Evaluation of renal protection from high doses of melatonin in an experimental model of renal ischemia and reperfusion in hyperglycemic rats.

BACKGROUND: Melatonin is a free radical scavenger with important actions in the study of renal ischemia and reperfusion (I/R). This study evaluated possible renal protection of high doses of melatonin in an experimental model of I/R in which rats were submitted to acute hyperglycemia under anesthesia with isoflurane. METHOD: Forty-four male Wistar rats, weighing more than 300 g, were randomly divided into 5 groups: G1, sham (n = 10); G2, melatonin (n = 10; 50 mg.kg(-1)); G3, hyperglycemia (n = 9; glucose 2.5 g.kg(-1)); G4, hyperglycemia/melatonin (n = 10; 2.5 g.kg(-1) glucose + melatonin 50 mg.kg(-1)); and G5, I/R (n = 5). In all groups, anesthesia was induced with 4% isoflurane and maintained with 1.5% to 2.0% isoflurane. Intraperitoneal injection of melatonin (G1, G4), glucose (G3, G4), or saline (G1, G5) was performed 40 minutes before left renal ischemia. Serum plasma values for creatinine and glucose were determined at baseline (M1), immediately following reperfusion (M2), and 24 hours after completion of the experiment (M3). Histological analysis was performed to evaluate tubular necrosis (0-5). RESULTS: Serum glucose was higher at M2 in the groups supplemented with glucose, hyperglycemia (356.00 ± 107.83), and hyperglycemia/melatonin (445.3 ± 148.32). Creatinine values were higher at T3 (P = .0001) for I/R (3.6 ± 0.37), hyperglycemia/melatonin (3.9 ± 0.46), and hyperglycemia (3.71 ± 0.69) and lower in the sham (0.79 ± 0.16) and melatonin (2.01 ± 1.01) groups, P < .05. Histology showed no necrosis injury in the G1, lesion grade 2 in the G2, and severe acute tubular necrosis in the G3: (grade 4), G4: (grade 5) and G5: (grade 4) groups (P < .0001). DISCUSSION: Melatonin protected the kidneys submitted to I/R in rats without hyperglycemia; however, this did not occur when the I/R lesion was associated with hyperglycemia. CONCLUSIONS: Due to its antioxidant and antiapoptotic action, melatonin was able to mitigate, but not prevent acute tubular necrosis in rats with hyperglycemia under anesthesia by isoflurane.

Orthognathic surgery with or without induced hypotension.

This study involved a retrospective evaluation of patients subjected to surgery for dentofacial deformities treated without induced controlled hypotension (group I, n=50) and a prospective evaluation of patients who were subjected to surgery under hypotensive general anaesthesia (group II, n=50). No statistical differences were found between the study groups with regard to the duration of surgery. However, there were statistically significant differences in the need for blood transfusion and the occurrence of bradycardia during the maxillary down-fracture. Hypotensive anaesthesia decreased the need for a blood transfusion and the occurrence of bradycardia, and is therefore considered highly beneficial for patients undergoing orthognathic surgery.

Caffeic acid phenethyl ester effects in the kidney during ischemia and reperfusion in rats anesthetized with isoflurane.

BACKGROUND: The purpose of this investigation was to examine the effect of caffeic acid phenethyl ester (CAPE) in renal ischemia/reperfusion injury in rats anesthetized with isoflurane (iso). METHODS: We randomly assigned 26 male Wistar rats anesthetized with isoflurane, intubated and mechanically ventilated to 3 groups: G1 (controls; n = 8), G2 (CAPE; n = 10), and G3 (ethanol; n = 8). Mean arterial pressure was monitored for anesthetic control. Intraperitoneal CAPE (G2) or ethanol (G3) injections were administered 40 minutes before left renal ischemia. All animals underwent right nephrectomy and the left kidney was submitted to ischemia for 25 minutes. Serum creatinine (cr) values were determined at the beginning (M1), end (M2), and 24 hours after the experiment (M3) upon intracardiac blood samples. The left kidney was removed for histologic analysis, using a scale for tubular necrosis (0-5, injury maximum). Statistical analysis was applied to serum creatinine and histological score injury considering statistical differences to be significant when P < .05. RESULTS: The cr values in the CAPE were significantly higher at M2 (0.8 mg/mL; P = .0012) and M3 (3.7 mg/mL; P = .0014) than the control (0.5 and 0.9 mg/mL) or G3 (0.6 and 1.0 mg/mL), respectively. Histologic examination showed the CAPE group to display more pericapsular tubular necrosis (3.0 [2.0; 3.0]) than the G1 group (2.0 [1.0; 2.0]) or G3 group (1.5 [1.0; 2.0]; P < .001). The CAPE group displayed more medullary tubular necrosis (2.0 [2.0; 3.0] than G1 (2.0 [1.0; 2.0] or G3 (1.0 [0.0; 2.0]; P < .001). CONCLUSION: CAPE promoted greater functional and anatomic renal injury when rats were anesthetized with iso than control or ethanol groups, as demonstrated by histologic analysis and serum values.

Erythropoietin attenuates apoptosis after ischemia-reperfusion-induced renal injury in transiently hyperglycemic Wister rats.

BACKGROUND: Hyperglycemia is associated with a decreased tolerance to ischemia and an increased severity of renal ischemia reperfusion (I/R) injury. It has been suggested that erythropoietin (EPO) attenuates this effect in normoglycemic animals. This study sought to examine the effects of EPO on treatment renal I/R injury (IRI) in transiently hyperglycemic rats. MATERIAL AND METHODS: Twenty-eight male Wister rats anesthetized with isoflurane received glucose (2.5 g.kg(-1) intraperitoneally) before right nephrectomy. They were randomly assigned to four groups: sham operation (S); IRI (ISO); IRI+EPO, (600 UI kg(-1) low-dose EPO [EL]); and IRI+EPO 5000 UI kg(-1) (high-dose EPO [EH]). IRI was induced by a 25-minute period of left renal ischemia followed by reperfusion for 24 hours. Serum creatinine and glucose levels were measure at baseline (M1), immediately after the ischemic period (M2), and at 24 hours after reperfusion (M3). After sacrificing the animals, left kidney specimens were submitted for histological analysis including flow cytometry to estimate tubular necrosis and the percentages of apoptotic, dead or intact cells. RESULTS: Scr in the ISO group was significantly higher at M3 than among the other groups. Percentages of early apoptotic cells in ISO group were significantly higher than the other groups. Percentages of late apoptotic cells in S and ISO groups were significantly greater than EL and EH groups. However, no significant intergroup differences were observed regarding the incidence of tubular necrosis. CONCLUSIONS: Our results suggested that, although not preventing the occurrence of tubular necrosis, EPO attenuated apoptosis and glomerular functional impairment among transiently hyperglycemic rats undergoing an ischemia/reperfusion insult.

Remifentanil, isoflurane, and preconditioning attenuate renal ischemia/reperfusion injury in rats.

BACKGROUND: The purpose of this investigation was to examine the effect of isoflurane, remifentanil, and preconditioning in renal ischemia/reperfusion injury (IRI). METHODS: All 52 male Wistar rats were anesthetized with isoflurane, intubated and mechanically ventilated. The animals were randomly divided into: S group (sham; n = 11) that underwent only right nephrectomy; as well as the I group of right nephrectomy and ischemia for 45 minutes by clamping of left renal artery. (n = 11); the IP (n = 9), the R (n = 10), and the RP (n = 11) groups. In addition, the R and RP animals received remifentanil (2 microg.kg(-1).min(-1)) during the entire experiment. The IP and RP group underwent ischemic preconditioning (IPC = three cycles of 5 minutes). Serum creatinine values were determined before and after IRI, as well as 24 hours later. In addition to an Histological study, cells from the left kidney were evaluated for apoptosis by flow cytometry (FCM). RESULTS: The Creatinine value of 0.8 +/- 0.2 mg/dl in the S group was significantly lower at 24 hours than the I 3.9 +/- 1.5 mg/dl; IP 2.6 +/- 1.7 mg/dl; R 3.3 +/- 2.8 mg/dl; or RP 1.8 +/- 0.5 mg/dl groups. The RP group value was significantly lower than those of the I, IP, and R groups (p < 0.05). The S group showed less proximal tubular cell damage than the I, IP, R, and RP groups (p < 0.05). The percentages of apoptotic cells (FITC(+)/PI(-)) were: S group = 11.6 +/- 6.5; I = 16.7 +/- 7.3; IP = 37.0 +/- 28.4; R = 11.7 +/- 6.6, and RP = 8.8 +/- 1.5. The difference between the IP vs RP group was significant. Similar percentages of necrotic cells (FITC(+)/PI(+)) and intact cells (FITC(-)/PI(-)) were observed among the groups. CONCLUSIONS: Ischemic preconditioning showed no protective effect in the isoflurane group (IP) but when isoflurane was administered associated with remifentanil (RP), there was a beneficial effect on the kidney, as demonstrated by flow cytometry and serum creatinine values.

Perioperative cardiac arrest: a study of 53,718 anaesthetics over 9 yr from a Brazilian teaching hospital.

BACKGROUND: Little information exists regarding factors influencing perioperative cardiac arrests and their outcome. This survey evaluated the incidence, causes and outcome of perioperative cardiac arrests in a Brazilian tertiary general teaching hospital between April 1996 and March 2005. METHODS: The incidence of cardiac arrest during anaesthesia was prospectively identified from an anaesthesia database. There were 53,718 anaesthetics during the study period. Data collected included patient characteristics, surgical procedures (elective, urgent or emergency), ASA physical status classification, anaesthesia provider information, type of surgery, surgical areas and outcome. All cardiac arrests were retrospectively reviewed and grouped by cause of arrest and death into one of four groups: totally anaesthesia related, partially anaesthesia related, totally surgery related or totally patient disease or condition related. RESULTS: One hundred and eighty-six cardiac arrests (34.6:10,000) and 118 deaths (21.97:10,000) were found. Major risk factors for cardiac arrest were neonates, children under 1 yr and the elderly (P<0.05), male patients with ASA III or poorer physical status (P<0.05), in emergency surgery (P<0.05) and under general anaesthesia (P<0.05). Patient disease/condition was the major cause of cardiac arrest or death (P<0.05). There were 18 anaesthesia-related cardiac arrests (3.35:10,000) -- 10 totally attributed (1.86:10,000) and 8 partially related to anaesthesia (1.49:10,000). There were 6 anaesthesia-related deaths (1.12:10,000) -- 3 totally attributable and 3 partially related to anaesthesia (0.56:10,000 in both cases). The main causes of anaesthesia-related cardiac arrest were respiratory events (55.5%) and medication-related events (44.5%). CONCLUSIONS: Perioperative cardiac arrests were relatively higher in neonates, infants, the elderly and in males with severe underlying disease and under emergency surgery. All anaesthesia-related cardiac arrests were related to airway management and medication administration which is important for prevention strategies.

Repercussöes da hipercapnia sobre a hemodinâmica renal do cäo / Effect of hypercapnia on renal haemodynamics

Hypercapnia is not deliberately used nowadays even in the anesthetic management of carotid endarterectomy. Nevertheless, high PaCO2 level may occur during anesthetic procedures. Such altered carbon dioxide concentration trigger important changes in cardiovascular and renal function. This paper was designed to study some effects of hypercapnia upon the renal function in dogs. Twelve dogs fasted overnight were anesthetized with intravenous sodium pentobarbital (30 mg.kg elevado a menos um). The animals were intubated with a cuffed endotracheal tube, and ventilated with a takoaka respirator, using room air at the respiratory rate of 12 - 14 min elevado a menos um. Pancuronium bromide (0,08 mg.kg elevado a menos um) was injected to facilitate the ventilation. Cannulation of artery and vein was performed for blood sampling and fluid administration. In six dogs it was added CO2 to the room air at a concentration betwen 10 and 15 per cents. The following parameters were analized: mean arterial pressure (MAP), renal plasmatic flow (RPF), renal blood flow (RBF), glomerular filtration rate (GFR), urine output, carbon dioxide partial pressure (PaCO2), and oxygen partial pressure (PaO2). In the control group there was not any significant change in the analized parameters. In the group of dogs with high PaCO2 a MAP progressive decrease was observed from the begining of the experiment, that coned be explained by the direct action of CO2 on the peripheral vascular bed. The RBF values increased initially and decreased thereafter. This last result can be explained by the release of catecholamines due to hypercapnia, or by other factors such as interaction with the renin-angiotensin system, or acid-base imbalance. The decreased urinary output variedconversely to the PaCO2 remained unchanged throughout the experiment. This study shows that renal hemodynamic changes do not occur until PaCO2 level achieves 6,66 kPa (50 mm Hg). At the PaCO2 level of 9,33 kPa (70 mm Hg) slight elevation of the RPF and of the RBF is observed possibly due to the direct action of CO2 on the smooth muscles of the vessels. When 9,33 kPa is achieved, significant changes do occur in renal hemodynamics