Hyperglycaemia emerging during general anaesthesia induces rat acute kidney injury via impaired microcirculation, augmented apoptosis and inhibited cell proliferation

Abstract

Anaesthesia-induced hyperglycaemia affects intra-renal auto-regulation via decreased renal perfusion, thus triggering renal function deterioration and tubular injury. Increased intra-renal Angiotensin-II aggravates the damage. Tight hypoglycaemic control might prevent or, at least, attenuate anaesthesia-induced renal injury.

Hyperglycaemia, inflammation, RAS activation: Three culprits to blame for acute kidney injury emerging in healthy rats during general anaesthesia

“…In accordance with our previous observations 15,20 normal animals invariably developed acute transient hyperglycaemia minutes after induction of general anaesthesia. Insulin secretion continuously increased in response to hyperglycaemia, positively correlating with the latter.…”

“…[1][2][3][4][5]18,19 In clinical practice, postoperative inflammation is generally believed to result from surgical stress and intraoperative interventions. [1][2][3][4][5] Our previous experience 15,20 prompted us to speculate that surgery-induced stress might either aggravate or disguise the role of anaesthesia per se in postoperative renal complications. Therefore, we intentionally isolated the effects of anaesthesia from the impacts of either surgery or intraoperative maintenance, demonstrating that our results were inflicted by anaesthesia regardless of unspecific stress conditions.…”

“…12 Furthermore, a strong link exists between the magnitude of inflammation and poor perioperative outcome, 13,14 whereas blunting the intraoperative inflammation improves the postoperative scenario. 1,4 In a previous study we have demonstrated that hyperglycaemia emerging during general anaesthesia not accompanied by stress caused by surgical intervention, induced AKI in experimental rats 15 as evidenced by impaired renal microcirculation, decreased GFR, augmented intra-renal apoptosis and inhibited renal cell proliferation. 15 The present study was aimed at investigating the possibility of interactive involvement of hyperglycaemia, inflammation and activated RAS in triggering AKI in experimental rats subjected to general anaesthesia.…”

Insulin alleviates mitochondrial oxidative stress involving upregulation of superoxide dismutase 2 and uncoupling protein 2 in septic acute kidney injury

“…However, the precise mechanisms of insulin on mitochondrial oxidative stress remain to be fully elucidated. Hyperglycemia is common in sepsis and can also induce inflammation, oxidative stress and apoptosis in sepsis or AKI models ( 24 , 25 ). Previous studies revealed that insulin therapy exerts the protective effect against mitochondrial oxidative stress via lowering blood glucose levels ( 26 ).…”

In situ assessment of the renal microcirculation in mechanically ventilated rats using sidestream dark‐field imaging

“…Based on our results, RMIC can be characterized as a capillary network with a proportion of perfused vessels reaching an average of 100% of all visible vessels and showing constantly continuous to hyperdynamic flow in all vessels as assessed by semiquantitative velocity classification. To our best knowledge, there are no similar studies evaluating RMIC by SDF imaging, however, some studies focus on changes in perfusion in different disease models and treatments (Mikhailichenko & Tikhomirova, ; Efrati et al ., ; Zhu et al ., ; Xu et al ., ). Understanding of renal microcirculation seems to play a crucial role in sepsis and acute kidney injury as the microcirculation is the integrative physiological compartment where all deleterious mechanisms come together and exert their integrative action that can be observed clinically (Le Dorze et al ., ; Ergin et al ., ).…”