Abstract
Small intestinal strangulation associated with ischaemia-reperfusion injury (IRI) is common in horses. In laboratory animals IRI can be ameliorated by ischaemic preconditioning (IPC) and pharmacological preconditioning (PPC) with dexmedetomidine. The aim of this study was to determine the effect of PPC with dexmedetomidine or IPC in an equine model of small intestinal ischaemia-reperfusion (IR). In a randomized controlled experimental trial, 15 horses were assigned to three groups: control (C), IPC, and PPC with dexmedetomidine (DEX). All horses were placed under general anaesthesia and 90% jejunal ischaemia was induced for 90 minutes, followed 30 minutes of reperfusion. In group IPC, three short bouts of ischaemia and reperfusion were implemented, and group DEX received a continuous rate infusion of dexmedetomidine prior to the main ischaemia. Jejunal biopsies were collected before ischaemia (P), and at the end of ischaemia (I) and reperfusion (R). Mucosal injury was assessed by the Chiu-Score, inflammatory cells were stained by cytosolic calprotectin. The degree of apoptosis and cell necrosis was assessed by cleaved-caspase-3 and TUNEL. Parametric data were analyzed by two-way ANOVA for repeated measurements followed by Dunnetts t-test. Non parametric data were compared between groups at the different time points by a Kruskal-Wallis-Test and a Wilcoxon-2-Sample-test. The mucosal injury score increased during I in all groups. After reperfusion, IRI further progressed in group C, but not in IPC and DEX. In all groups the number of cleaved caspase-3 and TUNEL positive cells increased from P to I. The number of TUNEL positive cells were lower in group DEX compared to group C after I and R. Infiltration with calprotectin positive cells was less pronounced in group DEX compared to group C, whereas in group IPC more calprotectin positive cells were seen. In conclusion, IPC and DEX exert protective effects in experimental small intestinal ischaemia in horses.
Highlights
Colic is one of the most common causes of death in horses [1,2]
The end-expiratory isoflurane concentrations to maintain an adequate depth of anaesthesia were 1.5 (0.05) vol %, 1.5 (0.1) vol % and 1.4 (0.1) vol % in group C, Ischaemic preconditioning (IPC) and DEX, respectively, with a significant difference between IPC and DEX (p = 0.04)
ischaemia/reperfusion injury (IRI) further progressed in group C (p = 0.010)
Summary
Colic is one of the most common causes of death in horses [1,2]. Even though the management of these patients has improved in the last decades, small intestinal strangulations with concurrent ischaemia/reperfusion injury (IRI), are still associated with a relatively high mortality rate after surgery [3]. The concept of IPC was first reported in 1986, where it was shown that brief periods of ischaemia reduced the myocardium infarct size in dogs to 25% of that seen in the control group [7]. The first involves the activation of pre-existing effector molecules like prosurvival kinases Akt and ERK-1/2 [8]. The latter emerges after 12–24 hours and relies on the expression of distal mediators such as iNOS, HSP and COX-2 [9]. Many authors have reported beneficial effects of preconditioning in different experimental models for IRI, including the small intestine [10,11]. The implementation of IPC has not been documented in horses
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