ABSTRACT
To study whether treatment with heparin (HEP) attenuates intestinal dysfunction caused by ischemia (I) and reperfusion (R), rats were treated with HEP (100 U/kg intravenously) or saline solution (SS) before I (60 min), which was produced by occlusion of the superior mesenteric artery, and R (120 min). After I or I/R, we mounted 2-cm jejunal segment in an organ bath to study neurogenic contractions stimulated by electrical pulses or KCl, using a digital recording system. Thin jejunal slices were stained with hematoxylin and eosin for optical microscopy. Compared with the sham group, jejunal contractions were similar in the I + HEP and the I/R + HEP groups, but reduced in the I + SS and the I/R + SS groups. The jejunal enteric nerves were damaged in the I + SS and the I/R + SS, but not in the I + HEP and the I/R + HEP cohorts. These results suggested that HEP attenuated intestinal dysfunction caused by I and I/R.
Subject(s)
Gastrointestinal Agents/pharmacology , Heparin/pharmacology , Jejunum/blood supply , Jejunum/drug effects , Reperfusion Injury/prevention & control , Animals , Cytoprotection , Disease Models, Animal , Electric Stimulation , Enteric Nervous System/drug effects , Enteric Nervous System/physiopathology , Gastrointestinal Motility/drug effects , Jejunum/innervation , Jejunum/pathology , Jejunum/physiopathology , Male , Potassium Chloride/pharmacology , Rats , Rats, Wistar , Reperfusion Injury/pathology , Reperfusion Injury/physiopathologyABSTRACT
To study whether ischemic preconditioning (IPC) attenuated intestinal dysfunction caused by ischemia (I) and reperfusion (R), rats were underwent 60 minutes of I which was produced by occlusion of the superior mesenteric artery, and/or 120 minutes R. The IPC group had the I procedure previously stimulated for 5 minutes and the R for 10 minutes. IPC and sham groups were injected with saline solution (SS) via the femoral vein 5 minutes before the I and R, and for R. After I or I/R, 2-cm jejunal segments were mounted in an organ bath to study neurogenic contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained with hematoxylin and eosin for optical microscopy. Compared with the sham group, jejunal contractions were similar in the IPC + I and the IPC + I/R groups, but reduced in the I + SS and the I/R + SS groups. The jejunal enteric nerves were damaged in the I + SS and the I/R + SS groups, but not in the IPC groups. These results suggested that ischemic preconditioning attenuated intestinal dysfunction caused by I and I/R.
Subject(s)
Ischemic Preconditioning , Jejunum/blood supply , Reperfusion Injury/prevention & control , Animals , Disease Models, Animal , Electric Stimulation , Enteric Nervous System/physiopathology , Gastrointestinal Motility , Jejunum/drug effects , Jejunum/innervation , Jejunum/pathology , Jejunum/physiopathology , Male , Potassium Chloride/pharmacology , Rats , Rats, Wistar , Reperfusion Injury/pathology , Reperfusion Injury/physiopathologyABSTRACT
To examine whether treatment with L-arginine (ARG), a substrate of nitric oxide biosynthesis, attenuated intestinal dysfunction caused by ischemia (I) and reperfusion (R), we treated rats with ARG (100 mg/kg intravenously) or saline solution (SS) before 60 minutes of I produced by occlusion of the superior mesenteric artery and/or during 120 minutes of R. After I or I/R, we isolated 2-cm jejunal segments for mounting in an organ bath to study neurogenic contractions stimulated by electrical pulses or KCl with the use of a digital recording system. Thin jejunal slices were stained with hematoxylin and eosin for optical microscopy. Jejunal contractions were similar in the sham and I+ARG, but reduced in I+SS, I/R+SS, and I/R+ARG groups. Jejunal enteric nerves were damaged in I+SS, IR+SS, and IR+ARG, but not in the I+ARG group, suggesting that ARG attenuate intestinal dysfunctions due to I but not to R.
Subject(s)
Arginine/pharmacology , Gastrointestinal Agents/pharmacology , Jejunum/blood supply , Jejunum/drug effects , Reperfusion Injury/drug therapy , Animals , Cytoprotection , Disease Models, Animal , Electric Stimulation , Enteric Nervous System/drug effects , Enteric Nervous System/physiopathology , Gastrointestinal Motility/drug effects , Jejunum/innervation , Jejunum/pathology , Jejunum/physiopathology , Male , Potassium Chloride/pharmacology , Rats , Rats, Wistar , Reperfusion Injury/pathology , Reperfusion Injury/physiopathologyABSTRACT
To study whether treatment with adenosine (ADO), an agonist of adenosine receptors, attenuates intestinal dysfunction caused by ischemia (I) and reperfusion (R), we treated rats with ADO (15 mg/kg or saline solution (SS) intravenously before 60 minutes occlusion of the superior mesenteric artery (I) and/or 120 minutes after its release (R). After I or I/R, isolated jejunal segments (2 cm) were mounted in an organ bath to study nerve-mediated contractions stimulated by electrical pulses or KCI with the use of a digital recording system. Thin jejunal slices were stained with hematoxylin and eosin for optical microscopy. Compared with the sham group, jejunal contractions were reduced in I+SS and IR+SS but similar after treatment with ADO (I+ADO and IR+ADO groups). We concluded that rat jejunal enteric nerves were damaged in I+SS and IR+SS but not in the I+ADO and IR+ADO groups. These results suggested that ADO attenuated intestinal dysfunction due to I and R.
Subject(s)
Adenosine/pharmacology , Gastrointestinal Agents/pharmacology , Jejunum/blood supply , Jejunum/drug effects , Reperfusion Injury/prevention & control , Animals , Cytoprotection , Disease Models, Animal , Electric Stimulation , Enteric Nervous System/drug effects , Enteric Nervous System/physiopathology , Gastrointestinal Motility/drug effects , Jejunum/innervation , Jejunum/pathology , Jejunum/physiopathology , Potassium Chloride/pharmacology , Rats , Rats, Wistar , Reperfusion Injury/pathology , Reperfusion Injury/physiopathologyABSTRACT
To study whether treatment with the beta-blocker atenolol (AT) attenuates intestinal dysfunction caused by ischemia (I) and reperfusion (R), rats were treated with AT (1.5 mg · kg(-1), intravenously) or saline solution (SS) prior to I (60 minutes), which was produced by occlusion of the superior mesenteric artery, and/or R (120 minutes). After I or I/R, 2-cm jejunal segments were mounted in an organ bath to study neurogenic contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained with hematoxylin and eosin for optical microscopy analysis. Compared to the sham group, jejunal contractions were similar in the I + AT and the I/R + AT groups, but reduced in the I + SS and the I/R + SS groups. The jejunal enteric nerves were damaged in the I + SS and the I/R + SS groups, but not in the I + AT and the I/R + AT. These results suggest that AT may attenuate intestinal dysfunction caused by I and I/R.
Subject(s)
Adrenergic beta-1 Receptor Antagonists/pharmacology , Atenolol/pharmacology , Gastrointestinal Agents/pharmacology , Jejunum/blood supply , Jejunum/drug effects , Reperfusion Injury/prevention & control , Animals , Cytoprotection , Disease Models, Animal , Electric Stimulation , Enteric Nervous System/drug effects , Enteric Nervous System/physiopathology , Gastrointestinal Motility/drug effects , Jejunum/innervation , Jejunum/pathology , Jejunum/physiopathology , Male , Potassium Chloride/pharmacology , Rats , Rats, Wistar , Reperfusion Injury/pathology , Reperfusion Injury/physiopathologyABSTRACT
To study whether treatment with L-arginine (ARG), a substrate of nitric oxide biosynthesis, attenuates intestinal dysfunction caused by ischemia (I) and reperfusion (R), rabbits treated with ARG (100 mgxkg(-1), intravenously) or saline solution (SS) prior to I (60 minutes) by occlusion of superior mesenteric artery and/or during R (120 minutes). After I or I/R, 2-cm jejunal segments were isolated and mounted in an organ bath to study of neurogenic contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained (hematoxylin and eosin) for analysis by optical microscopy. Compared to the sham group, jejunal contractions were similar in I + ARG, but reduced in I + SS, I/R + SS, and I/R + ARG groups. The jejunal enteric nerves were damaged in I + SS, I/R + SS, and I/R + ARG, but not in I + ARG group, suggesting that ARG can attenuate intestinal dysfunctions due to I, but not to R.
Subject(s)
Arginine/pharmacology , Intestines/blood supply , Nitric Oxide/biosynthesis , Reperfusion Injury/prevention & control , Animals , Arginine/therapeutic use , Blood Circulation , Femoral Vein/physiology , Gastrointestinal Motility/drug effects , Gastrointestinal Motility/physiology , Ischemia/physiopathology , Jejunum/blood supply , Jejunum/drug effects , Jejunum/pathology , Mesenteric Artery, Superior/physiology , Rabbits , Reperfusion/adverse effects , Reperfusion Injury/physiopathologyABSTRACT
To study whether treatment with the beta-blocker atenolol (AT) attenuates intestinal dysfunction caused by ischemia (I) and reperfusion (R), rabbits were treated with AT (1 mg.kg(-1), introvenously) or saline solution (SS) prior to I (60 minutes), which was produced by occlusion of the superior mesenteric artery, and/or R (120 minutes). After I or I/R, 2-cm jejunal segments were mounted in an organ bath to study neurogenic contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained hematoxylin and eosin for analysis by optical microscopy. Compared to the sham group, the jejunal contractions were similar in the I + AT and the I/R + AT groups, but reduced in the I + SS and the I/R + SS groups. The jejunal enteric nerves were damaged in the I + SS and the I/R + SS groups, but not in the I + AT and the I/R + AT. These results suggest that AT may attenuate intestinal dysfunction caused by I and I/R.
Subject(s)
Atenolol/therapeutic use , Intestinal Diseases/drug therapy , Intestines/blood supply , Jejunum/physiology , Reperfusion Injury/drug therapy , Animals , Blood Circulation , Electric Stimulation , Intestinal Diseases/etiology , Jejunum/blood supply , Jejunum/drug effects , Male , Mesenteric Artery, Superior/physiology , Muscle Contraction/drug effects , Muscle Contraction/physiology , Potassium Chloride/pharmacology , RabbitsABSTRACT
To study if the treatment with adenosine (ADO), an agonist of adenosine receptors, attenuates intestinal dysfunction caused by ischemia (I) and reperfusion (R), we treated rabbits with ADO (15 mg x kg(-1), intravenously) or saline solution (SS) to I (60 minutes) before occlusion of superior mesenteric artery and/or R (120 min). After I or I/R, isolated jejunal segments (2 cm) were mounted in an organ bath to study nerve-mediated contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained (hematoxylin and eosin) for analysis by optical microscopy. Compared to the sham group, the jejunal contractions were similar in I + ADO, but reduced in I + SS, I/R + SS, and I/R + ADO groups. We concluded that the jejunal enteric nerves were damaged in I + SS, I/R + SS, and I/R + ADO, but not in I + ADO group. These results suggested that ADO attenuated intestinal dysfunction due to I, but not to R.
Subject(s)
Adenosine/pharmacology , Intestines/blood supply , Reperfusion Injury/drug therapy , Animals , Blood Circulation , Electric Stimulation , Femoral Vein/drug effects , Femoral Vein/physiology , Jejunum/blood supply , Jejunum/drug effects , Jejunum/physiology , Male , Mesenteric Artery, Superior/physiology , Muscle Contraction/drug effects , Muscle Contraction/physiology , Potassium Chloride/pharmacology , Purinergic P1 Receptor Agonists , Rabbits , Sodium Chloride/pharmacologyABSTRACT
To study whether treatment with L-nitro-arginine methyl ester (L-NAME), an inhibitor of nitric oxide biosynthesis, attenuates intestinal dysfunction caused by ischemia (I) and/or reperfusion (R), rabbits were treated with L-NAME (15 mgxkg(-1), intervenously) or saline olution (SS) prior to I (60 minutes) induced by occlusion of superior mesenteric artery and/or R (120 minutes). After I or I/R, isolated jejunal segments (2 cm) were mounted in an organ bath to study nerve-mediated contractions stimulated by electrical pulses or KCI using a digital recording system. Thin jejunal slices were stained (hematoxylin and eosin) for analysis by optical microscopy. Compared with a sham group, the jejunal contractions were similar in the I/R + L-NAME, but reduced in I + SS, I/R + SS, and I + L-NAME groups. The jejunal enteric nerves were damaged in the I + SS, I/R + SS, and I + L-NAME cohorts, but not among the I/R + L-NAME cohort. These results suggested that L-NAME attenuated intestinal dysfunction caused by R but not by I.
Subject(s)
Gastrointestinal Motility/drug effects , Intestinal Diseases/prevention & control , NG-Nitroarginine Methyl Ester/pharmacology , Reperfusion Injury/prevention & control , Reperfusion Injury/physiopathology , Animals , Electric Stimulation , Ischemia/physiopathology , Jejunum/drug effects , Jejunum/innervation , Jejunum/physiology , Male , Muscle Contraction/drug effects , Muscle Contraction/physiology , Rabbits , Sodium Chloride/pharmacologyABSTRACT
To study whether treatment with 5'-adenosine triphosphate (ATP), an agonist of P2 purine receptors, attenuated intestinal dysfunction caused by ischemia (I) and/or reperfusion (R), rabbits were treated with ATP (15 mgxkg(-1), intravenously) or saline solution (SS) 60 minutes before I by occlusion of the superior mesenteric artery and/or R (120 minutes). After I or I/R isolated 2-cm jejunal segments were mounted in an organ bath to study nerve-mediated contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained (hematoxylin and eosin) for optical microscopy. Compared to a sham group, the jejunal contractions were similar to sham hosts among I + ATP, but reduced in I + SS, I/R + SS, and I/R + ATP groups. The jejunal-enteric nerves were damaged in I + SS, I/R + SS, and I/R + ATP, but not the I + ATP group. These results suggested that ATP attenuated intestinal dysfunction produced by I, but not that caused by R.
