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

Bulte, Carolien S. E.; Brom, Charissa E. van den; Loer, Stephan A.; Boer, Christa; Bouwman, R. Arthur

doi:10.1186/1475-2840-13-62

Cited by 8 publications

(7 citation statements)

References 37 publications

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“…Others reported a decline in CFR in obese, insulin resistant patients [ 19 , 24 ], which was largely explained by concurrent hypertension-related increases in basal myocardial blood flow [ 19 ]. Indeed, baseline myocardial blood flow was similar in healthy controls and diabetic patients without hypertension [ 47 ]. In obesity-prone pigs feeding a HFD for 10 weeks did not affect blood pressure and basal myocardial flow.…”

Section: Discussionmentioning

confidence: 99%

Early impairment of coronary microvascular perfusion capacity in rats on a high fat diet

Haare

Kooi

Vink

et al. 2015

Cardiovasc Diabetol

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BackgroundIt remains to be established if, and to what extent, the coronary microcirculation becomes compromised during the development of obesity and insulin resistance. Recent studies suggest that changes in endothelial glycocalyx properties contribute to microvascular dysfunction under (pre-)diabetic conditions. Accordingly, early effects of diet-induced obesity on myocardial perfusion and function were studied in rats under baseline and hyperaemic conditions.MethodsRats were fed a high fat diet (HFD) for 6 weeks and myocardial microvascular perfusion was determined using first-pass perfusion MRI before and after adenosine infusion. The effect of HFD on microcirculatory properties was also assessed by sidestream darkfield (SDF) imaging of the gastrocnemius muscle.ResultsHFD-fed rats developed central obesity and insulin sensitivity was reduced as evidenced by the marked reduction in insulin-induced phosphorylation of Akt in both cardiac and gastrocnemius muscle. Early diet-induced obesity did not lead to hypertension or cardiac hypertrophic remodeling. In chow-fed, control rats a robust increase in cardiac microvascular perfusion was observed upon adenosine infusion (+40 %; p < 0.05). In contrast, the adenosine response was abrogated in rats on a HFD (+8 %; N.S.). HFD neither resulted in rarefaction or loss of glycocalyx integrity in skeletal muscle, nor reduced staining intensity of the glycocalyx of cardiac capillaries.ConclusionsAlterations in coronary microcirculatory function as assessed by first-pass perfusion MRI represent one of the earliest obesity-related cardiac adaptations that can be assessed non-invasively. In this early stage of insulin resistance, disturbances in glycocalyx barrier properties appeared not to contribute to the observed changes in coronary microvascular function.

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Section: Discussionmentioning

confidence: 99%

Early impairment of coronary microvascular perfusion capacity in rats on a high fat diet

Haare

Kooi

Vink

et al. 2015

Cardiovasc Diabetol

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“…Sevoflurane is one of the most commonly used volatile anesthetic agents for the maintenance of anesthesia in surgical patients, including patients with type 2 DM ( Bulte et al, 2014 ). Sevoflurane has favorable clinical characteristics such as rapid pharmacokinetics and lack of airway irritability.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane Induces Exaggerated and Persistent Cognitive Decline in a Type II Diabetic Rat Model by Aggregating Hippocampal Inflammation

Liu

et al. 2017

Front. Pharmacol.

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Recent studies show that a moderate duration of sevoflurane, one of the most commonly used volatile anesthetics in clinical practice, does not induce cognitive impairment in animals under physiological conditions. However, the influence of sevoflurane on cognitive function under diabetic conditions remains unclear. The aim of this study was to determine whether sevoflurane causes cognitive decline in a rat model of type 2 diabetes mellitus (DM) and if so, to explore a possible underlying mechanism. Diabetic Goto–Kakizaki (GK) rats and non-diabetic Wistar rats underwent 2.6% sevoflurane for 4 h or sham (control) exposure. Cognitive function and hippocampal inflammation were assessed 1 week and 5 months after sevoflurane or sham exposure. Compared with Wistar control rats, GK control rats exhibited shorter freezing times in Trace fear conditioning task 1 week after exposure, took longer to locate the submerged platform and had shorter dwell-time in the target quadrant in Morris Water Maze task 5 months after exposure. GK rats that received sevoflurane not only exhibited less freezing times 1 week after exposure, but also spent more time to locate the submerged platform and had less dwell-time in the target quadrant, compared with GK control rats. Molecular studies revealed that the levels of pro-inflammatory cytokines and activated microglia in the hippocampus were higher in GK control rats than those in Wistar control rats at both time points and were further increased in GK rats receiving sevoflurane. Wistar rats that received sevoflurane and Wistar control rats did not differ in any cognitive performance and molecular assessment. The results suggest that diabetic GK rats exhibit cognitive dysfunction probably due to increased hippocampal inflammation, and that sevoflurane induces exaggerated and persistent cognitive decline in GK rat by aggregating hippocampal inflammation.

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“…Diabetes and obesity are both known to augment cardiovascular responses to anaesthetics [ 16 , 28 , 29 ]; and the well described cardioprotective effects of volatile anaesthetics are reduced under conditions of metabolic stress [ 30 ]. For instance, sevoflurane elicited greater impairments in myocardial blood flow in a pilot study of type 2 diabetic patients [ 31 ]. Isoflurane anaesthesia also impairs baroreflex responsiveness [ 32 ], and obesity is associated with impaired baroreflex sympatho-inhibition [ 33 ]; both effects which are thought to be mediated via augmentation of central nervous system pathways.…”

Section: Introductionmentioning

confidence: 99%

Increased haemodynamic adrenergic load with isoflurane anaesthesia in type 2 diabetic and obese rats in vivo

Bussey

Leeuw

Lamberts

2014

Cardiovasc Diabetol

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BackgroundIncreasing numbers of type 2 diabetic and obese patients with enhanced rates of cardiovascular complications require surgical interventions, however they have a higher incidence of perioperative haemodynamic complications, which has been linked to adrenergic dysfunction. Therefore, we aimed to determine how α- and β-adrenoceptor (AR)-mediated haemodynamic responses are affected by isoflurane anaesthesia in experimental type 2 diabetes and obesity in vivo.MethodsSixteen-week old male Zucker type 2 Diabetic Fatty (ZDF) rats, Zucker Obese rats and their lean counterparts (n = 7-9 per group) were instrumented with radio telemeters to record blood pressure and heart rate and with vascular access ports for non-invasive intravenous drug delivery in vivo. Haemodynamic effects of α-AR (phenylephrine; 1-100 μg.kg−1) or β-AR (dobutamine; 2-120 μg.kg−1) stimulation were assessed under conscious and anaesthetised (isoflurane; 2%) conditions.ResultsVascular α-AR sensitivity was increased in both diabetic (non-diabetic 80 ± 3 vs. diabetic 95 ± 4 ΔmmHg at 100 μg.kg−1; p < 0.05) and obese (lean 65 ± 6 vs. obese 84 ± 6 ΔmmHg at 20 μg.kg−1; p < 0.05) conscious rats. Interestingly, anaesthesia exacerbated and prolonged the increased α-AR function in both diabetic and obese animals (non-diabetic 51 ± 1 vs. diabetic 68 ± 4 ΔmmHg, lean 61 ± 5 vs. obese 84 ± 2 ΔmmHg at 20 μg.kg−1; p < 0.05). Meanwhile, β-AR chronotropic sensitivity was reduced in conscious diabetic and obese rats (non-diabetic 58 ± 7 vs. diabetic 27 ± 8 Δbpm, lean 103 ± 12 vs. obese 61 ± 9 Δbpm at 15 μg.kg−1; p < 0.05). Anaesthesia normalised chronotropic β-AR responses, via either a limited reduction in obese (lean 51 ± 3 vs. obese 66 ± 5 Δbpm; NS at 15 μg.kg−1) or increased responses in diabetic animals (non-diabetic 49 ± 8 vs. diabetic 63 ± 8 Δbpm, at 15 μg.kg−1; NS at 15 μg.kg−1).ConclusionsLong term metabolic stress, such as during type 2 diabetes and obesity, alters α- and β-AR function, its dynamics and the interaction with isoflurane anaesthesia. During anaesthesia, enhanced α-AR sensitivity and normalised β-AR function may impair cardiovascular function in experimental type 2 diabetes and obesity.

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

Cited by 8 publications

References 37 publications

Early impairment of coronary microvascular perfusion capacity in rats on a high fat diet

Early impairment of coronary microvascular perfusion capacity in rats on a high fat diet

Sevoflurane Induces Exaggerated and Persistent Cognitive Decline in a Type II Diabetic Rat Model by Aggregating Hippocampal Inflammation

Increased haemodynamic adrenergic load with isoflurane anaesthesia in type 2 diabetic and obese rats in vivo

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