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PubMed1994

Differential effect of esmolol on the fast and slow AV nodal pathways in patients with AV nodal reentrant tachycardia.

INTRODUCTION: AV nodal reentrant tachycardia (AVNRT) usually involves anterograde conduction over a slowly conducting ("slow") pathway and retrograde conduction over a rapidly conducting ("fast") pathway. A variety of drugs, such as beta blockers, digitalis, and calcium channel blockers, have been reported to prolong AV nodal refractoriness in both the anterograde and retrograde limbs of the circuit. However, few data are available that address whether the fast and slow pathways respond in a quantitatively different manner to drugs such as beta-adrenergic antagonists. In addition, it is not known whether the effects of these agents on refractoriness parallel the effects on conduction in the fast and slow pathways. The present study was performed to measure the effect of the intravenous beta-adrenergic agent, esmolol, on refractoriness and conduction in both the fast and slow AV nodal pathways in patients with AVNRT. METHODS AND RESULTS: Thirteen patients with discontinuous AV nodal conduction properties and typical AVNRT were studied. Anterograde and retrograde AV nodal functional assessment was performed at baseline and following steady-state drug infusion of intravenous esmolol at a dose of 500 micrograms/kg for 1 minute, 150 micrograms/kg per minute for the next 4 minutes, followed by a continuous maintenance infusion of 50 to 100 micrograms/kg per minute. The anterograde effective refractory period of the fast pathway increased from 381 +/- 75 msec at baseline to 453 +/- 92 msec during the infusion of esmolol (P = 0.003). The anterograde effective refractory period of the slow pathway was also prolonged by esmolol, from 289 +/- 26 msec to 310 +/- 17 msec (P = 0.005). However, the absolute magnitude of the change in the anterograde effective refractory period of the fast pathway (+72 +/- 59 msec) was significantly greater than the change in anterograde effective refractory period of the slow pathway (+21 +/- 16 msec, P = 0.01). The mean retrograde effective refractory period of the fast pathway increased from 276 +/- 46 msec to 376 +/- 61 msec during esmolol infusion (P = 0.03). Retrograde slow pathway conduction that could not be demonstrated at baseline became manifest in three patients during esmolol infusion. In contrast to the effects of esmolol on refractoriness, the AH interval during anterograde slow pathway conduction prolonged to a far greater extent (+84 msec) than the HA interval associated with retrograde fast pathway conduction (+5 msec, P = 0.04). CONCLUSION: The beta-adrenergic antagonist, esmolol, has a quantitatively greater effect on anterograde refractoriness of the fast than the slow AV nodal pathway. However, the effects on conduction intervals during AVNRT are greater in the anterograde slow pathway than in the retrograde fast pathway. These observations suggest that the fast and slow pathways may have differential sensitivities to autonomic influences. This difference in the response to beta-adrenergic antagonists may be exploited as a clinically useful method for demonstrating slow pathway conduction in some individuals with AVNRT.

Adrenergic beta-Antagonists↗
PubMed1986

Ventrolateral medullary neurons projecting to the medial preoptic/anterior hypothalamic area through the medial forebrain bundle: an electrophysiological study in the rat.

A total of 152 ventrolateral medullary neurons was antidromically stimulated from both the medial preoptic/anterior hypothalamic area (MPOAH) and the medial forebrain bundle (MFB) in urethane anesthetized rats. These neurons were located primarily dorsal to the lateral reticular nucleus and could be readily classified in at least two groups, type I and type II cells on the basis of electrophysiological properties. The action potentials of type I cells had a shorter duration, and their conduction velocities ranged from 0.45 to 3.1 m/s. By contrast, type II cells, most predominantly observed, were characterized by a longer duration and an unusual shape of their action potential, and the antidromic propagation into the somatodendritic complex was often blocked. The conduction velocity (mean = 0.21 m/s) and absolute refractory period (mean = 2.63 ms) of type II cells are consistent with them having fine non-myelinated axons. Injection of 6-hydroxydopamine (6-OHDA), but not 5,7-dihydroxytryptamine, directly into the MFB blocked antidromic responses of 57% of type II cells tested. The residual type II cells whose antidromic responses were not affected by 6-OHDA were located significantly rostral to the 6-OHDA sensitive cells. Neither antidromic response of type I cells tested, on the other hand, was affected by 6-OHDA. The majority of type I cells were dramatically activated by noxious pinches of the tail, whereas the noxious stimuli produced no detectable change in the firing of type II cells. These data demonstrate that ventrolateral medullary neurons projecting to the MPOAH through the MFB are comprised of at least three distinct populations: 6-OHDA resistant fast conducting cells with somatic afferents, 6-OHDA sensitive and resistant slow conducting cells.

Action Potentials↗
PubMed1993

Spontaneous activity, conduction velocity and segmental origin of different classes of thoracic preganglionic neurons projecting into the cat cervical sympathetic trunk.

Previously, in the anesthetized cat, thoracic preganglionic neurons projecting to the superior cervical ganglion were divided into four classes (groups I-IV) by way of their reflex pattern. Neurons of each class are probably involved in a distinct function, such as regulation of peripheral vascular resistance, regulation of blood flow through skin, regulation of pupil diameter, etc. Here it was tested whether the functionally different classes of thoracic preganglionic neurons also differ in the distribution of their segmental origin, their spontaneous activity and the conduction velocity of their axons. The segmental distribution of preganglionic neurons was almost identical to that determined previously with tracer methods. Distinct classes of neurons had different, although overlapping segmental distributions. Most group III neurons were located in segments T1 and T2, whereas group I, II and IV neurons showed a broader distribution. The subpopulations of preganglionic neurons did not differ in their rate of spontaneous activity. No significant difference was found in segmental distribution between neurons with spontaneous activity and silent neurons. No correlation was found between conduction velocity and spontaneous activity. The proportion of unmyelinated units was greater among group I (16.3%), group II (24.1%) and group IV (22.2%) neurons than among group III neurons (8%). The distributions of conduction velocity were significantly different between group I and group III and between group II and group III neurons. Axons of preganglionic neurons located in segments T1 and T2 conducted faster than axons of neurons located more caudally. The present study shows that distinct subpopulations of preganglionic neurons, as defined by their reflex patterns, differ in their segmental location within the spinal cord and with respect to the conduction velocity of their axons.

Animals↗
PubMed1964

A COMPARISON OF THE GANGLION POTENTIALS AND BLOCK PRODUCED BY ACETYLCHOLINE AND TETRAMETHYLAMMONIUM.

Potentials recorded from the surface of the superior cervical ganglion of cats after an intra-arterial injection of acetylcholine were characterized by a complex waveform which depended on the amount of drug administered. Small doses of acetylcholine evoked a potential consisting of low amplitude hyperpolarization followed by low amplitude depolarization. Somewhat larger doses of acetylcholine caused a triphasic potential containing an initial period of depolarization in addition to the periods of hyperpolarization and delayed depolarization. Still larger doses of acetylcholine produced usually a monophasic wave of depolarization. Small doses of atropine prolonged the initial period of depolarization and prevented the hyperpolarization and delayed depolarization. Hexamethonium reduced or abolished the initial depolarization and enhanced or unmasked the hyperpolarization. The block of transmission occurring during the falling phase of the initial depolarization or during the hyperpolarization was antagonized by atropine. Unlike acetylcholine, tetramethylammonium produced only a prolonged ganglion depolarization which was unaffected by atropine and blocked by hexamethonium. The block of transmission by tetramethylammonium was partially prevented by atropine. These findings support the proposals that three pharmacologically distinctive cholinoceptive sites are present in sympathetic ganglia and, further, that activation of a cholinoceptive site sensitive to atropine may be involved in the block of transmission produced by acetylcholine and related drugs.

Acetylcholine↗