PubMed · 5720947
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E Japiassú. 1968. [Postanesthesia complications].. https://pubmed.ncbi.nlm.nih.gov/5720947/
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1. In anaesthetized rats, using a focal recording technique, activity was recorded from single sympathetic postganglionic neurones innervating the lateral tail veins. On-going activity was examined in order to determine whether it had similar or different characteristics to those recorded from the caudal ventral artery in a previous study. 2. Animals were artificially ventilated, vagotomized, paralysed and given a pneumothorax. 3. The discharges of fourteen out of seventeen sympathetic postganglionic neurones were rhythmic. Such units had a mean firing frequency of 1.62 +/- 0. 70 Hz. The mean frequency of the dominant sympathetic rhythm under control conditions was 0.82 +/- 0.05 Hz. 4. The frequency of the dominant sympathetic rhythm was different from that of the phrenic rhythm in nine out of fourteen cases. 5. The mean frequency of the dominant sympathetic rhythm was: (i) not influenced significantly by hypocapnic apnoea, (ii) decreased by hyperthermia, which increased the frequency of the phrenic rhythm, (iii) in all cases different from that of the artificial ventilation cycle. 6. The above characteristics are similar to those recorded from the sympathetic supply to the caudal ventral artery of the same vascular bed under comparable conditions.
1. Bradycardia can be evoked by stimulation of both myelinated and non-myelinated vagal efferent fibres. The on-going activity and synaptic inputs to cardiac vagal preganglionic neurones with myelinated axons have been studied in detail, but there is little information regarding cardiac preganglionic neurones with non-myelinated axons. In the present study, the on-going discharge and afferent inputs to cardiac vagal efferents with non-myelinated axons were studied in anaesthetized rats and cats. 2. Extracellular recordings were made from vagal preganglionic neurones in the dorsal vagal motor nucleus (DVMN) of anaesthetized rats following electrical stimulation of the cervical vagus nerve. Based on calculated axonal conduction velocities, fifty-six neurones had non-myelinated axons. Sixteen of these C fibre neurones had on-going activity but this showed no relationship to central respiratory drive, lung inflation or the cardiac cycle. Activity of twenty-one of these fifty-six neurones was increased at short latency following right atrial injections of phenylbiguanide (PBG). 3. Eight presumed cardiac vagal preganglionic neurones were also recorded in the DVMN. Five of these were activated by PBG administration, and the one neurone with resting activity showed no indication of respiratory-related activity. 4. Finally, twenty-one single C fibres were recorded in peripheral branches of the cardiac vagus. They had a low rate of on-going activity, and in twelve fibres this on-going discharge was analysed in detail. On-going activity in seven of these fibres showed no relationship to central respiratory drive, lung inflation or the cardiac cycle, whereas the other five had prominent relationships with both central respiratory drive and lung inflation, and two of these also showed a relationship to heart period. PBG administration evoked an increased activity in fourteen of the fifteen fibres tested, and the latencies of nine of these responses (1.3 +/- 0.5 s) were within the pulmonary circulation time. 5. In anaesthetized cats, extracellular recordings were made in the DVMN from thirty-three cardiac vagal preganglionic neurones with C fibre axons. The on-going activity of these neurones, when present, never exhibited an on-going- or reflexly induced respiratory rhythm, nor any indication of an input from the arterial baroreceptors. Right atrial injection of PBG evoked a short-latency response in four of the five spontaneously active neurones but was without effect on the eight neurones tested which did not exhibit on-going activity. 6. In conclusion, the majority of cardiac vagal preganglionic neurones located in the DVMN have C fibre axons, show no obvious input from central or peripheral respiratory- or cardiac-related inputs, but are activated by stimulation of pulmonary C fibre afferent fibres.
1. The permeability response of slightly leaky pial venular capillaries to histamine was investigated using the single microvessel occlusion technique. 2. Histamine dose-response curves showed that concentrations between 5 nm and 5 microM increased permeability, while concentrations from 50 microM to 5 mM reduced it. 3. The H2 receptor antagonist cimetidine (2 microM) blocked the effects of lower concentrations of histamine, while the H1 receptor antagonist mepyramine (3 nM) blocked those of higher concentrations of histamine. 4. The effects of lower doses of histamine were mimicked by the H2 receptor agonist dimaprit, and the effects of higher doses of histamine were mimicked by the H1 receptor agonist alpha-2-(2-aminoethyl)pyridine (AEP). 5. Low concentrations of histamine, which normally increase the permeability of Lucifer Yellow (PLY), reduced it when co-applied with the phosphodiesterase 4 (PDE4) inhibitor rolipram. Rolipram also potentiated the response to AEP, but had no effect on that to dimaprit. 6. The effects of dimaprit were blocked by reducing extracellular Ca2+ from 2.5 mM to nominally Ca2+ free, or by applying the calcium entry blocker SKF 96365.