Assessment of the Cerebral Hemodynamic Benefits of Carotid Artery Stenting for Patients with Preoperative Hemodynamic Impairment Using Cerebral Single Photon Emission Computed Tomography (SPECT) and Carbon Dioxide Inhalation.

BACKGROUND The aim of this study was to evaluate the effects of carotid artery angioplasty and carotid artery stenting (CAS) on cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) in patients with preoperative cerebrovascular hemodynamic impairment. MATERIAL AND METHODS Seventeen patients with unilateral severe internal carotid artery (ICA) stenosis and ipsilateral CVR impairment underwent CAS. CBF and CVR were measured by single photon emission computed tomography (SPECT) with inhalation of carbon dioxide (CO2) one week before and three months after CAS. Sixty-eight ROIs in the middle cerebral artery (MCA) territory were analyzed in 17 patients. RESULTS Before CAS, CVR was impaired in all ROIs. CBF was impaired in 16 ROIs (23.5%). The percentage of ROIs with impaired CBF was significantly increased in patients with ≥90% carotid artery stenosis (p=0.047) without collateral flow through the circle of Willis (p=0.005). CAS significantly increased CVR in ROIs with a normal preoperative CBF and impaired CVR, indicating mild hemodynamic impairment (0.9±6.7% vs. 4.9±8.6%) (p=0.014). CAS significantly increased CBF in ROIs with preoperative impaired CBF and impaired CVR, indicating severe hemodynamic impairment (79.1±7.5% vs. 86.7±10.0%) (p<0.001). Following CAS, ROIs with normal CBF and impaired CVR had a significantly increased percentage of improved CVR (p=0.047); ROIs with impaired CBF and impaired CVR had a significantly increased percentage of improved CBF (p=0.027). CONCLUSIONS The severity of preoperative hemodynamic impairment, which is related to the degree of carotid artery stenosis and cerebral collateral flow, may influence hemodynamic benefits by CAS.

Multiple Silent Brain Infarcts Are Associated with Severer Stroke in Patients with First-Ever Ischemic Stroke without Advanced Leukoaraiosis.

BACKGROUND: Silent brain infarct (SBI) is associated with symptomatic stroke, but the association between SBI and acute ischemic stroke severity is uncertain. We aimed at investigating the association between SBI number and stroke severity in patients with first-ever ischemic stroke without advanced leukoaraiosis. METHODS: This study included 115 patients with first-ever ischemic stroke without advanced leukoaraiosis. National Institutes of Health Stroke Scale (NIHSS) scores were measured. Magnetic resonance imaging (MRI) was performed to detect the acute ischemic infarct and SBI. The location of infarct was divided into anterior and posterior circulations. The size of infarct was divided into large (≥15 mm) and small (<15 mm) infarctions. The number of SBIs was divided into single and multiple (r2) subgroups. The association between SBI and the NIHSS score was analyzed by stratification of stroke locations. The associations between SBI and the NIHSS score and the size of the acute ischemic infarct were analyzed by logistic regression. RESULTS: Of the 74 patients with SBI, single SBI was 30 (40.5%) and multiple SBIs were 44 (59.5%). Age (odds ratio [OR] = 1.125, P < .001) and hypertension (OR = 3.562, P < .05) were independent risk factors for SBI. When adjusted for all the other vascular risk factors, multiple SBIs had a higher percentage of more than 3 NIHSS scores (OR = 3.59, 95% confidence interval [CI]: 1.00-12.99, P = .048) and a large acute ischemic infarct (OR = 3.71, 95% CI: 1.23-11.22, P = .020) than no SBI. CONCLUSION: Multiple SBIs have severer neurological deficits and larger infarcts for ischemic stroke than no SBI, which may suggest the large-artery or cardiovascular vasculopathy evolution and poor collateral circulation in patients with multiple SBIs.

[Effects of acute hypobaric hypoxia on gastric emptying and intestinal propulsion: experiment with rats].

OBJECTIVE: To investigate the impact of acute hypobaric hypoxia on the gastrointestinal motility. METHODS: Eighty Wistar rats were randomly divided into 4 equal groups to be fed with (99)Tc(m)-labeled test food: ground level control group, put in the hypobaric chamber for 30 minutes; 3000 m simulated altitude group, exposed to the environment of simulated altitude of 3000 m for 30 minutes; 5000 m simulated altitude group, exposed to the environment of simulated altitude of 5000 m for 30 minutes; and mosapride + 5000 m simulated altitude group, fed with mosapride 2 mg/kg by perfusing stomach and fed with isotope-labeled test food 30 minutes later, and then exposed to 5000 m simulated altitude for 30 minutes. By the end of experiment the rats were killed, their stomachs were taken out to calculate the gastric emptying rate. Their intestine from pylorus to ileocecum was taken out to measure the intestinal propulsion function by using charcoal particle method. At the beginning and at the end of experiment abdominal arterial blood samples were collected to detect the plasma motilin and nitric oxide (NO) concentrations. RESULTS: The gastric emptying rate of the 5000 m simulated altitude group was 41% +/- 10%, significantly lower than that of the ground level group (62% +/- 12%, P < 0.01), and the charcoal transit rate of the 5000 m simulated altitude group was 37% +/- 8%, significantly lower than that of the ground level group (61% +/- 13%, P < 0.01). The gastric emptying rate and intestine propulsion rate of the 3000 m simulated altitude group were not significantly different from those of the ground level group. The gastric emptying rate of the mosapride + 5000 m simulated altitude group was 55% +/- 12%, significantly higher than that of the 5000 m simulated altitude group (P < 0.05), however, the intestine propulsion rate of the mosapride + 5000 m simulated altitude group was not significantly different from that of the 5000 m simulated altitude group (P > 0.05). The plasma motilin level of the 5000 m simulated altitude group was 88 pg/ml +/- 19 pg/ml, significantly lower than that of the ground level group (123 pg/ml +/- 28 pg/ml, P < 0.01), in contrast, the plasma NO level of the 5000 m simulated altitude group was 106 micromol/L +/- 24 micromol/L, significantly higher than that of the ground level group (80 micromol/L +/- 18 micromol/L, P < 0.01). CONCLUSION: Acute exposure to hypobaric hypoxia at the height of 5000 m inhibits the gastric emptying and intestinal propulsion. Mosapride may alleviate the inhibitory effect of hypobaric hypoxia on gastric emptying. Decrease of plasma motilin and elevation of NO level may be the main mechanism of inhibition of gastrointestinal motility by hypobaric hypoxia.