Heparin and hyperbaric oxygenation in enteric autonomic neuron preservation for transplant.

BACKGROUND: Previous studies have suggested that the addition of heparin to a preservation solution attenuated the autonomic dysfunction observed in rat jejunum and in addition that hypothermic hyperbaric oxygenation may play a role as a preservation technique. However, these studies did not address the lesion indices of the autonomic enteric neurons. We sought to investigate whether the autonomic enteric neurons are injured during cold ischemic preservation and whether administration of heparin or hyperbaric oxygenation prevents this lesion. METHODS: Jejunal segments (2 cm; n = 20) of Wistar rats (12-16 weeks old) were maintained in lactated Ringer's solution without or with heparin (H- and H+, respectively) at 4 degrees C under normobaric conditions. Other jejunal segments (n = 10) were maintained at 4 degrees C in H- under hyperbaric oxygenation conditions (HBO). After preservation for 12 hours, H-, H+, and HBO preparations fixed in 10% formaldehyde were stained with hematoxylin and eosin. The lesion indices were expressed as the mean number of affected neurons (karyorhexis, nuclear dislocation, cytoplasmic vacuolisation) per 100 neurons present in intramural ganglia. Statistical analysis was performed using the Mann-Whitney test (P < .05). RESULTS: The histologic studies showed that enteric autonomic neurons were damaged in H- jejunal segments. The lesion indices observed were: karyorhexis 90/100, nuclear dislocation 85/100, and cytoplasmic vacuolization 82/100. The autonomic neurons in H+ and HBO segments seemed to be normal and significantly well-preserved (P < .001). CONCLUSION: Hypothermic hyperbaric oxygenation and heparin prevented lesions in cold ischemic preservation of enteric autonomic neurons.

Role of purines on hepatic ischemia-reperfusion lesions in rabbit.

In this work, we evaluate the effects of adenosine 5' triphosphate (ATP) on hepatic lesions caused by ischemia/reperfusion (I/R) in liver rabbit. Rabbits were pretreated with ATP (15 mg/kg IV) or saline solution 0.9% (SS), before the hepatic I/R procedure. We evaluated the effects of ATP on hepatic injury before and after I/R. The warm hepatic I/R procedure caused profound acute liver injury, as indicated by elevated serum aspartate aminotransferase, alanine aminotransferase, and lactic dehydrogenase levels, as well as a high apoptotic cell count. All these changes were attenuate by ATP treatment before the hepatic I/R procedure. These results suggested that ATP exerted protective effects on hepatic I/R lesions in the rabbit. This ATP effect may be related to improved energy metabolism during reperfusion in ischemic livers protecting against functional damage of cellular and subcellular membranes during lipid peroxidation.

l-Arginine supplementation protects against hepatic ischemia-reperfusion lesions in rabbits.

We evaluated the effects of a substrate in the biosynthesis of nitric oxide (NO)-l-arginine (LARG)-on hepatic lesions caused by ischemia/reperfusion (I/R) injury in rabbit livers. Rabbits were pretreated with LARG (150 mg/kg IV) or saline solution 0.9% (SS) before the hepatic I/R procedure. The effects of LARG on hepatic injury were evaluated before and after I/R. The warm hepatic I/R procedure produced profound acute liver injury, as indicated by elevated values of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic dehydrogenase (LDH), as well as a high apoptotic cell count. All changes were attenuated by treatment with LARG before the hepatic I/R procedure. These results suggested that LARG produced protective effects on hepatic I/R lesions. This protective effect of LARG was probably associated with blocking generation of superoxide anions during the hepatic I/R procedure.

Effects of allopurinol on ischemia and reperfusion in rabbit livers.

In this work, we evaluated the effects of allopurinol (ALO), an inhibitor of xanthine oxidase (XO), on hepatic lesions caused by ischemia/reperfusion (I/R) in the rabbit liver. Rabbits were pretreated with ALO (10 mg/kg IV) or saline solution 0.9% before the hepatic I/R procedure. The effects of ALO on hepatic injury were evaluated before and after I/R. A standard, warm hepatic I/R procedure caused profound acute liver injury, as indicated by elevated serum aspartate aminotransferase, alanine aminotransferase, and lactic dehydrogenase levels, as well as a high apoptotic cell count. All of these changes were reversed by the administration of ALO before the hepatic I/R procedure. In conclusion, ALO exerted protective effects on hepatic I/R lesions. This protective effect of ALO was probably associated with blocking the generation of superoxide anions during the hepatic I/R procedure by inhibiting XO activity.

Protective effects of heparin on hepatic ischemia and reperfusion lesions in rabbits.

Because the role of heparin (HEP) in hepatic ischemia/reperfusion (I/R) injury is still not fully understood, we investigated the effects of treatment with HEP on hepatic I/R injury in rabbits. For I/R procedures, the portal vein and hepatic artery were occluded by a metallic clamp to promote ischemia. The clamp was removed after 30 minutes to allow reperfusion. Rabbits undergoing the I/R procedure were treated with HEP (100 U/kg) or saline solution 0.9% (SS). When compared with levels before I/R, the serum aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase, levels were increased by the hepatic I/R procedure, among rabbits treated with SS or HEP. However, the increase in these enzymes was lower among rabbits treated with HEP. Histologic analysis of hepatic tissue of rabbits undergoing I/R and treated with SS showed marked lesions in the central lobule with significant inflammatory infiltration. In contrast, a significant reduction in lesions caused by I/R was observed in the livers of rabbits treated with HEP. After starting reperfusion, we visualized apoptotic cells with nuclear staining among rabbits submitted to I/R and treated with SS, but not those treated with HEP. These results suggested that HEP was able to attenuate hepatic lesions caused by I/R in the livers of rabbits.

Evidence for the participation of calcium in non-genomic relaxations induced by androgenic steroids in rat vas deferens.

BACKGROUND AND PURPOSE: Androgens cause non-genomic relaxation in several smooth muscle preparations. However, such an effect has not been investigated in rat vas deferens yet. Our purpose was to study the effect of testosterone and derivatives in this tissue. EXPERIMENTAL APPROACH: The influence of androgens was tested on contraction and translocation of intracellular Ca(2+) induced by KCl in rat vas deferens in vitro. KEY RESULTS: The testosterone derivative 5alpha-dihydrotestosterone produced a rapid and reversible concentration-dependent relaxation of KCl-induced contractions. Other androgens were also effective, showing the following rank order of potency: androsterone >5beta-dihydrotestosterone >androstenedione >5alpha-dihydrotestosterone >testosterone. Calcium-induced contractions were also inhibited (about 45%) by 5alpha-dihydrotestosterone (30 microM). Moreover 5alpha-dihydrotestosterone blocked the increase of intracellular Ca(2+) induced by KCl, measured by the fluorescent dye fura-2. Relaxation to 5alpha-dihydrotestosterone was resistant to the K(+) channel antagonists glibenclamide, 4-aminopyridine and charybdotoxin. It was not affected by removal of epithelium or by L-NNA (300 microM), an inhibitor of nitric oxide biosynthesis, nor by selective inhibitors of soluble guanylate cyclase, ODQ or LY 83583, indicating that nitrergic or cGMP mediated mechanisms were not involved. The androgen-induced relaxation was also not blocked by the protein synthesis inhibitor cycloheximide (300 microM) or by the classical androgen receptor flutamide (up to 100 microM), corroborating that the effect is non-genomic. CONCLUSIONS AND IMPLICATIONS: Testosterone derivatives caused relaxation of the rat vas deferens, that did not involve epithelial tissue, K(+) channels, or nitric oxide-dependent mechanisms, but was related to a partial blockade of Ca(2+) influx.

Autonomic dysfunction of rat jejunum submitted to cold ischemic preservation is prevented by heparin.

Previous studies suggest that cold ischemic preservation (CIP) employed in small bowel transplantation promotes loss of intestinal motility due to severe lesions in autonomic enteric nerves. This autonomic dysfunction may be prevented by antioxidant agents. In this work, we investigated whether preservation with heparin prevented autonomic dysfunction of rat jejunum submitted to CIP for a long time. Jejunal segments (2 cm) of Wistar rats (12 to 16 weeks old) were preserved at 4 degrees C in Ringer's lactate solution without (-) or with (+) 100 UI/mL heparin (H). After preservation for 12 hours, H+ and H- preparations were mounted in parallel in isolated organ baths containing 10 mL Tyrode's solution at 37 degrees C for the study of neurogenic contractions evoked by electrical field stimulation (EFS; 10-30 Hz, 1-ms duration, 60 V) or by stimulation of nicotinic (NIC) or muscarinic (carbachol, CCh) cholinoceptors. The effects of NIC (hexamethonium, HEX) and muscarinic (atropine, ATR) antagonists were studied on these contractions. Contractions induced by EFS (30 Hz) were four times greater in H+ (1.02 +/- 0.12 g) versus H- (0.26 +/- 0.07 g), while contractions induced by NIC (1 mmol/L) were also four times higher in H+ (1.07 +/- 0.10 g) than H- (0.25 +/- 0.09 g) preparations. In addition, contractions induced by CCh (1 mmol/L) were two times higher in H+ (1.21 +/- 0.13 g) than in H- (0.65 +/- 0.10 g). EFS, NIC, and CCh contractions were inhibited by pretreatment of jejunum with HEX or ATR (1 mumol/L/30 min), in H+ and H-. These results indicated that addition of heparin to a preservation solution attenuated the autonomic dysfunction of rat jejunum submitted to CIP for a long time.

Atenolol attenuates autonomic dysfunction of rat jejunum submitted to cold ischemic preservation.

In vitro studies have demonstrated that cold ischemic preservation (CIP) employed in small bowel transplantation produces loss of intestinal motility due to severe lesions of autonomic enteric nerves and that this autonomic dysfunction is attenuated by antioxidant agents. In this work, we investigated whether preservation with atenolol attenuated autonomic dysfunction of rat jejunum submitted to long-term CIP. Jejunal segments (2 cm) of Wistar rats (12 to 16 weeks old) were surgically isolated and preserved at 4 degrees C in Ringer's lactate solution without (-) or with (+) 1 mumol/L atenolol (AT). After preservation for 12 hours, AT+ and AT- preparations were mounted in parallel in isolated organ baths containing 10 mL Tyrode's solution at 37 degrees C for the study of neurogenic contractions evoked by electrical field stimulation (EFS; 10 to 30 Hz, 1-ms duration, 60 V) or by stimulation with nicotinic (nicotine, NIC) or muscarinic (carbachol, CCh) cholinoceptor agents as well as nicotine (hexamethonium, HEX) and muscarinic (atropine, ATR) antagonists. Contractions induced by EFS (30 Hz) were 46% higher in AT+ (0.38 +/- 0.02 g) than AT- (0.26 +/- 0.01 g), while contractions induced by NIC (1 mmol/L) were 84% higher in AT+ (0.46 +/- 0.03 g) than in AT- (0.25 +/- 0.02 g). In addition, contractions induced by CCh (1 mmol/L) were 34% higher in AT+ (0.87 +/- 0.06 g) than in AT- (0.65 +/- 0.08 g). EFS-, NIC-, and CCh-induced contractions were inhibited by pretreatment of jejunum with HEX or ATR (1 mumol/30 min), in AT+ and AT-. These results suggest that addition of atenolol in the preservation solution attenuated autonomic dysfunction of rat jejunum submitted to long-term CIP.

Use of hyperbaric oxygenation in small bowel preservation for transplant.

INTRODUCTION: The aim of this work was to study the effects of hyperbaric oxygenation as a preservation technique for small bowel transplantation. METHODS: Twenty 2-month-old male Wistar rats weighting 250 g were divided into two groups: group A (n = 10) in which the small bowel was preserved for 12 hours, and group B (n = 10) in which the small bowel was preserved for 24 hours. After vascular and intraluminal perfusion, 3-cm segments were maintained in Ringer's solution at temperatures between 2 degrees C to 4 degrees C and in normobaric O2 conditions (groups A1, B1) or conditioned in an hyperbaric O2 metal chamber (100% oxygen at 5.5 absolute atmospheres) (groups A2, B2). After this preservation time, we studied intestinal tissue injury and morphometric analysis of the villi. RESULTS: Mucosal injury was significantly greater among group A1 compared to group A2 animals. The grade of the lesions was greater among group B1 compared to group B2 animals. Group A1 showed no difference from Group B1. For lesion grade, the range was smaller in group A2 and group B2 animals. The villi height was significantly smaller in groups A1 and B1 compared to the other groups; whereas it was higher in group A2 as compared with B2. CONCLUSION: Hyperbaric oxygenation may play a role as a preservation technique. Further research is necessary.

Epilepsy-induced electrocardiographic alterations following cardiac ischemia and reperfusion in rats.

The present study evaluated electrocardiographic alterations in rats with epilepsy submitted to an acute myocardial infarction (AMI) model induced by cardiac ischemia and reperfusion. Rats were randomly divided into two groups: control (n=12) and epilepsy (n=14). It was found that rats with epilepsy presented a significant reduction in atrioventricular block incidence following the ischemia and reperfusion procedure. In addition, significant alterations were observed in electrocardiogram intervals during the stabilization, ischemia, and reperfusion periods of rats with epilepsy compared to control rats. It was noted that rats with epilepsy presented a significant increase in the QRS interval during the stabilization period in relation to control rats (P<0.01). During the ischemia period, there was an increase in the QRS interval (P<0.05) and a reduction in the P wave and QT intervals (P<0.05 for both) in rats with epilepsy compared to control rats. During the reperfusion period, a significant reduction in the QT interval (P<0.01) was verified in the epilepsy group in relation to the control group. Our results indicate that rats submitted to an epilepsy model induced by pilocarpine presented electrical conductivity alterations of cardiac tissue, mainly during an AMI episode.

Low dihydropyridine receptor density in vasa deferentia of castrated rats.

Radioligand binding studies in crude membrane preparations of vasa deferentia of normal rats, with the 1,4-dihydropyridine (+)-[3H]-PN200-110 (isradipine) showed typical saturation isotherms. The binding exhibited a KD of 259 +/- 60 pM and Bmax of 144 +/- 20 fmol mg-1 protein. The low KD and the stereoselective displacement of (+)-[3H]-PN200-110 binding by (+)- and (-)-PN200-110 and by nifedipine suggests that these tissues contain dihydropyridine receptors probably coupled to voltage-sensitive, L-type calcium channels. In membrane preparations from vasa deferentia from rats castrated 30 days previously the maximum specific binding was 25 +/- 10 fmol mg-1 protein, representing only 11% of total binding; thus, the calculation of reliable KD values was not feasible. These findings suggest that a testicular hormone, possibly testosterone, plays an important role in the regulation of dihydropyridine-sensitive, voltage-dependent calcium channels in the rat vas deferens.

Down-regulation of Na(+)/K(+)-ATPase alpha(2) isoform in denervated rat vas deferens.

In the rat vas deferens, an organ richly innervated by peripheral sympathetic neurons, we have demonstrated recently the expression of alpha(1) and alpha(2), but not alpha(3) isoforms of the alpha subunit of Na(+)/K(+)-ATPase (EC 3.6.1.37), a membrane-bound enzyme of vital function for living cells (Noël et al., Biochem Pharmacol 55: 1531-1535, 1998). In the present work, we characterized, qualitatively and quantitatively, Na(+)/K(+)-ATPase alpha isoforms in denervated rat vasa deferentia. [(3)H]Ouabain binding at concentrations defined for high-affinity isoforms (alpha(2) and/or alpha(3)) detected only one class of specific binding sites in control (C) and denervated (D) vas deferens. Although the dissociation constant was similar for both groups [K(d) = 138 +/- 14 nM (C) and 125 +/- 8 nM (D)], a marked decrease in density was observed after denervation [716 +/- 81 fmol.mg protein(-1) (C) and 445 +/- 34 fmol.mg protein(-1) (D), P < 0.05]. In addition, western blotting revealed that denervated vasa deferentia produce the alpha(1) and alpha(2) isoforms but not alpha(3), just as we reported for the controls previously (Noël et al., Biochem Pharmacol 55: 1531-1535, 1998). Densitometric analysis showed a decrease of the alpha(2) isoform by about 40% in denervated organs, in very good agreement with what was shown with the [(3)H]ouabain binding technique, but no significant change in alpha(1) isoform density. Truncated alpha(1) (alpha(1)T), an isoform suggested to exist in the guinea pig vas deferens, was not detected. Altogether, our results demonstrated that Na(+)/K(+)-ATPase alpha(2) is down-regulated after sympathetic denervation of the rat vas deferens.

Quantitative analysis of the high-affinity binding sites for [3H]ouabain in the rat vas deferens and their immunological identification as the alpha 2 isoform of Na+/K(+)-ATPase.

Binding assays were performed with [3H]ouabain to investigate the presence of, and to characterize, a Na+/K(+)-ATPase isoform with high affinity for cardiac glycosides in the rat vas deferens. Nonlinear regression analysis of equilibrium experiments carried out with crude preparations in a Mg-Pi medium indicated the presence of high-affinity sites characterized with good precision (individual coefficients of variation = 11-35%) by their density (Bmax = 0.42 to 0.72 pmol/mg protein) and dissociation constant (Kd = 0.069 to 0.136 microM) values. The values of the dissociation rate constant (kappa-1) and the association rate constant (kappa+1) for these sites were 0.151 to 0.267 min-1 and 2.87 to 3.60 microM-1.min-1, respectively. A higher number of low-affinity sites (Kd around 15 microM), supposed to correspond to the alpha 1 isoform, was also identified, but their Kd and Bmax values were not quantified precisely in this crude preparation. Western blot assays indicated hybridization with specific anti-alpha 1 and anti-alpha 2 isoform antibodies but not with anti-alpha 3 isoform antibody. Taken together, the present results indicate the existence of a low proportion of the alpha 2 isoform of Na+/K(+)-ATPase in the rat vas deferens that can be quantified precisely by [3H]ouabain binding even in a crude membrane preparation that is suitable for studies under conditions of plasticity.

Increased density of alpha-adrenoceptors in vas deferens of spontaneously hypertensive rats (SHR), indicated by functional and receptor binding studies.

Pharmacological parameters were determined from contractile responses mediated by alpha-adrenoceptors in vas deferens from spontaneously hypertensive rats (SHR) and corresponding normotensive controls, Wistar Kyoto rats (WKY), and compared with data obtained from radioligand binding assays. Contractile responses induced in longitudinal and circular muscle layers by the alpha-adrenoceptor agonist noradrenaline (NA) and by barium chloride were recorded as described previously. In both muscle layers the maximal effects induced by NA, but not by BaCl2, were significantly greater in SHR. As a consequence, the relative responsiveness ratio (rho) for the alpha-adrenoceptor was also larger for SHR than for WKY. NA-induced contractions of both muscle layers were competitively antagonized by indoramine. The pA2 values for indoramine and pD2 values for NA were the same in SHR and WKY, indicating that alpha-adrenoceptor affinity was not changed in SHR. Additionally, binding studies with the alpha-adrenoceptor ligand [3H]WB4101 revealed that Bmax values were greater in the vas deferens of SHR, whereas Kd values were not significantly different from those of WKY controls. In summary, although differences could not be detected for affinity-related parameters, a greater density of alpha-adrenoceptors was shown for SHR in receptor binding studies and this was corroborated by functional studies.

A double perfusion system with two-channel recording for the simultaneous study of the contractile responses of the circular and longitudinal smooth muscle layers of the rat vas deferens.

A device for double perfusion of the vas deferens externally and through the lumen is described in detail. The perfusion system allows the simultaneous recording of drug-induced or spontaneous contractions of the circular and longitudinal smooth muscle layers of the organ. Isometric contractions of the longitudinal (external) layer are recorded through a tension transducer. The contractions of the circular (internal) smooth muscle layer are recorded as changes of the pressure of internal perfusion. Therefore, four different effects can be recorded for a given concentration of agonist by combining the variables related to the route of perfusion (external or internal) and type of muscle (longitudinal or circular). In addition, antagonism or synergism can be studied by simultaneously perfusing a second drug. Results can be expressed as single records or as mean concentration-response curves from which drug-receptor parameters can be directly or indirectly obtained. The importance of employing this method for the analysis of some less usual problems related to the mechanism of drug action is discussed.

Study of heparin in intestinal ischemia and reperfusion in rats: morphologic and functional evaluation.

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.

Effect of ischemic preconditioning on injuries caused by ischemia and reperfusion in rat intestine.

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.

Study of L-arginine in intestinal lesions caused by ischemia-reperfusion in rats.

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.

Effect of adenosine on injury caused by ischemia and reperfusion in rats: functional and morphologic study.

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.

Atenolol to treat intestinal ischemia and reperfusion in rats.

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.