Glibenclamide attenuates ischemia-induced acidosis and loss of cardiac function in rats

Legtenberg, Roger J.; Houston, R.; Heerschap, Arend; Oeseburg, B.; Smits, Paul

doi:10.1016/s0014-2999(01)01483-2

Cited by 2 publications

(2 citation statements)

References 26 publications

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“…Also, metformin improved endothelium-dependent vasodilation in both nondiabetic and diabetic subjects [31,32]. In isolated rat hearts, sulfonylurea derivatives reduced myocardial perfusion under ischemic conditions, while perfusion under normal conditions was unaffected [33,34]. In humans, these oral diabetics deteriorated both resting and hyperaemic myocardial blood flow [35].…”

Section: Discussionmentioning

confidence: 99%

Myocardial blood flow under general anaesthesia with sevoflurane in type 2 diabetic patients: a pilot study

Bulte

Brom

Loer

et al. 2014

Cardiovasc Diabetol

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BackgroundIn type 2 diabetic patients, cardiac events in the perioperative period may be associated with diminished myocardial vasomotor function and endothelial dysfunction. The influence of sevoflurane anaesthesia on myocardial endothelial dysfunction in type 2 diabetic mellitus is investigated in this pilot study.MethodsSix males with type 2 diabetes mellitus and eight healthy controls were included. Using myocardial contrast echocardiography, myocardial blood flow (MBF) was measured at rest, during adenosine-induced hyperaemia (endothelium-independent vasodilation) and after sympathetic stimulation by the cold pressor test (endothelium-dependent vasodilation). Measurements were performed before and after induction of sevoflurane anaesthesia.ResultsSevoflurane anaesthesia decreased resting MBF in diabetics but not in controls (P = 0.03), while baseline MBF did not differ between diabetics and controls. Without anaesthesia, adenosine-induced hyperaemia increased MBF in both groups compared to resting values. Adenosine combined with sevoflurane resulted in a lower hyperaemic MBF in both groups compared to no anaesthesia. Differences in MBF in response to adenosine before and after sevoflurane administration were larger in diabetic patients, however not statistically significant in this pilot group (P = 0.08). Myocardial blood flow parameters after the cold pressor test were not different between groups.ConclusionThese pilot data in type 2 diabetic patients show that sevoflurane anaesthesia decreases resting myocardial blood flow compared to healthy controls. Further, we observed a trend towards a lower endothelium-independent vasodilation capacity in diabetic patients under sevoflurane anaesthesia. Endothelium-dependent vasodilation was not affected by sevoflurane in diabetic patients. These data provide preliminary insight into myocardial responses in type 2 diabetic patients under general anaesthesia.Trial registrationhttp://www.clinicialtrials.gov, NCT00866801

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Section: Discussionmentioning

confidence: 99%

Myocardial blood flow under general anaesthesia with sevoflurane in type 2 diabetic patients: a pilot study

Bulte

Brom

Loer

et al. 2014

Cardiovasc Diabetol

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“…In groups randomized to receive naloxone or glibenclamide, the agent was added to the tissue bath at 5 min before the administration of the normoxic PC concentrate or at the corresponding time point (20 min preischemia) in the drug-treated control groups. Doses of both agents were within the micromolar range used previously in isolated buffer-perfused heart preparations (5,16). For glibenclamide, the agent was initially dissolved in dimethyl sulfoxide (DMSO, 12.5 mM), and 0.01 ml of the stock solution was added to the bath, yielding final concentrations of 5 M of the antagonist and 0.04 vol% of DMSO.…”

Section: Protocol 1: Transfer Of Precipitate From Heart To Mesentericmentioning

confidence: 99%

Myocardial preconditioning factors evoke mesenteric ischemic tolerance via opioid receptors and K_ATPchannels

Dickson

Tubbs²,

Porcaro³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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We have shown that a reverse-phase concentrate generated from the effluent of preconditioned (PC) rabbit hearts evokes a cardioprotective effect in virgin acceptor hearts. With the use of a model of sustained (1 h) simulated ischemia in isolated, spontaneously contracting rabbit jejunum, our current aims were to 1) determine whether protective factor(s) released from PC hearts can improve ischemic tolerance in noncardiac tissue; and 2) obtain preliminary insight into the mediator(s) involved in triggering and eliciting this remote protection. Recovery of contractile force following reoxygenation (our index of ischemic tolerance) was enhanced in jejunal segments pretreated with concentrate generated from PC hearts (33 ± 3% of baseline, P < 0.01) versus segments that received no concentrate (21 ± 2%) and segments treated with concentrate from normoxic hearts (16 ± 3%; P < 0.01). Protection achieved with PC concentrate was attenuated by coadministration of naloxone or glibenclamide, thereby implicating the involvement of opioids and ATP-sensitive potassium channels. Moreover, evaluation of purified subfractions of the crude PC concentrate identified a specific bioactive fraction that may participate in triggering the improved jejunal ischemic tolerance.

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Glibenclamide attenuates ischemia-induced acidosis and loss of cardiac function in rats

Cited by 2 publications

References 26 publications

Myocardial blood flow under general anaesthesia with sevoflurane in type 2 diabetic patients: a pilot study

Myocardial blood flow under general anaesthesia with sevoflurane in type 2 diabetic patients: a pilot study

Myocardial preconditioning factors evoke mesenteric ischemic tolerance via opioid receptors and K_ATPchannels

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Glibenclamide attenuates ischemia-induced acidosis and loss of cardiac function in rats

Cited by 2 publications

References 26 publications

Myocardial blood flow under general anaesthesia with sevoflurane in type 2 diabetic patients: a pilot study

Myocardial blood flow under general anaesthesia with sevoflurane in type 2 diabetic patients: a pilot study

Myocardial preconditioning factors evoke mesenteric ischemic tolerance via opioid receptors and KATPchannels

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Myocardial preconditioning factors evoke mesenteric ischemic tolerance via opioid receptors and K_ATPchannels