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PubMed1968

The ganglion-stimulating effects of some amino-acid esters.

1. The effects of some amino-acid esters possessing both muscarinic and nicotinic activity have been investigated on the cat superior cervical ganglion. The compounds were applied to the ganglion in vivo by close intra-arterial injection and responses were measured by contraction of the nictitating membrane or by recording post ganglionic compound action potentials.2. The esters, like carbachol, produced effects which were blocked by hexamethonium and reduced by atropine. Pretreatment with an anticholinesterase agent had no effect on the response and the chronically denervated ganglion was, if anything, slightly more sensitive to the drugs.3. Effects of standard muscarinic and nicotinic drugs were also studied and the results support the view that both muscarinic and nicotinic receptors are present in the ganglion.4. From the results of this investigation it appears that the amino-acid esters and carbachol produce their effects by interacting with post synaptic receptors in the ganglion. This is in contrast to other results in the literature which suggest that the receptors might be presynaptic. Further studies are required to resolve this difference.

Action Potentials↗
PubMedDate not supplied

Significance of cardiac innervation on spontaneous ventricular arrhythmias elicited by left stellate ganglion stimulation in dogs 4 days after myocardial infarction: comparison of two experimental models.

The effects of cardiac sympathetic overactivity on spontaneous arrhythmias and transmural left ventricular effective refractory period (LVERP) were assessed by left stellate stimulation (LSS) in 16 anesthetized dogs. The experiments were performed 4 days after proximal occlusion of the left anterior descending (LAD) coronary artery produced by either ligation (9 dogs) or embolization with histoacryl (7 dogs). The innervation of left ventricular myocardium was studied by light and electron microscopies. Synaptophysin (SYN)- and neuropeptide Y (NPY)-immunoreactive nerve fibers and terminals were thereby detected. In dogs subjected to ligation, LSS elicited negligible arrhythmias in spite of a decrease in LVERP by 6.9 +/- 2.2% (mean +/- SD, p < 0.001). However, dogs with intravascular occlusion were more susceptible to LSS, as indicated by development of sustained ventricular rhythms. In these animals, the LVERP decreased with LSS by 14.6 +/- 3.4% (p < 0.001). The innervation of the anterior left ventricular wall distal to the place of occlusion revealed a higher reduction of SYN- and NPY-immunoreactive nerves in infarcted myocardium and a more heterogeneous distribution of nerves in undamaged regions after ligation, compared to intravascular occlusion. Ultrastructurally, nerve terminals containing small agranular and large dense-core vesicles were found innervating ischemically damaged myocardiocytes. Our findings indicate a higher preservation of nerves in infarcted and noninfarcted myocardium of animals subjected to embolic occlusion of the LAD. Because LSS apparently elicited more arrhythmias in these animals, we suggested a proarrhythmic effect of intact myocardial innervation after infarction.

Animals↗
PubMed1978

Effects of hydralazine on canine muscarinic ganglion stimulation.

The effects of hydralazine upon the caudal pressor responses during occlusion of the abdominal aorta and vena cava evoked by: (1) preganglionic electrical stimulation of the lumbar sympathetic chain, (2) neostigmine and (3) McN-A-343 were investigated in the anesthetized dog. Hydralazine (10 microgram/kg, i.v.) produced a small but significant reduction of the pressor response to lumbar electrical stimulation prior and following blockade of nicotinic transmission with chlorisondamine (1.0 mg/kg). However, hydralazine was not effective in blocking the pressor responses elicited by neostigmine and McN-A-343. On the other hand, small doses of atropine (20 microgram/kg) produced a blockade of residual pressor responses evoked by all three stimuli. On the basis of these findings, the site of action of hydralazine appears to be different from that of atropine. It is proposed that hydralazine affects ganglionic transmission by acting at sites other than muscarinic in nature.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗