Investigation of the effects of thymoquinone on erythrocyte deformability in sepsis treatment which created by cecal perforation in rat.

AIM: We aimed to study the effects of thymoquinone on erythrocyte deformability in an experimental model of sepsis given before or after the initiation of the sepsis model. METHOD: The animals were grouped as (n = 6) control, nigella sativa, sepsis, sepsis group with administration of nigella sativa before sepsis development and sepsis group with nigella sativa administration after sepsis development. Cecal ligation and puncture model (CLP) was used to induce sepsis in the animals. The thymoquinone was given 1 hour before or after the CLP in the study groups with a dose of 500 mg·kg(-1). Erythrocyte deformability and relative resistance was calculated. RESULT: Relative resistance was increased in the sepsis groups when compared to the control group (p < 0.0001). Deformability index was increased in the sepsis group when compared to the other groups (p < 0.0001 in all groups). Sepsis group with after nigella sativa groups deformability index was significantly different from the deformability index in control group (p = 0.002). The use of nigella sativa before the initiation of sepsis corrected the deformability index significantly and the results were comparable to the control group (p = 0.078). CONCLUSION: Thymoquinone administration before induction of CLP was observed to have protective effects on these alterations in CLP sepsis (Tab. 1, Fig. 1, Ref. 26).

Effect of cerium oxide on erythrocyte deformability in rat lower extremity ischemia reperfusion injury.

BACKGROUND: Cerium oxide is the oxide form of cerium, which has protective effects in ischemia reperfusion (I/R) injury. The purpose of our study was to look into the effects of this rare-earth metal on erythrocyte deformability in rat lower extremity I/R injury model. MATERIALS AND METHODS: We used 24 Wistar albino rats as subjects in our study. They were divided into 4 groups; randomized control group (group C; n = 6), cerium oxide group 0.5 mg.kg-1, intraperitoneal (group CO; n = 6), I/R group (group I/R; n = 6) and I/R group with cerium oxide 0.5 mg.kg-1 intraperitoneally (group I/R-CO; n = 6). Erythrocyte packs were prepared from heparinized blood samples and deformability measurements were performed. RESULTS: We obtained similar results from the control and I/R-CO groups (p = 0.158). The results in I/R group were evidently higher than those of the control, CO, and IR-CO groups (p < 0.0001, p < 0.0001, p = 0.001, respectively). CONCLUSION: We detected unfavorable effects of I/R on erythrocyte deformability, which may impair blood flow and hence tissue perfusion in infrarenal rat aorta. We also found that cerium oxide had beneficial effects by reversing undesirable effects of I/R. Further studies with larger volume are required to support our promising results (Fig. 1, Ref. 24).

Effects of dexmedetomidine and thymoquinone on erythrocyte deformability in lower limb ischemia reperfusion injury in streptozotocin-induced diabetic rats.

OBJECTIVE: In this study we aimed to evaluate the effect of dexmedetomidine and thymoquinone on erythrocyte deformability in lower limb ischaemia-reperfusion (IR) injury in streptozotocin-induced diabetic rats. MATERIAL AND METHODS: Thirty Wistar albino rats were equally divided into 5 groups (n = 6); randomized control group (Group C), diabetes control group (Group DC), DIR group (Group DIR), DIR group with thymoquinone 25 mg.kg‒1 intraperitoneally (Group DIRT) and Group DIR with dexmedetomidine 100 µg.kg‒1 intraperitoneally (Group DIRD). Erythrocyte packs were prepared from heparinized blood samples and deformability measurements were performed. RESULTS: IR significantly increased the relative resistance, a marker of erythrocyte deformability when compared to control group (p < 0.05). There were significant differences among the groups in comparisons with ANOVA test (p < 0.0001). Comparisons of the groups DIRD and DIRT revealed similar results (p = 0.824). The values of Group DIR were significantly higher than those of the control, DC, DIRD and DIRT groups (p < 0.0001, p = 0.001, p = 0.004, p = 0.002, respectively). The values of the DC, DIR, DIRD and DIRT groups were significantly higher than those of the control group (p < 0.0001, all). CONCLUSION: Erythrocyte deformability may cause more problems in microcirculation. Dexmedetomidine and thymoquinone may be useful in reducing the adverse effects of this type of injury (Fig. 1, Ref. 41).

Effect of apelin-13 on erythrocyte deformability during ischaemia-reperfusion injury of heart in diabetic rats.

OBJECTIVES: Erythrocyte deformability and plasma viscosity are of crucial importance for the perfusion of tissues and organs. The aim of this study was to evaluate the effect of apelin-13 on erythrocyte deformability during IR heart injury in diabetic rats. METHODS: Eighteen Wistar Albino rats were included in the study after streptozotocin (55 mg/kg) treatment for four weeks of observation for diabetes existence. The animals were randomly assigned to one of five experimental groups. In the Group C, DC (sham-control group) and DCA (sham-control group-apelin-13), the coronary artery was not occluded or re-perfused. In the Group DIR, a branch of the left coronary artery was occluded for 30 minutes followed by 90 minutes of re-perfusion to produce IR. In the Group DIRA, a branch of the left coronary artery was occluded for 30 minutes followed by 90 minutes of re-perfusion to produce IR, and apelin-13 was administrated via 10 µg.kg-1 IP route 30 minutes before ligating the left coronary artery.Deformability measurements were performed in erythrocyte suspensions containing Htc 5% in a PBS buffer. RESULTS: The deformability index was significantly increased in diabetic rats; however, it was similar in Group DC, DCA and DIRA. It was significantly increased in the Group DIR when compared to the Group C, DIRA, DCA and DC. The relative resistance was increased in IR models. CONCLUSION: Erythrocyte deformability was decreased in rats having diabetes and IR injury. This injury might lead to further problems in microcirculation. It was shown that apeline-13 may be useful in enhancing the adverse effects of this type of injury (Fig. 1, Ref. 35).

Vitamin C ameliorates high dose Dexmedetomidine induced liver injury.

BACKGROUND: We investigated whether vitamin C has protective effects on rat liver tissue treated with different dexmedetomidine doses. MATERIAL AND METHODS: Thirty five wistar albino rats were randomly divided into 5 groups (Control (0.9% NaCl intraperitoneally (i.p.), Dexmedetomidine 5 µg.kg(-1) (i.p.), Dexmedetomidine 5 µg.kg(-1) i.p. plus Vitamin C (100 mg.kg(-1)), Dexmedetomidine 10 µg.kg(-1) i.p. and Dexmedetomidine 10 µg.kg(-1) i.p. plus Vitamin C (100 mg.kg(-1)). Histopathological liver injury, superoxide dismutase (SOD) activity and tissue Malondialdehyde levels were investigated. RESULTS: Hepatocyte degeneration was significantly higher in D10 group than those in other study groups (p < 0.0001, p = 0.002, p < 0.0001, p = 0.005, respectively). Similarly, liver tissue sinusoidal dilatation and hepatocyte necrosis were significantly higher in D10 group than those in other groups (p < 0.0001, p < 0.0001, p = 0.002, p < 0.0001 and p < 0.0001, p = 0.046, p < 0.0001 and p = 0.002, respectively). Tissue MDA levels in D10 group were significantly higher than those in control, D5+Vit C and D10+Vit C groups (p = 0.028, p = 0.004, p = 0.031, respectively). SOD enzyme activity in D10 group was significantly lower than in control, D5+Vit C and D10+Vit C groups (p < 0.0001, p = 0.023 and p = 0.031, respectively). CONCLUSION: High dose dexmedetomidine can induce hepatic injury and oxidative stress in rats while pre-treatment with vitamin C may be effective in protecting liver tissue against this newly recognized undesirable dexmedetomidine effect (Tab. 2, Fig. 5, Ref. 30).

Effects of intravenous ibuprofen and lornoxicam on erythrocyte deformability in rats undergoing hind limb ischemia reperfusion injury.

BACKGROUND AND AIM: Acute hind limb ischemia reperfusion (I/R) injury is a common consequence of abdominal aorta cross­clamping during aortic surgery. Erythrocyte deformability is affected by I/R process and may lead to increased tissue and organ injury. Lornoxicam and intravenous ibuprofen are becoming commonly used as non-steroidal anti-inflammatory drugs (NSAID) for postoperative analgesia. In this study, we aimed to investigate the effects of lornoxicam (2 mg/kg iv) and intravenous ibuprofen (30 mg/kg iv) on erythrocyte deformability in I/R model in rats. MATERIALS AND METHODS: Four study groups, each containing 6 Wistar rats were created. Laparotomy was performed in all groups under general anesthesia with ketamine and xylazine. In all groups except sham group, ischemia and reperfusion were achieved by clamping and declamping the infrarenal abdominal aorta for 120 minutes. Rats in Group IR+L received intravenous infusion of lornoxicam (2 mg/kg) while rats in Group IR+I received intravenous infusion of ibubrofen (30 mg/kg) following 2 hours of ischemic period. At the end of reperfusion period, erythrocyte packs were prepared from heparinized blood samples. Erythrocyte suspensions with hematocrit at a concentration of 5% in a phosphate­buffered saline (PBS) were used in order to perform deformability measurements. The value of p<0.05 was considered statistically significant. RESULTS: Relative resistance has increased in ischemia reperfusion group when compared to control group (p < 0.0001). Lornoxicam or ibuprofen intravenous treatments did not change the erythrocyte deformability during ischemia reperfusion period in rats (p=0.851, p=0.690). CONCLUSION: Intravenous ibuprofen or lornoxicam administrations during ischemia reperfusion period in rats have no negative effect on erythrocyte deformability. The findings of the study should be supported with more detailed and extensive clinical/experimental studies in the future (Fig. 1, Ref. 18).

Effects of iron overload and exenatide on erythrocyte deformability in a rat model.

Iron overload is known to affect erythrocyte membrane properties and erythrocyte shape. We hypothesized that iron overload which directly affects the erythrocyte morphology may also interfere with erythrocyte deformability (ED). Exenatide, a glucagon like peptide -1 (GLP-1) analogue used in the treatment of diabetes, is known to have beneficial pleiotropic effects on endothelial function and blood flow which are different from its glucose-lowering effects. In our study we aimed to test the effect of iron overload on ED in a rat model (1) and to evaluate the effect of exenatide on ED in the same model (2). For this purpose, the animals were randomly divided into three groups, each containing 6 rats. Rats in the control group (Group C) were given intraperitoneal injections of saline as placebo. The second group (Group Fe) was given intraperitoneal iron dextran (60 mg/kg/day) five days a week for 4 weeks to develop iron overload. The third group (Group Fe +E) received subcutaneous injections of 10 mcg exenatide (Byetta® Lilly Pharma) in two divided doses for 4 weeks in addition to iron dextran. We observed that ED index was significantly higher in Group Fe when compared to Group C and Group Fe+E (p Keywords: erythrocyte deformability, iron, exenatide.

Effect of levosimendan on erythrocyte deformability during myocardial ischaemia-reperfusion injury.

UNLABELLED: Diabetes mellitus (DM) is a chronic metabolic disorder accompanied by an increase in oxidative stress. Ischaemia-reperfusion (IR) injury is a cascade of events initiated by tissue ischaemia. The cellular damage produced by reperfusion leads to an active inflammatory response. Erythrocyte deformability and plasma viscosity are of crucial importance for the perfusion of tissues and organs. The aim of this study was to evaluate the effect of levosimendan on erythrocyte deformability during IR myocardial injury in diabetic rats. METHODS: Twenty-four Wistar albino rats were included in the study after streptozocin (55 mg/kg) treatment for 4 weeks to observe the existence of diabetes. The animals were randomly assigned to one of four experimental groups. In Group C and DC (sham-control group), the coronary artery was not occluded or reperfused in the control rats. Myocardial IR was induced by ligation of the left anterior descending coronary artery for 30 min, followed by 2 h of reperfusion in the diabetes-IR (DIR) and diabetes-IR-levosimendan (DIRL) group. Deformability measurements were performed in erythrocyte suspensions containing Htc 5 % in a phosphate-buffered saline (PBS) buffer. RESULTS: The deformability index was significantly increased in the diabetic rats. It was similar in Group DC and DIRL It was significantly increased in the DIR group compared to Group C, DIRL and DC. The relative resistance was increased in the IR models. CONCLUSION: Erythrocyte deformability was decreased in rats with diabetes and IR injury. This injury might lead to further problems in microcirculation. Levosimendan may be useful in enhancing the adverse effects of this type of injury (Fig. 2, Ref. 41). KEYWORDS: erythrocyte deformability, myocardial ischaemia reperfusion, experimental diabetes, levosimendan, rat.

Effect of alprostadil on erythrocyte deformability in ischemia reperfusion injury.

BACKGROUND: Ischemia reperfusion injury (I/R) in lower extremity is a frequent and important clinical phenomenon. Protective effect of alprostadil on local and distant organ injury due to I/R has been well-documented but its effect on erythrocyte deformability needs further investigation. Our aim was to investigate the effect of alprostadil on erythrocyte deformability in infrarenal aorta of rats undergoing I/R. MATERIALS AND METHODS: Our study was conducted with 18 Wistar albino rats. Rats were divided into 3 groups; randomized control group (group C; n=6), I/R group without alprostadil (group I/R; n=6) and I/R group with alprostadil 20 mcg.kg(-1), intraperitoneal (group I/R-A; n=6). Packs of erythrocytes were prepared from heparinized blood samples and deformability measurements were done. RESULTS: Comparisons of the control and I/R-A groups revealed similar results (p=0.240). The values of the IR group were significantly higher than those of the control and IR-A groups (p=0.009, p=0.026, respectively). CONCLUSION: In our study, we detected unfavourable effects of I/R on erythrocyte deformability, which may lead to disturbance in blood flow and hence tissue perfusion in infrarenal rat aorta. We also found that alprostadil had beneficial effects by reversing undesirable effects of I/R (Fig. 1, Ref. 22).

The effects of low and high doses of sugammadex on kidney tissue in streptozotocin-induced diabetic rats.

BACKGROUND: Sugammadex is primarily excreted via renal route. We investigated effects of low and high doses of sugammadex (16 mg/kg versus 96 mg/kg) on renal tissue samples of streptozotocin-induced diabetic rats. MATERIAL AND METHODS: Twenty-four Wistar albino rats were divided into 4 groups. Group C (control - 0.9 % NaCl), Group DC (diabetes control; 55 mg/kg streptozotocin, IP, only), Group DR-16S (diabetes-rocuronium - 16 mg sugammadex, IV.) and Group DR-96S (diabetes- rocuronium - 96 mg sugammadex, IV). Renal tissue histopathological evaluation and antioxidant status (measurements of MDA levels and NO activities) were studied. RESULTS: Significantly higher levels of all inflammation parameters (inflammation, degeneration/necrosis, tubular dilatation, tubular cell degeneration, dilatation in Bowman's space, tubular hyaline casts, and lymphocyte infiltration) were found in the 96 mg/kg sugammadex group. Higher MDA tissue levels and lower NO activity were found in the 96 mg/kg sugammadex group. DISCUSSION: We can conclude that high-dose (96 mg/kg) sugammadex administration resulted in significant renal tissue damage in diabetic rats. As a consequence, low doses of sugammadex have to be preferred in diabetic patients (Tab. 2, Fig. 4, Ref. 26).

Effect of dexmedetomidine on erythrocyte deformability during ischaemia-reperfusion injury of heart in diabetic rats.

UNLABELLED: The aim of this study is to evaluate the effect of dexmedetomidine on erythrocyte deformability during IR heart injury in diabetic rats. METHODS: Eighteen Wistar Albino rats were included in the study after streptozocin (55 mg/kg) treatment for four weeks. In the Group C and DC (sham-control group), the coronary artery was not occluded or reperfused in the control rats. In the Group DIR, a branch of the left coronary artery was occluded for 30 minutes followed by two hours of reperfusion to produce IR. In the Group DIRD, a branch of the left coronary artery was occluded for 30 minutes followed by two hours of reperfusion to produce IR, and dexmedetomidine was administrated via 100 µg/kg IP route 30 minutes before ligating the left coronary artery. Deformability measurements were performed in erythrocyte suspensions containing Htc 5 % in a PBS buffer. RESULTS: The deformability index was significantly increased in diabetic rats; however, it was similar in the Group DC and DIRD. It was significantly increased in the Group DIR when compared to the Group C, DIRD and DC. The relative resistance was increased in IR models. CONCLUSION: Erythrocyte deformability was decreased in rats having diabetes and IR injury. This injury might lead to further problems in microcirculation. It was shown that dexmedetomidine might be useful in enhancing the adverse effects of this type of injury (Fig. 1, Ref. 39).

The protective effects of dexmedetomidine on hepatic ischemia reperfusion injury.

OBJECTIVE: The aim of this study was to evaluate the effect of dexmedetomidine (100 µg/kg-ip) on liver ischemia and reperfusion (I/R) in rats. METHODS: Twenty-four Wistar Albino rats were separated into three groups as control (C), ischemia-reperfusion injury (I/R) and dexmedetomidine group (I/R-D). Ischemia was induced with portal clampage for 45 minutes and reperfusion period was 45 minutes after declampage. Group I/R-D was received dexmedetomidine 100 µg/kg i.p. 30 min before portal clampage. Thiobarbutiric Acid-Reactive Substances (TBARS), glutathioneS-transferase (GST), superoxide dismutase (SOD), Catalase (CAT), and Paraoxonase 1 (PON-1) were investigated in blood samples. Also HSP60 and p53-positive hepatocytes were counted under ImageJ image analysis program. RESULTS: All parameters, except GST levels, were significant between the groups (p < 0.05). Although HSP60 expression was significantly increased between I/R, I/R-D and C groups there were no significant differences between I/R-D and C (p = 0.443). On the other hand, p53 expression was also significantly increased between I/R, I/R-D and C groups At the same time, there were no significant differences between I/R-D and C groups (p = 0.354). CONCLUSION: All the results suggest that dexmedetomidine has beneficial effects on liver ischemia/reperfusion stress (Tab. 1, Fig. 2, Ref. 49).

The effects of propofol and memantine on erythrocyte deformability.

OBJECTIVE: Propofol is an intravenous general anesthetic with a primary hypnotic effect. Memantine is an NMDA receptor antagonist that has been shown to reverse changes in memory and synaptic plasticity in animal models. This study aims to investigates whether propofol and/or memantine has any effects on erythrocyte deformability. METHODS: 24 Wistar albino rats were divided randomly into four groups. Group P received 150 mg.kg-1 propofol intraperitoneally (ip); Group M received 1 mg.kg-1 memantine (ip); Group PM received 1 mg.kg-1 memantine mg.kg-1 ip 30 minutes before the administration of 150 mg.kg-1 propofol; and the control group (Group C) received saline ip. Euthanasia was performed in all rats by using intraabdominal blood uptake. The heparinized whole blood samples were used to prepare erythrocyte suspensions, from which erythrocyte suspensions were formed with a PBS buffer solution containing 5% htc, and the deformability parameters were measured. RESULTS: Erythrocyte deformability was significantly higher in Groups P, M and PM when compared to the Group C (p = 0.007 and p = 0.001, p <0.0001, respectively); while the erythrocyte deformability indices were similar in groups P, M and PM. CONCLUSION: The administration of propofol and memantine altered the erythrocyte deformability in the rats, which may lead to further problems in microcirculation. The administration of memantine to the propofol-treated rats did not alter the erythrocyte deformability; however the early results should be verified through further experimental and clinical studies (Fig. 1, Ref. 23).

Investigation of the effects of propofol and vitamin C administration on erythrocyte deformability in rats with streptozotocin-induced diabetes mellitis.

PURPOSE: In the current study we aim to investigate the effects of vitamin C and profol on red blood cell deformability in diabetic rats. MATERIALS AND METHODS: Twenty- eight Wistar Albino rats were included in the study after streptozocin (60 mg/kg) treatment for 4 weeks of observation for diabetes presence. Twenty-eight rats were allocated to 4 groups. In group DP (n = 7) 150 mg.kg-1 of propofol was injected intraperitoneally. In group DP-vit C (n = 7) rats 100 mg/kg of vitamin C (Ascorbic acid, Redoxon® 1000 mg/5 mL - Roche) were applied one hour before administrating 150 mg.kg-1 of propofol, while rats in control group (n = 7), and diabetic control group (n = 7) received intraperitoneally physiological saline. Deformability measurements were achieved by using erythrocyte suspensions with hematocrit level of 5 % in PBS buffer. RESULTS: Erythrocyte deformability was significantly higher in diabetic control group than in control and vitamin C plus propofol groups (p = 0.00, p = 0.025, respectively). Erythrocyte deformability indexes were found similar in control group and vitamin C plus propofol group (p = 0.949). Relative resistance was increased in diabetic rat model. CONCLUSIONS: Erythrocyte deformability was damaged in rats with diabetes. This injury might lead to further problems in microcirculation. Application of propofol did not alter red cell deformability in diabetic rats. Vitamin C supplementation seems to reverse those negative effects and variations in erythrocyte deformability (Fig. 2, Ref. 57).

The effects of iloprost on lung injury induced by skeletal muscle ischemia-reperfusion.

PURPOSE: The aim of this study was to investigate the effects of iloprost (I) on lung injury as a remote organ following skeletal muscle ischemia-reperfusion injury in a rat model. MATERIALS AND METHODS: Twenty-four Wistar Albino rats were randomized into four groups (n = 6). Laparotomy was performed in all groups under general anesthesia. Only laparotomy was applied in Group S (Sham). Ischemia reperfusion group (Group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 minutes. Group iloprost (Group I) received intravenous infusion of iloprost 0.5 ng/kg/min, without ischemia and reperfusion. Group I/R/I received intravenous infusion of iloprost 0.5 ng/kg/min immediately after 2 hours of ischemia. At the end of the study, lung tissue was obtained for determining total oxidant status (TOS) and total antioxidant status (TAS) levels, histochemical and immunohistochemical determination. RESULTS: Diffuse lymphocyte infiltration was detected in immunohistochemical examination of lung tissue in Group I/R. The connective tissue around bronchi, bronchioles and vessel walls was found to be increased. Although minimal local lymphocyte infiltration was detected in some fields in Group I/R/I, the overall tissue was found to be similar to Group S. iNOS expression was significantly higher in Group I/R, when compared with Group S and significantly lower in Group I/R/I compared to Group I/R.TOS levels were significantly higher in Group I/R, when compared with groups S and I (p = 0.028, p = 0.016, respectively) and significantly lower in group I/R/I, when compared with Group I/R (p = 0.048). TAS levels were significantly higher in Group I/R, when compared with groups S, I (p = 0.014, p = 0.027, respectively) and significantly lower in Group I/R/I, when compared with Group I/R (p = 0.032). CONCLUSION: These results indicate that administration of iloprost may have protective effects against ischemia reperfusion injury (Fig. 8, Tab. 1, Ref. 30)

Effect of iloprost on erythrocyte deformability in rat's lower extremity undergoing an ischemia reperfusion injury.

AIM: Ischemia reperfusion injury (I/R) in lower extremity is a frequent and important clinical phenomenon. The protective effect of iloprost on local and distant organ injury due to I/R has been well documented but its effect on erythrocyte deformability needs further investigation. Our aim was to investigate the effect of iloprost on erythrocyte deformability in the infrarenal aorta of rats undergoing I/R. MATERIALS AND METHODS: Our study was conducted with 18 Wistar albino rats. Rats were divided into the 3 groups; the randomized control group (group C; n=6), I/R group without iloprost (group I/R; n=6) and I/R group with iloprost - 10 mcg.kg-1, 30 min infusion (group I/R-I; n=6). Packs of erythrocytes were prepared from heparinized blood samples and deformability measurements were done. RESULTS: The comparisons of the control and I/R-I groups revealed similar results (p=0.951). The values of the IR group were significantly higher than those of the control and IR-I groups (p=0.006, p=0.011, respectively). CONCLUSION: In our study, we detected the unfavourable effects of I/R on erythrocyte deformability, which may lead to disturbance in blood flow and hence tissue perfusion in the infrarenal rat aorta. We also found that Iloprost had beneficial effects by reversing the undesirable effects of I/R (Fig. 1, Ref. 15).

Antioxidative effects of adrenomedullin and vascular endothelial growth factor on lung injury induced by skeletal muscle ischemia-reperfusion.

PURPOSE: The aim of this study was to investigate the effects of adrenomedullin (AM) and vascular endothelial growth factor (VEGF) on lung injury as a remote organ following skeletal muscle ischemia-reperfusion injury in a rat model. MATERIALS AND METHODS: Thirty-six Wistar rats were randomized into six groups (n=6). Laparotomy was performed in all groups under general anesthesia. Nothing else was done in Group S (Sham). Ischemia reperfusion group (Group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 minutes, respectively. Group VEGF and Group AM received intravenous infusion of VEGF (0.8 µg/kg) or AM (12 µg /kg) respectively, without ischemia and reperfusion. Group IR+VEGF and Group IR+AM received intravenous infusion of VEGF (0.8 µg/kg) or AM (12 µg /kg) respectively immediately after 2 hours period of ischemia. At the end of reperfusion period. Lung tissue samples were taken for biochemical examination. Total oxidant status (TOS) and total antioxidant status (TAS) levels in lung tissue were determined by using a novel automated method. p<0.05 was considered as statistically significant. RESULTS: TOS levels were significantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.004, p=0.011, p=0.017, respectively) and significantly lower in groups I/R+AM and I/R+VEGF, when compared with Group I/R (p=0.018, p=0.006, respectively). TAS levels were significantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.006 p=0.016, p=0.016, respectively) and significantly lower in Group I/R+AM, when compared with Group I/R (p=0.016). CONCLUSION: These findings indicate that AM and VEGF acted effectively on the prevention of lung injury induced by skeletal muscle ischemia-reperfusion injury in a rat model (Fig. 2, Ref. 30).

The effects of low-high doses of dexmedetomidine on erythrocyte deformability in rats.

BACKGROUND: Dexmedetomidine is an anesthetic agent frequently used for sedation, intensive care units, and general anesthesia. The purpose of our study was to investigate the effect of two different doses of dexmedetomidine on erythrocyte deformability in rats. MATERIALS AND METHODS: The study was performed on 21 male rats, with 7 rats in each study group and the control group. The rats in the study groups were administered dexmedetomidine (low dose 5 µg.kg-, high dose 10 µg.kg-) intraperitoneally, and the rats in the control group were administered physiological saline. Erythrocyte packs were prepared using heparinized total blood samples. Deformability measurements were done by erythrocyte suspensions in phosphate buffered saline (PBS) buffer. A constant flow filtrometer system was used to measure erythrocyte deformability, and the relative resistance was calculated. RESULTS: Use of a high dose dexmedetomidine resulted in an increase in relative resistance, which is an indicator for erythrocyte deformability in control rats (p=0.014). CONCLUSIONS: High dose dexmedetomidine via negative change in erythrocyte deformability may cause a functional deterioration in blood flow and tissue perfusion. Our results showed that low dose dexmedetomidine protects erythrocyte deformability better than the high dose (Fig. 1, Ref. 23).

Effect of dexmedetomidine on erythrocyte deformability during ischemia-reperfusion injury of liver in diabetic rats.

AIM: The aim of this study is to evaluate the effect of dexmedetomidine on erythrocyte deformability during IR injury of liver in diabetic rats. METHODS: Twenty- eight Wistar Albino rats were included in the study after a 4 week streptozocin (65 mg/kg) treatment to observe the existence of diabetes. The animals were randomly assigned to one of the four experimental groups: GroupC and DC (sham-control group): The abdomen was dissected with a median laparotomy and the liver was collected. GroupDIR: The liver was collected after IR following the abdominal median laparotomy. GroupDIRD: The liver was collected after IR following the abdominal median laparotomy and 30 min of infusion of dexmedetomidine 100 µg/kg ip The deformability measurements were performed in erythrocyte suspensions containing Htc 5% in PBS buffer. RESULTS: The deformability index was significantly increased in diabetic rats, however it was similar in the GroupC and DIRD. It was significantly increased in the GroupDIR when compared to the GroupC, DIRD and DC. The relative resistance was increased in IR models. CONCLUSION: Erythrocyte deformability was damaged in rats having diabetes and IR injury. This injury might lead to further problems in microcirculation. It was shown that dexmedetomidine may be useful in enhancing the adverse effects of this injury (Tab. 1, Fig. 2, Ref. 41).

Does vitamin C prevent the effects of high dose dexmedetomidine on rat erythrocyte deformability?

PURPOSE: Dexmedetomidine is an anesthetic agent frequently used for sedation at the intensive care units and during general anesthesia. The purpose of our study was to investigate whether vitamin C prevents the effect of high dose dexmedetomidine on erythrocyte deformability in rats. METHODS: The study was performed on 21 male rats, with 7 rats in each study groups and the control group. The rats in the study groups were treated with intraperitoneal dexmedetomidine (10 µg/kg) and intraperitoneal dexmedetomidine plus Vitamin C (ascorbic acid) (100 mg/kg ascorbic acid administered 1 hour before administration of 10 µg/kg dexmedetomidine), respectively. Intraperitoneal physiological saline was administered in the control group. Erythrocyte packs were prepared using heparinized total blood samples. Deformability measurements were done by erythrocyte suspensions in phosphate buffered saline (PBS) buffer. A constant flow filtrometer system was used to measure erythrocyte deformability and the relative resistance was calculated. RESULTS: Erythrocyte deformability was significantly higher in dexmedetomidine group than in control and vitamin C plus dexmedetomidine groups (p=0.003, p=0.013, respectively). Erythrocyte deformability indexes were found similar in the control group and in the vitamin C plus dexmedetomidine group (p=0.383). CONCLUSIONS: High dose dexmedetomidine may cause functional deterioration in blood flow and tissue perfusion with negative effects in erythrocyte deformability. Vitamin C supplementation seems to reverse those negative effects and variations in erythrocyte deformability. However, our preliminary results should be confirmed in wider serious of experimental and clinical trials (Fig. 1, Ref. 27).