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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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Background and Purpose: Hypercapnia leads to increased cerebral blood flow and impaired autoregulation by changing the cerebrovascular resistance (CVR). We studied the effect of hypercapnia on critical closing pressure (CCP) and resistance area product (RAP) which effectively reflects the role of vascular tone and resistance respectively in altering cerebrovascular resistance and maintaining cerebral autoregulation during transient hypotension. Methods: –26 healthy subjects had continuous cerebral blood flow velocity and arterial blood pressure recording. Transient hypotension was induced by sudden release of thigh cuff after suprasystolic inflation for 3 minutes. 3 trials of thigh cuff maneuver were performed with normal breathing, 3% CO 2 breathing and 5% CO 2 breathing. CO 2 inhalation was given for last 45 seconds of thigh cuff maneuver and continued for 90 seconds after release. Autoregulatory Index (ARI) was calculated for each trial with Tieck’s model. CCP and RAP were computed for 10 seconds’ window each at 1 minute after inflation (Baseline), immediately before release (Prerelease) and immediately after release (Release) of inflated thigh cuff. Results: –ARI values decreased significantly (p < 0.0001) from 5.46 ± 1.47 to 2.0 ± 1.35 and 1.63 ± 1.09 during 3% CO 2 and 5% CO 2 trial respectively. No significant changes were observed in CCP value during thigh cuff release with all three trials. RAP significantly dropped from prerelease value after thigh cuff release in all 3 trials. Drop in RAP attenuated during hypercapnia trial and had significant (p < 0.0001) difference between RAP Prerelease – Release ( d RAP) for Normal breathing (0.20 ± 0.12) and 3% and 5 % CO 2 trials (0.089 ± 0.090, 0.081 ± 0.093). d RAP was significantly correlated (Spearmen r = 0.42, p = 0.0004) with the ARI values where higher d RAP had better autoregulation. Conclusion: – Cerebral autoregulation during transient hypotension acts by changing vascular resistance i.e. RAP without any effect on vascular tone i.e. CCP and had been suggested to reflect myogenic component of autoregulation to blood pressure changes. We concluded that hypercapnia leads to impairment of myogenic component of autoregulation during transient arterial blood pressure changes as suggested by attenuated d RAP.

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