Responses of cerebral circulation produced by adrenoceptor agonists and antagonists in rats

Tsai, Mei-Ling; Lee, C. Y.; Lin, Mao Tsun

doi:10.1016/0028-3908(89)90120-2

Cited by 10 publications

(4 citation statements)

References 17 publications

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“…These data suggest that the initial, short-lived MA-induced increase in CBF may be related to MA-mediated α-adrenergic stimulation (Tsai et al, 1989), since MAP remained within autoregulatory range (Ruland and Aiyagari, 2007). However, there are conflicting reports on role of the sympathetic nervous system in CBF regulation (Busija et al, 1980; Heistad et al, 1977; Meyer et al, 1973; Skinhoj, 1972), suggesting that future followup studies may be required to precisely define the mechanism underlying the initial, transient MA-induced increase in CBF.…”

Section: Discussionmentioning

confidence: 88%

Methamphetamine causes sustained depression in cerebral blood flow

et al. 2011

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The use prevalence of the highly addictive psychostimulant methamphetamine (MA) has been steadily increasing over the past decade. MA abuse has been associated with both transient and permanent alterations in cerebral blood flow (CBF), hemorrhage, cerebrovascular accidents and death. To understand MA-induced changes in CBF, we exposed C56BL/6 mice to an acute bolus of MA (5 mg/kg MA, delivered IP). This elicited a biphasic CBF response, characterized by an initial transient increase (~5 min) followed by a prolonged decrease (~30 min) of approximately 25% relative to baseline CBF -as measured by laser Doppler flowmetry over the somatosensory cortex. To assess if this was due to catecholamine derived vasoconstriction, phentolamine, an α-adrenergic antagonist was administered prior to MA treatment. This reduced the initial increase in CBF but failed to prevent the subsequent, sustained decrease in CBF. Consistent with prior reports, MA caused a transient increase in mean arterial blood pressure, body temperature and respiratory rate. Elevated respiratory rate resulted in hypocapnia. When respiratory rate was Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access

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Section: Discussionmentioning

confidence: 88%

Methamphetamine causes sustained depression in cerebral blood flow

et al. 2011

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“…In rats anaesthetized with volatile agents, the infusion of NE caused a significant reduction in flow that was reversed by PHO (Edvinsson et al, 1979) unless excessive and non-physiologic increases in blood pressure were induced (i.e. 80-100 mmHg) (Tsai et al, 1989). The use of inhaled anaesthetics in these studies is likely to have interfered with the autoregulatory response to changes in pressure unmasking the a-adrenoceptor response.…”

Section: Discussionmentioning

confidence: 92%

“…The current observation of increased MFV despite no change in blood pressure during PHO infusion alone supports this conclusion. 80-100 mmHg) (Tsai et al, 1989). In rats anaesthetized with volatile agents, the infusion of NE caused a significant reduction in flow that was reversed by PHO (Edvinsson et al, 1979) unless excessive and non-physiologic increases in blood pressure were induced (i.e.…”

Section: Discussionmentioning

confidence: 99%

Circulating norepinephrine and cerebrovascular control in conscious humans

Kimmerly

Tutungi

Wilson

et al. 2003

Clin Physio Funct Imaging

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“…Phentolamine and propranolol, however, increased EEG spike latencies, whether administered before or after HBO 2 , at the transition from phase I to phase II. The immediate decrease in rCBF following phentolamine may be due to a breakthrough of cerebral autoregulation, as suggested to occur with acute hypertension at sea level (41). The eventual or rebound regional cerebral hyperemia observed with phentolamine, however, suggests that excessive sympathetic outflow and increased NO • production overrides this temporary relief and predominates in regulating cerebral blood flow in phase II of HBO 2 (19).…”

Section: Discussionmentioning

confidence: 94%

Adrenoceptor blockade modifies regional cerebral blood flow responses to hyperbaric hyperoxia: protection against CNS oxygen toxicity

Gasier

Demchenko

Zhilyaev

et al. 2018

Journal of Applied Physiology

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Exposure to extreme-hyperbaric oxygen (HBO2), > 5-6 atmospheres absolute (ATA), produces baroreflex impairment, sympathetic hyperactivation, hypertension, tachycardia, and cerebral hyperemia, known as Phase II, culminating in seizures. We hypothesized that attenuation of the effects of high sympathetic outflow would preserve regional cerebral blood flow (rCBF) and protect against HBO2-induced seizures. To explore this possibility, we tested four adrenoceptor antagonists in conscious and anesthetized rats exposed to HBO2 at 5 and 6 ATA, respectively: phentolamine (nonselective α1 and 2), prazosin (selective α1), propranolol (nonselective β1 and 2) and atenolol (selective β1). In conscious rats, 4 drug-doses were administered to rats prior to HBO2 exposures, and seizure latencies were recorded. Drug-doses that provided similar protection against seizures were administered before HBO2 exposures in anesthetized rats to determine the effects of adrenoceptor blockade on mean arterial pressure, heart rate, rCBF and EEG spikes. All four drugs modified cardiovascular and rCBF responses in HBO2 that aligned with epileptiform discharges, but only phentolamine and propranolol effectively increased EEG spike latencies by ~20 and 36 min, respectively. When phentolamine and propranolol were delivered during HBO2 at the onset of phase II, only propranolol led to sustained reductions in heart rate and rCBF, preventing the appearance of epileptiform discharges. The enhanced effectiveness of propranolol may extend beyond β-adrenoceptor blockade, i.e. membrane stability and reduced metabolic activity. These results indicate that adrenoceptor drug pre-treatment will minimize the effects of excessive sympathetic outflow on rCBF and extend HBO2 exposure time.

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Responses of cerebral circulation produced by adrenoceptor agonists and antagonists in rats

Cited by 10 publications

References 17 publications

Methamphetamine causes sustained depression in cerebral blood flow

Methamphetamine causes sustained depression in cerebral blood flow

Circulating norepinephrine and cerebrovascular control in conscious humans

Adrenoceptor blockade modifies regional cerebral blood flow responses to hyperbaric hyperoxia: protection against CNS oxygen toxicity

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