This study was undertaken to test the hypothesis that group III and IV afferents with endings in skeletal muscle signal the distension of the peripheral vascular network. The responses of these slowly conducting afferents to pharmacologically induced vasodilation and to acute obstruction of the venous drainage of the hindlimbs were studied in barbiturate-anesthetized cats. Afferent impulses arising from endings in the triceps surae muscles were recorded from the L(7) and S(1) dorsal roots. Fifteen of the 48 group IV and 3 of the 19 group III afferents tested were stimulated by intra-aortic injections of papaverine (2-2.5 mg/kg). Sixty-two percent of the afferents that responded to papaverine also responded to isoproterenol (50 microg/kg). Seven of the 36 group IV and 2 of the 12 group III afferents tested were excited by acute distension of the hindlimb venous system. Four of the seven group IV afferents responding to venous distension also responded to papaverine (57 vs. 13% for the nonresponding). Finally, we observed that most of the group IV afferents that were excited by dynamic contractions of the triceps surae muscles also responded either to venous distension or to vasodilatory agents. These results are consistent with the histological findings that a large number of group IV endings have their receptive fields close to the venules and suggest that they can be stimulated by the deformation of these vascular structures when peripheral conductance increases. Moreover, such a mechanism offers the possibility of encoding both the effects of muscle contraction through intramuscular pressure changes and the distension of the venular system, thereby monitoring the activity of the veno-muscular pump.

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Over the 38-28 degrees C range, changes in minimum alveolar anesthetic concentration (MAC) parallel changes in lipid solubility of the anesthetics studied. We hypothesized that there would be minimal change in N2OMAC, since N2O lipid solubility is relatively unaltered by temperature changes. We determined N2OMAC in rats using a hyperbaric chamber. In Group N (normothermia, n = 10) rectal temperature was maintained at 37.5 +/- 1 degrees C (mean +/- SD). In Group H (hypothermia, n = 9) temperature was maintained at 29.7 +/- 1.8 degrees C. The hyperbaric chamber was pressurized with N2O and oxygen partial pressure was 0.4 +/- 0.1 atm. Chamber pressure was adjusted approximately 15% up or down, stabilized for approximately 15 min, and the noxious stimulus (electrical current) was applied. This process was continued until two N2O partial pressures were determined which just prevented and just permitted gross, purposeful movement. Nitrous oxide MAC for Group N and Group H were 1.9 +/- 0.2 atm and 1.6 +/- 0.2 atm, respectively, P < 0.01. Temperature and MAC correlated: r = 0.59, P < 0.01. We conclude that hypothermia minimally decreases N2OMAC, which is consistent with the effects of hypothermia on N2O solubility in lipid membranes.

Airway dilation is one of the many autonomic responses to exercise. Two neural mechanisms are believed to evoke these responses: central command and the muscle reflex. Previously, we found that activation of central command, evoked by electrical and chemical stimulation of the mesencephalic locomotor region, constricted the airways rather than dilated them. In the present study we examined in decerebrate paralyzed cats the role played by the hypothalamic locomotor region, the activation of which also evokes central command, in causing the airway dilator response to exercise. We found that activation of the hypothalamic locomotor region by electrical and chemical stimuli evoked fictive locomotion and, for the most part, airway constriction. Fictive locomotion also occurred spontaneously, and this too, for the most part, was accompanied by airway constriction. We conclude that central command plays a minor role in the airway dilator response to exercise.

Cholinesterase inhibitors antagonize neuromuscular block produced by mivacurium, but some may also decrease its metabolism by inhibiting pseudocholinesterase. These opposing interactions were examined in rats anaesthetized with pentobarbitone. After spontaneous recovery from an initial bolus dose of 0.03 mg kg-1, mivacurium was infused to produce 80-90% block of gastrocnemius muscle twitch. After 15 min, the infusion was discontinued and saline, edrophonium, pyridostigmine or neostigmine was administered. Fifteen minutes later, a second bolus dose of mivacurium was given. Edrophonium, pyridostigmine and neostigmine reduced the subsequent maximum block, compared with the change in saline control, by 3%, 19% and 35%, respectively. Correspondingly, the time to recovery of T1 to 50% was decreased by 20%, 58% and 62%. In rats, acetylcholinesterase-mediated antagonism of neuromuscular block predominated over decreased pseudocholinesterase-mediated metabolism, such that prior administration of a cholinesterase inhibitor did not prolong the neuromuscular blocking effects of mivacurium.

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