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PubMed · 8104728

Dexmedetomidine-induced decrease in cerebral blood flow is attenuated by verapamil in rats: a laser Doppler study.

Abstract

This study was performed to examine the changes in local cortical blood flow (CoBF) after simultaneous administration of an alpha 2 adrenergic agonist (dexmedetomidine) and a calcium channel antagonist (verapamil) to urethane-anaesthetized rats. Dexmedetomidine (100 micrograms.kg-1) given intraperitoneally alone resulted in decreases in mean arterial blood pressure (MABP) (F[27,140] = 3.43; P < 0.01) and CoBF (F[27,140] = 4.22; P < 0.01), whereas the heart rate (HR) was increased (F[27,140] = 2.33; P < 0.01). Verapamil (2.5 mg.kg-1) given subcutaneously reduced the MABP (F[27,140] = 3.41; P < 0.01), but the HR and CoBF were not changed. Combined administration of the drugs decreased MAPB (F[27,140] = 5.37; P < 0.01), with no changes in CoBF and HR. The present data indicate that the calcium channel antagonist verapamil did not potentiate the haemodynamic effects of dexmedetomidine in rats, but rather attenuated the effect of dexmedetomidine on CoBF. This favourable interaction suggests a potential therapeutic role of these agents in maintaining cardiovascular stability during surgical interventions.

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BibTeXRIS

F Bari, G Horváth, G Benedek. 1993. Dexmedetomidine-induced decrease in cerebral blood flow is attenuated by verapamil in rats: a laser Doppler study.. https://doi.org/10.1007/bf03009771

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Adrenergic alpha-Agonists↗

Presynaptic alpha-adrenoceptors in median preoptic nucleus modulate inhibitory neurotransmission from subfornical organ and organum vasculosum lamina terminalis.

The median preoptic nucleus (MnPO) in the lamina terminalis receives a prominent catecholaminergic innervation from the dorsomedial and ventrolateral medulla. The present investigation used whole cell patch-clamp recordings in rat brain slice preparations to evaluate the hypothesis that presynaptic adrenoceptors could modulate GABAergic inputs to MnPO neurons. Bath applications of norepinephrine (NE; 20-50 microM) induced a prolonged and reversible suppression of inhibitory postsynaptic currents (IPSCs) and reduced paired-pulse depression evoked by stimulation in the subfornical organ and organum vasculosum lamina terminalis. These events were not correlated with any observed changes in membrane conductance arising from NE activity at postsynaptic alpha(1)- or alpha(2)-adrenoceptors. Consistent with a role for presynaptic alpha(2)-adrenoceptors, responses were selectively mimicked by an alpha(2)-adrenoceptor agonist (UK-14304) and blockable with an alpha(2)-adrenoceptor antagonist (idazoxan). Although the alpha(1)-adrenoceptor agonist cirazoline and the alpha(1)-adrenoceptor antagonist prazosin were without effect on these evoked IPSCs, NE was noted to increase (via alpha(1)-adrenoceptors) or decrease (via alpha(2)-adrenoceptors) the frequency of spontaneous and tetrodotoxin-resistant miniature IPSCs. Collectively, these observations imply that both presynaptic and postsynaptic alpha(1)- and alpha(2)-adrenoceptors in MnPO are capable of selective modulation of rapid GABA(A) receptor-mediated inhibitory synaptic transmission along the lamina terminalis and therefore likely to exert a prominent influence in regulating cell excitability within the MnPO.

Adrenergic alpha-Agonists↗