Cerebral Vascular Responsiveness in Chronic Hypercapnia

Transcranial Doppler estimation of cerebral blood flow and cerebrovascular conductance during modified rebreathing

“…The linear regression slope of the C B F V -P etco 2 relationship (CVMR0, 5%/Torr) over the entire range of changes in P e tc o 2 is consistent with previous findings (8,14,27,40). However, this method of analysis, although practical, evidently underes timates the maximal cerebral vasodilatory effect of CO2, as indicated by the estimates of CVMRmax using either the first-order derivatives of the identified logistic function (8%/ Torr) or the specific linear regressions in the steep portion of sigmoidal curves (7%/Torr) ( Table 2).…”

Decreased cerebrovascular response to CO2in post-menopausal females with COPD: role of oxidative stress

“…We did not find evidence of chronic cerebrovascular dilation in COPD patients. Our results are supported in both an animal model [22], and hypercapnic patients with severe COPD [6]. Cigarette smoking is known to induce both acute and chronic cerebrovascular dilation in healthy individuals, but cerebrovascular reactivity appears to be maintained.…”

“…Recent literature suggests that cerebrovascular sensitivity and ventilatory response are tightly linked in healthy individuals [5]. However, evidence suggests that COPD patients exhibit cerebrovascular disturbances [3,6,7], although the pathological onset and cause of these disturbances have not yet been comprehensively studied.…”

“…While a few studies have looked at cerebrovascular health in COPD patients [3,6,7,11], no study has investigated how oxidative stress and antioxidant activity could be involved in the CBF regulation observed in COPD. Oestrogen is a sex hormone with beneficial vasoactive and antioxidant properties.…”

Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity

“…15,35,37,39 However, previous animal and human data have shown that the cerebral circulation adapts to chronic sustained hypercapnia for more than 6 hours because of normalization of the CSF pH secondary to increased CSF bicarbonate levels. 34,39,[47][48][49][50][51] Our data showed no statistically significant difference in CBF between the acute and chronic respiratory acidosis groups. This result may indicate a physiologic CSF pH compensation limit.…”