Effect of labetalol on cerebral blood flow and middle cerebral arterial flow velocity in healthy volunteers

Schroeder, Torben V; Schierbeck, Jens; Howardy, Paul; Knudsen, L.; Skafte-Holm, Philipp; Gefke, Kaj

doi:10.1080/01616412.1991.11739958

Cited by 27 publications

(11 citation statements)

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“…The results of the present study showed that labetalol did not influence global CBF, rCBF or CMRO2. This is in accordance with studies on global CBF, in which xenon-133 inhalation and stationary detectors [15,18] or transcranial Doppler [15] were used for measurement of CBF. The effect of labetalol on rCBF or CBF autoregulation has not been studied previously in humans.…”

Section: Discussionsupporting

confidence: 86%

“…If necessary MAP was maintained unchanged by infusion of angiotensin, which does not influence CBF [13], The second CBF value was corrected for any differences in 2 CO a P from the first measurement using reactivity of CBF to changes in 2 CO a P (carbon dioxide reactivity) of 30 % kPa 91 [14]. It has been shown that labetalol does not influence carbon dioxide reactivity [15].…”

Section: Measurement Of Global and Regional Cbfmentioning

confidence: 99%

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Effect of labetalol on cerebral blood flow, oxygen metabolism and autoregulation in healthy humans

Olsen

Svendsen

Larsen

et al. 1995

British Journal of Anaesthesia

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We have studied the effects of labetalol on cerebral blood flow (CBF) and cerebral oxygen metabolism (CMRO2) in eight healthy volunteers. CBF was measured by single photon emission computerized tomography before and during infusion of labetalol. CMRO2 was calculated as CBF x cerebral arteriovenous oxygen content difference (CaO2-CvO2). CBF autoregulation was tested during infusion of labetalol by changing arterial pressure and estimating relative changes in global CBF from changes in (CaO2-CvO2). CBF before and during infusion of labetalol was 67 and 65 ml/100 g min-1, respectively (P > 0.05). CMRO2 was 2.9 and 2.8 ml/100 g min-1, respectively (P > 0.05). CBF autoregulation was preserved in all subjects. The lower limit of CBF autoregulation was 88 mm Hg (94% of baseline mean arterial pressure). We conclude that labetalol did not influence global or regional CBF, or CMRO2, and CBF autoregulation was preserved.

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Section: Discussionsupporting

confidence: 86%

Section: Measurement Of Global and Regional Cbfmentioning

confidence: 99%

Effect of labetalol on cerebral blood flow, oxygen metabolism and autoregulation in healthy humans

Olsen

Svendsen

Larsen

et al. 1995

British Journal of Anaesthesia

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“…The pathophysiological mechanisms that underlie this disruption are not yet clear. Although there are data suggesting that the sympathetic nervous system restrains cerebrovascular responses to CO 2 ,32 neither agonists nor antagonists of the sympathetic system demonstrate any direct effect on vasoreactivity 33 34. The role of myogenic mechanisms is also unclear.…”

Section: Discussionmentioning

confidence: 99%

Cerebrovascular reactivity assessed by transcranial Doppler ultrasound in sport-related concussion: a systematic review

et al. 2014

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“…While it is unknown if a similar effect is observed in cerebrovascular resistance and/or conductance, this result suggests that the sympathetic system may restrain cerebral blood flow responses to CO 2 . On the other hand, neither agonists nor antagonists of the sympathetic system demonstrate any effect on cerebrovascular vasoreactivity (Moppett et al, 2004;Schroeder et al, 1991), Thus, while sympathetic pathways may play a role in the interaction between cerebral autoregulation and vasoreactivity, the specifics of this interaction remain largely unknown.…”

Section: Interactions Between Autoregulation and Other Effectors Omentioning

confidence: 99%

Integrative physiological and computational approaches to understand autonomic control of cerebral autoregulation

Tan

Taylor

2013

Experimental Physiology

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The brain requires steady delivery of oxygen and glucose, without which neurodegeneration occurs within minutes. Thus, the ability of the cerebral vasculature to maintain relatively steady blood flow in the face of changing systemic pressure, i.e., cerebral autoregulation, is critical to neurophysiologic health. Although the study of autoregulation dates to the early 20th century, only the recent availability of cerebral blood flow measures with high temporal resolution has allowed rapid, beat-by-beat measurements to explore the characteristics and mechanisms of autoregulation. These explorations have been further enhanced by the ability to apply sophisticated computational approaches that exploit the large amounts of data that can be acquired. These advances have led to unique insights. For example, recent studies have revealed characteristic time scales wherein cerebral autoregulation is most active, and specific regions wherein autonomic mechanisms are prepotent. However, given that effective cerebral autoregulation against pressure fluctuations results in relatively unchanging flow despite changing pressure, estimating the pressure-flow relationship can be limited by the error inherent in computational models of autoregulatory function. This review will focus on the autonomic neural control of the cerebral vasculature in health and disease from an integrative physiologic and perspective. It will also provide a critical overview of the current analytic approaches to understand cerebral autoregulation.

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Effect of labetalol on cerebral blood flow and middle cerebral arterial flow velocity in healthy volunteers

Cited by 27 publications

References 0 publications

Effect of labetalol on cerebral blood flow, oxygen metabolism and autoregulation in healthy humans

Effect of labetalol on cerebral blood flow, oxygen metabolism and autoregulation in healthy humans

Cerebrovascular reactivity assessed by transcranial Doppler ultrasound in sport-related concussion: a systematic review

Integrative physiological and computational approaches to understand autonomic control of cerebral autoregulation

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