Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

Abstract

showed significantly less injury in rats that received ketamine than in rats that did not (2.35 ± 1.14 vs 4.58 ± 0.50, P < 0.0001). The distance traveled by a marker, expressed as percentage of total intestinal length, in rats that received pentobarbital sodium was 20% ± 2% in comparison with 25.9% ± 1.64% in rats that received ketamine (P = 0.017 INTRODUCTIONMesenteric ischemia is a clinical entity with a mortality rate between 60% and 100% that usually requires surgical resection of the necrotic intestinal segment [1] . Although there have been advancements in the treatment of ischemic injury, an ideal treatment has not been defined, and new options should be considered. A promising strategy is the use of anesthetic and sedative agents that might exert protective effects on the injured tissue. Ketamine is an agent that has been recommended for this purpose in clinical situations of sepsis, renal ischemia, cerebral ischemia and serious burn injuries [2][3][4] . The small intestine is very sensitive to ischemic insult [5] . Reperfusion causes additional damage through the release of free radicals, pro-inflammatory cytokines, leukotrienes and other related products [6] . Intestinal Abstract AIM: To investigate the effects of ketamine anesthesia on the motility alterations and tissue injury caused by ischemia/reperfusion in rats. METHODS: T h i r ty m a l e W i s t a r ra t s w e i g h i n g 200-250 g were used. Ischemia was induced by obstructing blood flow in 25% of the total small intestinal length (ileum) with a vascular clamp for 45 min, after which either 60 min or 24 h of reperfusion was allowed. Rats were either anesthetized with pentobarbital sodium (50 mg/kg) or ketamine (100 mg/kg). Control groups received sham surgery. After 60 min of reperfusion, the intestine was examined for morphological alterations, and after 24 h intestinal basic electrical rhythm (BER) frequency was calculated, and intestinal transit determined in all groups. RESULTS: The intestinal mucosa in rats that were anesthetized with ketamine showed moderate alterations such as epithelial lifting, while ulceration and hemorrhage was observed in rats that received pentobarbital sodium after 60 min of reperfusion. Quantitative analysis of structural damage using the Chiu scale

Ketamine reduces intestinal injury and inflammatory cell infiltration after ischemia/reperfusion in rats

“…19 The current study confi rmed those earlier fi ndings, and demonstrated that ketamine acts in a dose-dependent manner. Ischemia/reperfusion injury in the intestine and other tissues is thought to be mediated by the release of proinfl ammatory cytokines, induction of complement, leukocyte activity, increased vascular permeability, and loss of barrier function.…”

“…A previous study showed that total ketamine anesthesia reduced intestinal mucosal damage and motility alterations after I/R, in comparison to pentobarbital anesthesia. 19 The current study investigated the effects of pretreatment with various anesthetic and subanesthetic doses of ketamine on intestinal mucosal injury, infl ammatory cell infi ltration, and myenteric plexus neuron morphology.…”

Simvastatin nanoparticles attenuated intestinal ischemia/reperfusion injury by downregulating BMP4/COX-2 pathway in rats

“…-/NO 3 -content and dry/wet intestine ratios As shown in Figure 5D and E, NO 2 -/NO 3 -content in serum in I/R group rats was lower than that in the Sham group (P,0.01). 3 -content in serum in I/R group rats (P,0.01).…”

“…3 -content in serum in I/R group rats (P,0.01). Administration of simvastatin/PEG-b-PBLG 50 remarkably increased NO 2 -/NO 3 -content (12.3±0.65 μmol), which was remarkably greater than that in the I/R group (P,0.01); the dry/wet (D/W) intestine ratios in I/R groups rats were lower than those in Sham group (P,0.01). The D/W intestine ratios reached 3.08±0.06 in Sham group, whereas the D/W intestine ratios in I/R groups reached 6.25±0.09.…”

“…1,2 The mortality rates from II/RI are very high and reach more than 60% and it often requires clinical operation to cut off the necrotic intestinal segment. 3,4 It causes the tissue injury through inadequate blood and oxygen supply relative to cellular energy stores exhaustion, tissue metabolic disorder, and toxic metabolites accumulation in intestinal ischemia phase and leads to reactive oxygen species (ROS), inflammatory factors, calcium overload, and so on, mediating the further damage of intestine in reperfusion phase. 5 It is well known that oxygen supply reestablishment results in ROS production, causing lipid oxidation reaction in cell membranes, 6 and blood supply reestablishment leads to production of a lot of inflammatory factors to aggravate tissue injury and intestinal barrier dysfunction, and toxic metabolite products enter the systemic blood circulation and threaten life.…”