Cerebrovascular reactivity is impaired in patients with non-insulin-dependent diabetes mellitus and microangiopathy

Petrică, Ligia; Petrica, Maxim; Vlad, Adrian; Bob, Flaviu; Gluhovschi, Cristina; Gluhovschi, Gheorghe; Jianu, Dragoș Cătălin; Ursoniu, Sorin; Schiller, Adalbert; Velciov, Silvia; Trandafirescu, Virginia; Bozdog, Gheorghe

doi:10.1007/s00508-007-0809-0

Cited by 33 publications

(31 citation statements)

References 32 publications

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“…Among demographic factors examined in our study (sex, age and weight) and underlying diseases (DM and hypertension), only DM was found to be a significant covariate, decreasing the slope related to the reactivity of rSO 2 in response to changes in EtCO 2 , which is consistent with the previous result that Type 2 DM is associated with impaired cerebrovascular reactivity to PaCO 2 compared to healthy agematched controls [15][16][17]. It has been reported that one reason for reduced cerebrovascular reactivity in patients with DM is endothelial dysfunction caused by an imbalance between endothelium-derived vasodilator and vasoconstrictor substances [25].…”

Section: Discussionsupporting

confidence: 81%

“…Meanwhile, changing partial pressure of carbon dioxide in arterial blood (PaCO 2 ) is the strongest modulator of CBF because a linear relationship exists between PaCO 2 and CBF within a normal physiological range of PaCO 2 (20-75 mmHg) [12]. However, when considering cerebrovascular reactivity to PaCO 2 , other factors such as MAP, use of anaesthetic agents and disease states should be taken into account [12][13][14][15][16][17][18][19].In practice, cerebrovascular reactivity to PaCO 2 can be assessed by measuring cerebral oxygen saturation (rSO 2 ) with a near-infrared spectroscopy device [20], which has been used as a non-invasive and continuous monitoring method for detecting cerebral ischaemia in various clinical situations [8]. It measures the ratio of oxygenated haemoglobin and deoxygenated haemoglobin, and rSO 2 values are calculated based on the assumption of a fixed reference ratio of 25% arterial and 75% venous contribution [21].…”

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confidence: 99%

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confidence: 99%

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Modelling of the Effect of End‐Tidal Carbon Dioxide on Cerebral Oxygen Saturation in Beach Chair Position under General Anaesthesia

Kim¹,

Chae

Chun

et al. 2016

Basic Clin Pharma Tox

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Patients undergoing shoulder surgery in the beach chair position (BCP) under general anaesthesia may be at risk of cerebral desaturation. Increasing end-tidal carbon dioxide (EtCO 2 ) is the most convenient and powerful method for the management of cerebral desaturation. The purpose of this study was to investigate the quantitative relationship between EtCO 2 and cerebral oxygen saturation (rSO 2 ) and to identify the associated influencing factors. Fifty-one patients undergoing arthroscopic shoulder surgery in the BCP under general anaesthesia completed this study. Desflurane and remifentanil were used, and EtCO 2 was steadily increased and then decreased by adjusting the ventilator settings every 3 min. so that time lag of rSO 2 response to EtCO 2 changes could be delineated. Near-infrared spectroscopy was used to monitor rSO 2 response. An indirect response model was used to examine the relationship between EtCO 2 and rSO 2 . To determine the relevant covariates, a stepwise approach was used. There was a linear relationship between rSO 2 and EtCO 2 with a slight delay in the peak of rSO 2 relative to EtCO 2 . Increase in end-tidal desflurane concentration led to a slower response of rSO 2 to the changes of EtCO 2 (p = 0.0002). The presence of diabetes mellitus reduced the reactivity of rSO 2 to EtCO 2 changes (p < 0.0001). This model-based approach revealed that diabetes mellitus attenuates the response of rSO 2 to changes in EtCO 2 . The management of cerebral desaturation by hypercapnia in patients with diabetes may be less effective than in non-diabetic patients under general anaesthesia with BCP.The beach chair position (BCP) under general anaesthesia with induced hypotension is commonly used in arthroscopic shoulder surgery [1]. Unlike the BCP in an awake state in which the compensatory mechanism to increase blood pressure occurs, the BCP under general anaesthesia is associated with significant hypotension and cerebral desaturation [2][3][4]. Further hypotension induced for better visualization of the surgical field might aggravate cerebral desaturation [4,5]. As cerebral desaturation during surgery is associated with postoperative cognitive dysfunction and stroke [6,7], prevention and treatment of cerebral desaturation is necessary.As cerebral oxygenation is dependent on cerebral perfusion and oxygen transport, interventions for the prevention and treatment of cerebral desaturation during shoulder surgery include increasing systemic arterial pressure with vasopressors, increasing end-tidal carbon dioxide (EtCO 2 ) with ventilation adjustment and increasing fraction of inspired oxygen (FiO 2 ) [3,4,8,9]. Although increases in systemic arterial pressure may cause rapid increases in cerebral blood flow (CBF), CBF returns to its baseline value within a few seconds by the mechanism of cerebral autoregulation, which aims to maintain a stable CBF over a wide range of mean arterial pressures (MAP) of 70-150 mmHg [10][11][12]. Moreover, increases in arterial pressure may worsen visualization of the sur...

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Section: Discussionsupporting

confidence: 81%

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confidence: 99%

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confidence: 99%

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Modelling of the Effect of End‐Tidal Carbon Dioxide on Cerebral Oxygen Saturation in Beach Chair Position under General Anaesthesia

Kim¹,

Chae

Chun

et al. 2016

Basic Clin Pharma Tox

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“…Moreover, ECD and TCD ultrasound, by utilizing the PI and RI, proved a reliable tool in the assessment of structural and functional changes in the cerebral vessels in asymptomatic non-diabetic and diabetic CKD patients, modifications which correlated with classic and non-classic cerebrovascular risk factors [17][18][19][20][21][22].…”

Section: Cerebral Vessels Modificationsmentioning

confidence: 99%

“Does chronic kidney disease define a particular risk pattern of cerebral vessels modifications in patients with symptomatic ischemic cerebrovascular disease?”

et al. 2010

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AbstractCardiovascular complications, including stroke, may be attributed the highest rate of morbidity and mortality in patients with chronic kidney disease (CKD). The aim of our study was to evaluate the prevalence of CKD in patients with symptomatic ischaemic cerebrovascular disease and to establish of whether CKD may define a particular risk pattern of cerebral vessels modifications in this category of patients. The prevalence of CKD was evaluated in 590 consecutive patients with symptomatic ischaemic cerebrovascular disease admitted to a department of neurology. The types of stroke, the vascular territories, the vascular modifications and the haemodynamic changes (resistance index- RI) found by neurosonology (extracranial and transcranial Doppler ultrasound) were analysed in relation to classic and non-classic cerebrovascular risk factors, as well as to stages of CKD (defined by estimated glomerular filtration rate-eGFR-MDRD4 formula-K/DOQI 2002). The prevalence of CKD in the studied patients was 70.84%. Atherosclerosis in a diffuse pattern was detected in 79.7% of CKD patients, while carotid artery stenoses were found in 10% of cases, occlusions- 5.3%, stenoses + occlusions-1.2%, and multiple stenoses- 3.8% of cases. The RI evaluated in the internal carotid arteries correlated with fibrinogen(P<0.0001) and GFR(P<0.0001), while IR in the middle cerebral arteries correlated with fibrinogen(P<0.05), C-reactive protein(P<0.0001), and GFR(P<0.0001). There is a strong relation between symptomatic cerebrovascular disease and CKD, a fact demonstrated by the increased prevalence of CKD in these patients and by the severity of the cerebral vessels lesions.

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“…1,2 Endothelial dysfunction precedes the development of clinically evident vascular complications 3,4 and in many vascular beds has been shown to be proportional to the severity of DM or IR. 5,6 Endothelial function can be assessed by quantifying the vascular reactivity (VR) of any vascular bed in response to a stimulus.…”

Section: Introductionmentioning

confidence: 99%

Correlations between endothelial function in the systemic and cerebral circulation and insulin resistance in type 2 diabetes mellitus

Prakash

Chandran

Khadgawat

et al. 2015

Diabetes and Vascular Disease Research

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Insulin resistance is associated with endothelial dysfunction in type 2 diabetes mellitus, which can lead to impaired vascular reactivities of both systemic and cerebral circulations. Appropriate 'correction' of vascular reactivity results for non-endothelium-dependent systemic effects avoids misinterpretation of endothelial function. Therefore, we 'corrected' vascular reactivity results and explored the potential correlations between systemic vascular reactivity, cerebrovascular reactivity and insulin resistance. In 34 patients, 'systemic vascular reactivity' was assessed by quantifying reactive hyperaemia. Cerebrovascular reactivity was assessed by quantifying changes in cerebral blood flow velocity during hypercapnia. To minimize the influence of non-endothelium-dependent systemic effects on vascular reactivity results, 'corrected systemic vascular reactivity' was calculated by normalizing systemic vascular reactivity using the measurements from the contralateral side; and cerebrovascular reactivity results were corrected by calculating percentage and absolute changes in cerebrovascular conductance index ('percent cerebrovascular conductance index' and 'delta cerebrovascular conductance index', respectively). Insulin resistance was estimated by homeostatic model assessment. Correlation between conventional cerebrovascular reactivity and systemic vascular reactivity was not significant. But correlations between 'corrected systemic vascular reactivity' and 'percent cerebrovascular conductance index' (r = 0.51; p = 0.002) and 'corrected systemic vascular reactivity' and 'delta cerebrovascular conductance index' (r = 0.50; p = 0.003) were significant. Among all vascular reactivity parameters, only 'delta cerebrovascular conductance index' was significantly correlated with homeostatic model assessment of insulin resistance (r = −0.38; p = 0.029). In conclusion, endothelial function in the systemic and cerebral circulations is moderately correlated, provided that vascular reactivity estimates are corrected for non-endothelium-dependent influences.

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Cerebrovascular reactivity is impaired in patients with non-insulin-dependent diabetes mellitus and microangiopathy

Abstract: CVR is impaired in normotensive NIDDM patients. These cerebral hemodynamic changes correlate significantly with the duration of DM, parameters of inflammation, proteinuria and serum creatinine.

Cited by 33 publications

References 32 publications

Modelling of the Effect of End‐Tidal Carbon Dioxide on Cerebral Oxygen Saturation in Beach Chair Position under General Anaesthesia

Modelling of the Effect of End‐Tidal Carbon Dioxide on Cerebral Oxygen Saturation in Beach Chair Position under General Anaesthesia

“Does chronic kidney disease define a particular risk pattern of cerebral vessels modifications in patients with symptomatic ischemic cerebrovascular disease?”

Correlations between endothelial function in the systemic and cerebral circulation and insulin resistance in type 2 diabetes mellitus

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