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Alpha agonist drug usage during CPR.

Abstract

As a result of many investigations, the role of adrenergic drugs in cardiopulmonary resuscitation (CPR) has been identified, but the choice of drug and drug dosage are yet to be defined. It has been suggested that the successful return of circulation following cardiac arrest is linked with the ability to achieve a diastolic arterial pressure of 30 to 40 mm Hg. Since the turn of this century, the addition of epinephrine to resuscitation procedures has been shown to increase greatly diastolic arterial pressures and resuscitation success. The key to epinephrine's action lies in its alpha agonist properties (which promote peripheral vasoconstriction, leading ultimately to increased coronary perfusion) rather than its direct beta effects (which increase the workload of the fibrillating myocardium). Indeed, pure alpha agonist drugs work as effectively as epinephrine in restoring the circulation, and beta agonists are totally ineffective when used during the arrest period. The hypothesis that pure alpha agonists may be superior to epinephrine during CPR is the subject of current investigations. To date, drug dosage has been largely empirical. During CPR other factors play a role in drug effectiveness, including the injection site, rate of blood flow, and current metabolic status. Because the early use of effective alpha agonists can improve survival, the search for the best drug, via the best route and at the best dosage deserves additional investigation.

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BibTeXRIS

S H Ralston. 1984. Alpha agonist drug usage during CPR.. https://doi.org/10.1016/s0196-0644(84)80437-0

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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↗