The effect of ketamine on acute muscular ischaemia reperfusion in rats

Salman, A. Ebru; Dal, Didem; Salman, M. A.; İskit, Alper B.; Aypar, Ülkü

doi:10.1017/s0265021505001171

Cited by 16 publications

(9 citation statements)

References 24 publications

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“…Hct 10 % (CA1: 11,44 ± 2,52; cortex: 13,65 ± 2,31) que dans le groupe Hct 20 % (CA1 : 8,29 ± 1,31 ; cortex : 10,68 ± 1,24 ; P < 0,05) …”

Section: Discussionunclassified

“…In the present study, we developed a HCA model using rats, which was designed to mirror clinical circulatory arrest to the greatest extent possible. 11 As with other related rodent models, 23,24 we used chloral hydrate as the primary anesthetic. Our findings provide convincing evidence that low Hct worsens cerebral injury after prolonged HCA.…”

Section: Discussionmentioning

confidence: 99%

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Un niveau réduit d’hématocrite aggrave les lésions cérébrales après un arrêt circulatoire hypothermique prolongé chez le rat

Wang

Zheng

et al. 2006

Can J Anesth/J Can Anesth

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Purpose: This study tests the hypothesis that low hematocrit (Hct) worsens cerebral injury after prolonged hypothermic circulatory arrest (HCA) in rats, and the mechanism involves variable expression of the genes C-Fos, Bcl-2 and Bax.Methods: A rat HCA model was developed, and 40 animals were randomly assigned to four groups: Sham (sham) group, or Hct groups of Hct 10%, Hct 20% and Hct 30%. After 90 min of HCA at 18°C, physiologic variables were recorded and brain morphological changes were evaluated with light and electron microscopy. Expressions of C-Fos, Bcl-2, Bax in various brain areas were measured by the reverse transcriptase polymerase chain reaction and standard immunohistochemistry techniques. Results:The number of injured neurons in the hippocampus CA1 and parietal cortex in the Hct 10% group (CA1: 11.44 ± 2.52; cortex: 13.65 ± 2.31) exceeded the mean number of injured neurons in the Hct 20% group (CA1: 8.29 ± 1.31; cortex: 10.68 ± 1.24; P < 0.05) and the Hct 30% group. Mean mitochondrial injury scores were greatest at lower Hct levels, while the expression of C-Fos and Bax were highest in the Hct 10% group and lowest in the Hct30% group (P < 0.05). In contrast, the expression of the Bcl-2 mRNA was greatest in the Hct 30% group (P < 0.05). Conclusion:Low Hct worsens cerebral injury after prolonged HCA and CPB in rats, which may relate in part to the variable expression of the genes C-Fos, Bcl-2 and Bax. Hct 10 % (CA1: 11,44 ± 2,52; cortex: 13,65 ± 2,31) que dans le groupe Hct 20 % (CA1 : 8,29 ± 1,31 ; cortex : 10,68 ± 1,24 ; P < 0,05) Méthode : Un modèle d'ACH a été développé chez le rat et on a réparti de façon aléatoire 40 animaux dans quatre groupes : un groupe sans intervention et des groupes Hct de 10 %, 20 % et 30 %. Après un ACH pendant 90 min à 18°C, on a mesuré les variables physiologiques et on a évalué les changements morphologiques dans le cerveau avec la microscopie optique et électronique. On a mesuré l'expression de C-Fos, Bcl-2 et Bax dans différentes régions du cerveau par la réaction en chaîne transcriptase inverse -polymérase et par des techniques habituelles d'immunohistochimie. Résultats : Les neurones CA1 de l'hippocampe et du cortex pariétal ont été atteints en plus grand nombre dans le groupe

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“…Hct 10 % (CA1: 11,44 ± 2,52; cortex: 13,65 ± 2,31) que dans le groupe Hct 20 % (CA1 : 8,29 ± 1,31 ; cortex : 10,68 ± 1,24 ; P < 0,05) …”

Section: Discussionunclassified

Section: Discussionmentioning

confidence: 99%

Un niveau réduit d’hématocrite aggrave les lésions cérébrales après un arrêt circulatoire hypothermique prolongé chez le rat

Wang

Zheng

et al. 2006

Can J Anesth/J Can Anesth

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“…Ketamine has shown protective properties on I/R injury of the brain, 15 kidney, 16 skeletal muscle, 17 and heart, 18 among other tissues. A previous study showed that total ketamine anesthesia reduced intestinal mucosal damage and motility alterations after I/R, in comparison to pentobarbital anesthesia.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2010

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“…Ketamine is a parenteral anesthetic that non-competitively blocks the NMDA receptor [9] . It has been shown that ketamine protects various tissues from I/R injury, such as brain [10] , myocardium [11] and skeletal muscle [12] . To the best of our knowledge, no previous studies have evaluated the effects of ketamine on intestinal motility impairment and tissue damage induced by I/R.…”

Section: Introductionmentioning

confidence: 99%

Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

Cámara¹,

Guzmán²,

Barrera³

et al. 2008

WJG

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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

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The effect of ketamine on acute muscular ischaemia reperfusion in rats

Abstract: Ketamine was found to attenuate acute ischaemia-reperfusion injury in muscle tissue in rats (muscular protective). Ketamine may attenuate lipid peroxidation in muscle tissue in tourniquet-requiring manoeuvres.

Cited by 16 publications

References 24 publications

Un niveau réduit d’hématocrite aggrave les lésions cérébrales après un arrêt circulatoire hypothermique prolongé chez le rat

Un niveau réduit d’hématocrite aggrave les lésions cérébrales après un arrêt circulatoire hypothermique prolongé chez le rat

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

Ketamine anesthesia reduces intestinal ischemia/reperfusion injury in rats

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