of neurons immunoreactive (IR) for the P2X2 receptor, a 26.4% reduction in NOS-IR neuron, a 25% reduction in ChAT-IR neuron, and a 47% reduction in calretinin-IR neuron. The density of P2X2 receptor and calretinin-IR neurons also decreased in the submucosal plexus of the I/R-i group. In the myenteric plexus, P2X2-IR, NOS-IR, ChAT-IR and calretinin-IR neurons were reduced in size by 50%, 49.7%, 42%, and 33%, respectively, in the I/R-i group; in the submucosal plexus, P2X2-IR and calretinin-IR neurons were reduced in size by 56% and 72.6%, respectively.Conclusions: These data demonstrate that ischemia/reperfusion of the intestine affects the expression of the P2X2 receptor in neurons of the myenteric and submucosal plexus, as well as density and size of neurons in this population. Our findings indicate that I/R-i induces changes in P2X2-IR enteric neurons that could result in alterations in intestinal motility. [ABSTRACT FROM AUTHOR]

The atrial natriuretic peptide (ANP) is a peptide hormone that is mainly produced in the cardiocytes of the atria and auricles, where it is stored within secretory granules. The aim of the present work was to analyze the effects of pre- and postnatal protein malnutrition on weight gain, the size of the heart and the number and sizes of the ANP-granules in the cardiocytes of the rat’s right auricle. This study was conducted on 21-day-old rats from mothers exposed to 73% protein restriction during the gestation and lactation and on age-matched control animals. At this stage, both control and protein-deprived animals were killed by a lethal intraperitonial injection of sodic pentobarbital. The weight and the size of the heart were determined and ANP-granules of auricular cardiocytes were examined by transmission electron microscopy and ultrastructural morphometry. Protein deprivation of the mother throughout pregnancy, and the mother and unweaned rat pups in the first 21 postnatal days reduced the weights of pups to about 60% of the normally fed group. The weight and size of the heart were also reduced, by about 50%. Despite this, perinatal malnutrition did not significantly affect the numbers of ANP-granules/field in the cardiocytes. However, there was a small but significant reduction in the sizes of granules. It is concluded that ANP-granules are protected from loss even when there is a substantial reduction in body weight and organ size caused by protein deprivation. [ABSTRACT FROM AUTHOR]

The early responses of the myocardium ultrastructure under thyroid dysfunction conditions, hemodynamic parameters, cardiac hypertrophy and ultrastructural evaluations were performed in hypothyroid and hyperthyroid rats submitted to different doses [T4-25 and T4-100; 0.025 mg and 0.1 mg kg(-1) body weight (BW).per day, respectively)]. All groups were treated for 7 days. The animals were sacrificed, the hearts were excised and weighed and the left ventricle tissue samples were processed for transmission election microscopy. Systolic blood pressure (SBP) was not altered by administration of T4. An increased heart rate and ratio of heart weight to body weight (HW/BW) were found in the hyperthyroid rats. However, the SBP and HW/BW decreased significantly in hypothyroid rats. No significant ultrastructural alterations were detected when the hypothyroid and T4-25 groups were compared with the control group. Alterations of cardiomyocytes nuclei of these groups were also not detected. Notably, disorganization of intercellular junctions was observed in many cardiomyocytes of T4-100 group. The present results indicate that in the early stages of hyperthyroidism, the cardiac hypertrophy development was mainly due to direct effects of thyroid hormone. Despite cardiac hypertrophy development, there is no ultrastructural evidence of myocardial degeneration. [ABSTRACT FROM AUTHOR]