Nilay Boztas

Efeitos de dexmedetomidina em conjunto com o pré-condicionamento isquêmico remoto em lesão de isquemia-reperfusão renal em ratos

BACKGROUND AND OBJECTIVES The aim of this study was to evaluate the effects of remote ischemic preconditioning by brief ischemia of unilateral hind limb when combined with dexmedetomidine on renal ischemia-reperfusion injury by histopathology and active caspase-3 immunoreactivity in rats. METHODS 28 Wistar albino male rats were divided into 4 groups. Group I (Sham, n=7): Laparotomy and renal pedicle dissection were performed at 65th minute of anesthesia and the rats were observed under anesthesia for 130min. Group II (ischemia-reperfusion, n=7): At 65th minute of anesthesia bilateral renal pedicles were clamped. After 60min ischemia 24h of reperfusion was performed. Group III (ischemia-reperfusion+dexmedetomidine, n=7): At the fifth minute of reperfusion (100μg/kg intra-peritoneal) dexmedetomidine was administered with ischemia-reperfusion group. Reperfusion lasted 24h. Group IV (ischemia-reperfusion+remote ischemic preconditioning+dexmedetomidine, n=7): After laparotomy, three cycles of ischemic preconditioning (10min ischemia and 10min reperfusion) were applied to the left hind limb and after 5min with group III. RESULTS Histopathological injury scores and active caspase-3 immunoreactivity were significantly lower in the Sham group compared to the other groups. Histopathological injury scores in groups III and IV were significantly lower than group II (p=0.03 and p=0.05). Active caspase-3 immunoreactivity was significantly lower in the group IV than group II (p=0.01) and there was no significant difference between group II and group III (p=0.06). CONCLUSIONS Pharmacologic conditioning with dexmedetomidine and remote ischemic preconditioning when combined with dexmedetomidine significantly decreases renal ischemia-reperfusion injury histomorphologically. Combined use of two methods prevents apoptosis via active caspase-3.

Renal Ischemia/Reperfusion Injury in Diabetic Rats: The Role of Local Ischemic Preconditioning

Background. The aim of this study was to evaluate the effects of local ischemic preconditioning using biochemical markers and histopathologically in the diabetic rat renal IR injury model. Methods. DM was induced using streptozotocin. Rats were divided into four groups: Group I, nondiabetic sham group (n = 7), Group II, diabetic sham group (n = 6), Group III, diabetic IR group (diabetic IR group, n = 6), and Group IV, diabetic IR + local ischemic preconditioning group (diabetic IR + LIPC group, n = 6). Ischemic renal injury was induced by clamping the bilateral renal artery for 45 min. 4 h following ischemia, clearance protocols were applied to assess biochemical markers and histopathologically in rat kidneys. Results. The histomorphologic total cell injury scores of the nondiabetic sham group were significantly lower than diabetic sham, diabetic IR, and diabetic IR + LIPC groups. Diabetic IR group scores were not significantly different than the diabetic sham group. But diabetic IR + LIPC group scores were significantly higher than the diabetic sham and diabetic IR groups. Conclusion. Local ischemic preconditioning does not reduce the risk of renal injury induced by ischemia/reperfusion in diabetic rat model.

Intravenous lipid emulsion prolongs survival in rats intoxicated with digoxin.

BACKGROUND Intravenous lipid emulsion eliminates the toxicity-related symptoms of several drugs. We hypothesized that intravenous lipid emulsion prolongs the survival time in digoxin-intoxicated rats. METHODS Electrocardiograms of 14 anesthesized Wistar rats were monitored. All of the rats received digoxin infusion at a rate of 12 mL/h (0.25 mg/mL). Five minutes after the start of digoxin infusion, animals were treated either with 12.4 mL/kg intravenous lipid emulsion (group L) or saline (group C). The primary outcome variable was time elapsed until asystole development. Cumulative dose of digoxin required to induce asystole was also recorded. RESULTS Mean time until asystole development in groups C and L were 21.28 ± 8.61 and 32.00 ± 5.41 minutes, respectively (P< .05). The mean lethal doses of digoxin in the groups C and L were 3.97 ± 1.54 and 6.09 ± 0.96 mg/kg, respectively (P< .05). CONCLUSION Intravenous lipid emulsion prolonged the time until asystole development and increased cumulative lethal dose in rats intoxicated with digoxin.

Protective effects of dexmedetomidine and remote ischemic preconditioning on renal ischemia reperfusion injury in rats

BACKGROUND The aim of this study was to evaluate the effects of remote ischemic preconditioning (RIPC) and dexmedetomidine as pharmacological conditioning in a rat renal ischemia/reperfusion (IR) injury model. METHODS Total of 28 male Wistar Albino rats weighing 250 to 300 g were divided into 4 equal groups. Group I (Sham; n=7): Laparotomy and renal pedicle dissection were performed, and the rats were observed under anesthesia without any intervention. Group II (IR; n=7): Following laparotomy and 45 minutes of left renal pedicle occlusion, 4 hours of reperfusion was performed. Group III (IR+D; n=7): Following laparotomy and ischemia, dexmedetomidine was administrated intraperitoneally (100 µg/kg) at fifth minute of reperfusion. Group IV (RIPC+IR; n=7): Under anesthesia, 3 cycles of ischemic preconditioning were applied to the left hind leg, and after 5 minutes, renal IR was performed. All rats were sacrificed after the left kidney was processed for conventional histomorphology. RESULTS Total histomorphological renal injury score was significantly lower in the Sham group compared with the other groups (p<0.01). Total renal injury score of IR group was significantly higher than IR+D and RIPC+IR groups (p<0.01). There was no significant difference in the total renal injury score between the dexmedetomidine and RIPC groups (p=0.89). CONCLUSION In the present study, it was demonstrated histomorphologically that both dexmedetomidine and RIPC decreased renal IR injury significantly. In addition, no significant difference was found between dexmedetomidine and RIPC groups.

Effects of different doses of remifentanil on hemodynamic response to anesthesia induction in healthy elderly patients

Abstract Objective: We compared the effects of three different doses of remifentanil infusion, which were performed for the induction of anesthesia in elder patients, on cardiovascular response. Research design and methods: The present study was designed as a randomized, prospective and double-blind study. A total of 90 ASA I–II patients over the age of 65 years were enrolled. The patients were randomly (by lot) assigned to receive one of the three doses of remifentanil infusion (0.1, 0.2 or 0.3 μg/kg/min) for two minutes. Subsequently, 0.5 mg/kg propofol was administered via IV route and 0.5 mg/kg rocuronium was administered via IV route at the time eyelash reflex disappeared. Intubation was performed after 2 minutes. Patients who had an allergy against opioids, were chronic substance users, were obese, expected to have difficult airway, had hypertension, or were receiving any drug influencing the cardiovascular system were excluded. Main outcome measures: In this study after recording baseline values of heart rate (HR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and mean arterial pressure (MAP), these values were recorded at the 1st, 2nd, 3rd, 4th and 5th minutes of induction. Results: A significant increase was observed in heart rate at the 1st and 2nd minutes of induction versus baseline in the Remi 0.1 group and at the 2nd minute of induction versus baseline in the Remi 0.2 group, with no additional significant change in heart rate. A significant decrease was determined in the systolic, diastolic and mean arterial pressures in all groups from the 1st minute of induction of anesthesia to the pre-intubation period compared to baseline (p < .05). Conclusions: It was determined that each dose of remifentanil used was quite high for patients of this age-group. ClinicalTrials.gov trial number: NCT02763098.

Avaliação dos efeitos de sugamadex e dexmedetomidina intra‐arterial: estudo experimental

BACKGROUND Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1μg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.

Evaluation of the effects of intra-arterial sugammadex and dexmedetomidine: an experimental study

BACKGROUND Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1μg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.