Reactivity of cerebral blood flow to carbon dioxide in various types of ischemic cerebrovascular disease: evaluation by the transcranial Doppler method.

Abstract

The response of cerebral blood flow to changes in the arterial carbon dioxide partial pressure (i.e., carbon dioxide reactivity) has been evaluated as a parameter of cerebral perfusion reserve in patients with cerebrovascular disease. In this study, variations in this reactivity in various ischemic cerebrovascular diseases were evaluated by a newly established method, a transcranial Doppler technique. Thirty-three patients with symptomatic cerebrovascular disease, 13 patients with asymptomatic cerebral infarction, and 25 age-matched normal control subjects were investigated. The symptomatic patients were divided into three groups; those with unilateral carotid artery obstruction, those with cortical infarction, and those with lacunar infarction. The carbon dioxide reactivity of each subject was determined by simultaneously measuring the mean spatial Doppler frequency in the middle cerebral artery and the end-tidal carbon dioxide partial pressure under normocapnic, hypercapnic, and hypocapnic conditions. In the patients with carotid obstruction, the carbon dioxide reactivity of the hemisphere ipsilateral to the obstruction was more impaired than the reactivity of the symptomatic hemispheres in any other group, and was significantly less than in the contralateral asymptomatic hemisphere (p < 0.01). In patients with cortical infarction, the carbon dioxide reactivity of the symptomatic hemisphere was significantly less than in normal control subjects (p < 0.05) and was also less than that of the contralateral asymptomatic hemisphere (p < 0.05). In patients with lacunar infarction, the carbon dioxide reactivity of both hemispheres was significantly less than that in normal controls (p < 0.01), although there was no difference between the symptomatic and asymptomatic hemispheres. In patients with asymptomatic infarction, the carbon dioxide reactivity was also less than that in normal controls (p < 0.01). The carbon dioxide reactivity of cerebral blood flow measured by this transcranial Doppler technique may be useful for characterizing the hemodynamic changes that occur in various types of ischemic cerebrovascular disease.

A Systematic Review of Dynamic Cerebral and Peripheral Endothelial Function in Lacunar Stroke Versus Controls

“…35 For the cerebral comparisons, we used the test results from the asymptomatic side of the brain, because vascular reactivity was reduced in ipsilateral versus contralateral arteries in patients with cortical stroke due to tissue damage resulting from the stroke (Table). Although individual studies showed differences in endothelial function between patients with lacunar stroke and those with cortical stroke, 35,37,38,42,44 the combined data showed no difference in vascular reactivity between lacunar and cortical stroke in either cerebral (SMD Ϫ0.29, 95% CI Ϫ0.69 to 0.11, Pϭ0.16) or in peripheral (SMD Ϫ0.23, 95% CI Ϫ0.55 to 0.08, Pϭ0.15) circulation. There was no significant heterogeneity between studies.…”

“…30,32,39,40,42 Three studies recruited age-and risk-factor matched control subjects (with longstanding hypertension and hypercholesterolemia in 2 32,34 ; with hypertension only in 1 43 ). Five papers compared patients with lacunar ischemic stroke with patients with cortical ischemic stroke, 35,37,38,42,44 confirming the infarct subtype with CT or MRI. Four studies included patients with Ͼ1 lacunar infarct on CT, 30,37,40,45 MR, 40,45 or both.…”

Diabetes Mellitus Does Not Affect Jugular Bulb Oxygen Saturation in Patients Undergoing Off-Pump Coronary Artery Bypass Graft Surgery

“…16,17 One of the possible causes of increased postoperative neurologic deficits in diabetic patients is impaired cerebrovascular circulatory and vasodilatory reserve. 18,19 Hyperglycemia leads to impaired vascular function by altering endothelial cell function. The pathway that appears most affected by DM is that of nitric oxide 20 and CPB might alter the cerebral endothelial function more extensively in diabetic patients than in non-diabetic patients.…”

Alterations in Nitric Oxide and Endothelin-1 Bioactivity Underlie Cerebrovascular Dysfunction in ApoE-Deficient Mice

“…Altered vascular reactivity associated with atherosclerotic disease in patients has been attributed to hypercholesterolemiainduced 'endothelial dysfunction,' which is characterized specifically by a decrease in the bioavailability of the vasodilator endothelium-derived nitric oxide (NO) (Casino et al, 1993). This view, that endothelial vasodilator NO production is reduced in stroke, is supported by observations that patients with ischemic stroke have impaired cerebral blood flow (Maeda et al, 1993), an effect that is predictive of lacunar infarction (Molina et al, 1999) and is associated with a higher risk of stroke (Yonas et al, 1993). In addition, recent work suggests that reduced capacity to generate NO, reflected by decreased levels of the metabolites of NO in plasma, correlates with risk of stroke (Rashid et al, 2003) and may be due to the presence of specific genetic polymorphisms in the endothelial form of the NO synthase enzyme, eNOS, gene (Tao and Chen, 2009).…”