RESUMO
Spinal cord injury (SCI) is associated with severe autonomic changes, including inhibition of gastrointestinal (GI) motility. GI motility changes are known to affect electrolytes transport and these changes have not been adequately studied after SCI. We studied the ileal permeability to fluid and electrolytes in rats submitted to experimental spinal cord transection (SCT), between T4 and T5, throughout the first week after SCT. SCT increased ileal secretion of Na+ (P<0.05) and decreased the Cl(-) absorption during the first week post SCI (P<0.05). Water transport was also significantly altered, leading to increased water secretion following the Na+ gradient. Ileal secretion of K+ was significantly increased 1 and 7 days after spinal cord injury. To our knowledge, the present findings are the first direct evidence that SCT alters ileal electrolyte transport in rats. Further studies are necessary to evaluate the mechanisms involved in this phenomenon.
Assuntos
Eletrólitos/metabolismo , Íleo/fisiopatologia , Traumatismos da Medula Espinal , Análise de Variância , Animais , Transporte Biológico/fisiologia , Masculino , Ratos , Ratos Wistar , Traumatismos da Medula Espinal/metabolismo , Traumatismos da Medula Espinal/patologia , Traumatismos da Medula Espinal/fisiopatologia , Fatores de Tempo , Água/metabolismoRESUMO
The outcome of acute myocardial infarction (AMI) on gastrointestinal motor behavior was assessed in awake rats. Under anesthesia, they were submitted to thoracotomy followed or not by occlusion of the left coronary artery. Next day, they were gavage fed (1.5 ml) with phenol red in 5% glucose solution and sacrificed 10, 20, or 30 min later. Each subset consisted of 7 to 19 animals. Dye recovery in the stomach, proximal, mid, and distal small intestine was obtained by spectrophotometry. Infarcted left ventricle plus septum area was about 48.9 +/- 2.8, 55.1 +/- 6.7, and 54.1 +/- 8.1% (respectively, for 10-, 20-, and 30-min subsets). AMI increased gastric dye retention by 25.5, 51.3, and 65.1% (respectively, for 10-, 20-, and 30-min subsets), while it decreased mid small intestine retention at 30 min (45.3%) as well as distal retention at 10 min (90.5%) and 20 min (90%). A positive correlation (rS = 0.64) was found between infarcted area and gastric retention values at 10 min. AMI also increased (P < 0.05) central venous pressure values in all subsets (3.8 +/- 0.2 vs. -2.1 +/- 1.5, 1.4 +/- 0.1 vs. 0.5 +/- 0.2, and 1.6 +/- 0.4 vs. -0.2 +/- 0.3 cm H2O), while it decreased (P < 0.05) mean arterial pressure (95.0 +/- 2.6 vs. 110.0 +/- 3.9 and 106.0 +/- 2.0 vs. 113.0 +/- 3.0 mm Hg, respectively, at 10 and 30 min), and increased (P < 0.05) the 10-min heart rate values (429.6 +/- 11.3 vs. 374.0 +/- 19.8 bpm). Omeprazole pretreatment did not alter this phenomenon. In another group of rats, cardiac chemoreflex stimulation by i.v. phenylbiguanide increased gastric dye retention by 51.1%. In conclusion, AMI delays the gastric emptying and gastrointestinal transit of liquid in awake rats.