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Item does not contain fulltext, Carotid artery (CCA) dilation occurs in healthy subjects during cold pressor test (CPT), while the magnitude of dilation relates to cardiovascular risk. To further explore this phenomenon and mechanism, we examined carotid artery responses to different sympathetic tests, with and without alpha1-receptor blockade and assessed similarity to these responses between carotid and coronary arteries. In randomized order, 10 healthy participants (25 +/- 3 yr) underwent sympathetic stimulation using the CPT (3-min left-hand immersion in ice-slush) and lower-body negative pressure (LBNP). Before and during sympathetic tests, CCA diameter and velocity (Doppler ultrasound) and left anterior descending (LAD) coronary artery velocity (echocardiography) were recorded across 3 min. Measures were repeated 90 min following selective alpha1-receptor blockade via oral prazosin (0.05 mg/kg body wt). CPT significantly increased CCA diameter, LAD maximal velocity, and velocity-time integral area-under-the-curve (all P < 0.05). In contrast, LBNP resulted in a decrease in CCA diameter, LAD maximal velocity, and velocity time integral (VTI; all P < 0.05). Following alpha1-receptor blockade, CCA and LAD velocity responses to CPT were diminished. In contrast, during LBNP (-30 mmHg), alpha1-receptor blockade did not alter CCA or LAD responses. Finally, changes in CCA diameter and LAD VTI responses to sympathetic stimulation were positively correlated ( r = 0.66, P < 0.01). We found distinct carotid artery responses to different tests of sympathetic stimulation, where alpha1 receptors partly contribute to CPT-induced responses. Finally, we found agreement between carotid and coronary artery responses. These data indicate similarity between carotid and coronary responses to sympathetic tests and the role of alpha1 receptors that is dependent on the nature of the sympathetic challenge. NEW & NOTEWORTHY We showed distinct carotid artery responses to cold pressor test (CPT; i.e., dilation) and lower

Item does not contain fulltext, AIM OF THE STUDY: Estimation of cerebral anaerobic metabolism in survivors and non-survivors after cardiac arrest. METHODS: We performed an observational study in twenty comatose patients after cardiac arrest and 19 healthy control subjects. We measured mean flow velocity in the middle cerebral artery (MFVMCA) by transcranial Doppler. Arterial and jugular blood samples were used for calculation of the jugular venous-to-arterial CO2/arterial to-jugular venous O2 content difference ratio. RESULTS: After cardiac arrest, MFVMCA increased from 26.0[18.6-40.4]cm/sec on admission to 63.9[48.3-73.1]cm/sec after 72h (p<0.0001), with no significant differences between survivors and non-survivors (p=0.4853). The MFVMCA in controls was 59.1[52.8-69.0]cm/sec. The oxygen extraction fraction (O2EF) was 38.9[24.4-47.7]% on admission and decreased significantly to 17.3[12.1-26.2]% at 72h (p<0.0001). The decrease in O2EF was more pronounced in non-survivors (p=0.0173). O2EF in the control group was 35.4[32.4-38.7]%. The jugular bulb-arterial CO2 to arterial-jugular bulb O2 content difference ratio was >1 at all time points after cardiac arrest and did not change during admission, with no differences between survivors and non-survivors. Values in cardiac arrest patients were similar to those in normal subjects. CONCLUSIONS: In this study, low CBF after cardiac arrest is not associated with anaerobic metabolism. Hypoperfusion appears to be the consequence of a decrease of neuronal functioning and metabolic needs. Alternatively, hypoperfusion may decrease cerebral metabolism. Subsequently, metabolism increases in survivors, consistent with resumption of neuronal activity, whereas in non-survivors lasting low metabolism reflects irreversible neuronal damage.

Item does not contain fulltext, KEY POINTS: Previous studies indicate a transient reduction in arterial function following large muscle group exercise, but the mechanisms involved are unknown. Sympathetic nervous system activation may contribute to such reductions through direct effects in the artery wall, or because of decreases in arterial shear stress. Administration of prazosin (an alpha1 -adrenoreceptor blocker) abolished the transient reduction in vascular function observed under placebo conditions following exercise. This effect could not be explained by drug-induced changes in arterial shear stress. These results suggest that sympathetic vasoconstriction directly competes with endothelium-dependent dilator activity to influence post-exercise vascular function. These findings have implications for understanding the stimuli responsible for exercise-induced adaptations in arterial function and health in humans. ABSTRACT: Transient reduction in vascular function following systemic large muscle group exercise has previously been reported in humans. The mechanisms responsible are currently unknown. We hypothesised that sympathetic nervous system activation, induced by cycle ergometer exercise, would contribute to post-exercise reductions in flow-mediated dilatation (FMD). Ten healthy male subjects (28 +/- 5 years) undertook two 30 min sessions of cycle exercise at 75% HRmax . Prior to exercise, individuals ingested either a placebo or an alpha1 -adrenoreceptor blocker (prazosin; 0.05 mg kg(-1) ). Central haemodynamics, brachial artery shear rate (SR) and blood flow profiles were assessed throughout each exercise bout and in response to brachial artery FMD, measured prior to, immediately after and 60 min after exercise. Cycle exercise increased both mean and antegrade SR (P < 0.001) with retrograde SR also elevated under both conditions (P < 0.001). Pre-exercise FMD was similar on both occasions, and was significantly reduced (27%) immediately following exercise in the placebo condition (t-test