Dynamic cerebral autoregulation in acute lacunar and middle cerebral artery territory ischemic stroke

Background and Purpose - We addressed whether dynamic cerebral autoregulation (dCA) is affected in middle cerebral artery (MCA) territory (MCAS) and lacunar ischemic stroke (LS). Methods - Blood pressure (MAP) and MCA velocity (V) were measured in 10 patients with large MCAS (National Institutes of Health Stroke score, 17 +/- 2; mean +/- SEM), in 10 with LS (score, 9 +/- 1), and in 10 reference subjects. dCA was evaluated in time (delay of the MCA V-mean counter-regulation during changes in MAP) and frequency domains (cross-spectral MCA V-mean-to-MAP phase lead). Results - In reference subjects, latencies for MAP increments (5.3 +/- 0.5 seconds) and decrements (5.6 +/- 0.5 seconds) were comparable, and low frequency MCA V-mean-to-MAP phase lead was 56 +/- 5 and 59 +/- 5 degrees (left and right hemisphere). In MCAS, these latencies were 4.6 +/- 0.7 and 5.6 +/- 0.5 seconds in the nonischemic hemisphere and not detectable in the ischemic hemisphere. In the unaffected hemisphere, phase lead was 61 +/- 6 degrees versus 26 +/- 6 degrees on the ischemic side (P <0.05). In LS, no latency and smaller phase lead bilaterally (32 +/- 6 and 33 +/- 5 degrees) conformed to globally impaired dCA. Conclusions - In large MCAS infarcts, dynamic cerebral autoregulation was impaired in the affected hemisphere. In LS, dynamic cerebral autoregulation was impaired bilaterally, a finding consistent with the hypothesis of bilateral small vessel disease in patients with lacunar infarct

Diabetic autonomic neuropathy: conventional cardiovascular laboratory testing and new developments

Cardiovascular reflex tests remain the investigational cornerstone for the assessment of patients in the clinical autonomic laboratory. Three cardiovagal tests have been found suitable for testing: the instantaneous heart rate responses induced by deep breathing, Valsalva's manoeuvre and standing up. Suitable laboratory indices of adrenergic function include continuous monitoring of blood pressure responses induced by Valsalva's manoeuvre and standing up, which is now possible through tracking of beat-to-beat blood pressure changes at the finger. Spectral analysis of heart rate and blood pressure and pulse wave analysis for stroke volume changes are promising approaches to evaluate abnormalities in arterial baroreflex regulatory mechanisms in diabetic patient

The role of carotid chemoreceptors in the sympathetic activation by adenosine in humans.

Contains fulltext : 59280.pdf (publisher's version ) (Open Access)The direct vasodilatory and negative chronotropic effects of adenosine in humans are counterbalanced by a reflex increase in sympathetic nerve traffic. A suggested mechanism for this reflex includes peripheral chemoreceptor activation. We, therefore, assessed the contribution of carotid chemoreceptors to sympatho-excitation by adenosine. Muscle sympathetic nerve activity was recorded during adenosine infusion (140 microg.kg(-1).min(-1) for 5 min) in five patients lacking carotid chemoreceptors after bilateral carotid body tumour resection (one male and four female, mean age 51 +/- 11 years) and in six healthy controls (two male and four female, mean age 50 +/- 7 years). Sympathetic responses to sodium nitroprusside injections were assessed to measure baroreceptor-mediated sympathetic activation. In response to adenosine, controls showed no change in blood pressure, an increase in heart rate (+48.2 +/- 13.2%; P<0.003) and an increase in sympathetic nerve activity (+195 +/- 103%; P<0.022). In contrast, patients showed a decrease in blood pressure (-14.6 +/- 4.9/-17.6 +/- 6.0%; P<0.05), an increase in heart rate (+25.3 +/- 8.4%; P<0.032) and no significant change in sympathetic activity. Adenosine-induced hypotension in individual patients elicited less sympathetic activation than equihypotensive sodium nitroprusside injections. In humans lacking carotid chemoreceptors, adenosine infusion elicits hypotension due to the absence of significant sympatho-excitation. Chemoreceptor activation is essential for counterbalancing the direct vasodilation by adenosine. In addition, blunting of the baroreflex sympathetic response to adenosine-induced hypotension may indicate a direct sympatho-inhibitory effect of adenosine

Baroreflex failure following radiation therapy for nasopharyngeal carcinoma

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Baroreflex failure: a neglected type of secondary hypertension.

Contains fulltext : 58150.pdf (publisher's version ) (Closed access)The arterial baroreflex buffers abrupt transients of blood pressure and prevents pressure from rising or falling excessively. In experimental animals, baroreceptor denervation results in temporary or permanent increases in blood pressure level and variability, depending on the extent of denervation. In humans, the clinical syndrome of baroreflex failure may arise from denervation of carotid baroreceptors following carotid body tumour resection, carotid artery surgery, neck irradiation and neck trauma. The syndrome is characterised by acute malignant hypertension and tachycardia followed by labile hypertension and hypotension. Baroreflex failure can be a cause of hypertension and should also be considered in the differential diagnosis of pheochromocytoma. Patients with suspected baroreflex failure should be referred to specialised centres for diagnostic testing and treatment

Cardiovascular responses to stress after carotid baroreceptor denervation in humans.

Contains fulltext : 58704.pdf (publisher's version ) (Closed access)Iatrogenic bilateral denervation of carotid sinus baroreceptors may occur as a complication of carotid body tumor resection and radiation therapy of the neck. The acute phase of the resulting syndrome of baroreflex failure is characterized by a limited blood pressure buffering capacity against excessive rise or fall in response to emotional and physical stimuli like sexual arousal and cold. Paroxysms of severe hypertension and tachycardia, accompanied by excessive increments in sympathetic tone and catecholamine plasma levels, were ascribed to loss of tonic inhibitory influence of baroreceptors on sympathetic tone. Bilateral anesthetic blockade of baroreceptor afferent nerves was shown to result in a strong increase in muscle sympathetic nerve activity and disruption of its normal patterning. This chapter reviews our findings on the long-term effects of iatrogenic baroreflex trauma on the hemodynamic responses to pharmacological, physical, and emotional stress in the autonomic function laboratory as well as under daily life conditions. Chronic attenuation of baroreflex sensitivity after carotid body tumor resection and neck irradiation results in an increased blood pressure variability. However, unopposed sympathetic activation in response to physical and emotional stress appears to be limited to the acute phase of baroreflex failure