Journal of the autonomic nervous system最新文献

The time constant (T) obtained by fitting post-exercise heart rate (HR) recovery to a first order exponential decay curve has been promoted as an index of parasympathetic activity. However, acceptance has been limited because reported data are inadequate to assess goodness of fit for the model, determine the best exercise protocol, or optimize the duration of post exercise monitoring. Consequently, we evaluated T for nine healthy volunteers (age 24–46) following treadmill exercise at maximal (max) and two stages sub-max exercise (Bruce protocol). T stabilized only after 3 min of post-exercise monitoring. With max exercise, T varied unacceptably with small changes in onset of monitoring, e.g. −16.7±16.6 (−13.2%) in the first 5 s, and residuals of the fitted curve were non-random. In contrast, sub-max exercise produced consistent T values, e.g. −1.9±3.2 (−4.2%) in the first 5 s, and residuals were more nearly random. In conclusion, first order decay is an inadequate model for HR recovery following max exercise, but may be reasonable for sub-max levels.

Cyanide intoxication, which has been used as a model of energy depletion at cardiac sympathetic nerve terminals, causes non-exocytotic release of norepinephrine (NE). However, the effect of cyanide intoxication on cardiac epinephrine (Epi) release remains unknown. Using cardiac microdialysis in the rabbit, we measured dialysate Epi and NE concentrations as indices of myocardial interstitial Epi and NE levels, respectively. Local administration of sodium cyanide (30 mM) through the dialysis probe increased both Epi and NE levels (from 11.3±2.3 to 32.3±4.4 pg/ml and from 33.6±6.1 to 389.0±71.8 pg/ml, respectively, mean±S.E., P<0.01). Local desipramine (100 μM) administration suppressed the cyanide induced NE response without affecting the Epi response. In contrast, local ω-conotoxin GVIA (10 μM) administration partially suppressed the cyanide induced NE response and totally abolished the Epi response. In conclusion, cyanide intoxication causes N-type Ca²⁺ channel dependent exocytotic Epi release as well as inducing N-type Ca²⁺ channel independent non-exocytotic NE release.

The ultrastructure of the wild-type (+/+) mice small intestine was compared with c-kit mutant (W/W^ν) mice which only have few interstitial cells of Cajal (ICC) associated with Auerbach’s plexus, in order to elucidate whether the specialized membrane contacts are general features of so-called fibroblast-like cells that are widely distributed in the tunica muscularis of the alimentary tract. Fibroblast-like cells in the Auerbach region were found in approximately equal number in W/W^ν mice as in +/+ mice, while ICC associated with Auerbach’s plexus (ICC-AP) could not be demonstrated in W/W^ν mice in the present investigation. Fibroblast-like cells were characterized by cytoplasm of moderate to high electron density, well developed rough endoplasmic reticulum and nuclei with thick peripheral accumulations of heterochromatin. There were no basal lamina and caveolae along the cell membrane. It was observed that single fibroblast-like cells formed probable small gap junctions with muscle cells of both circular and longitudinal layers. Fibroblast-like cells with the same features were also observed in the region of the deep muscular plexus in both +/+ and W/W^ν mice. The present observation, together with our previous studies on rats and guinea-pigs, suggest the common presence of gap junctions or gap junction-like structures on fibroblast-like cells in the gastrointestinal musculature and their involvement in the regulatory system of gastrointestinal motility by passing electrical or molecular signals to influence the state of muscle tonus.

We examined whether a higher plasma lactic acid (LA) concentration resulting from carbohydrate (CHO)-loading affects the cardiovascular responses to exercise through a greater activation of LA-induced metaboreflex. Before and after CHO-loading, LA concentration, mean arterial blood pressure (MAP), heart rate (HR), cardiac output (CO), rating perceived exertion (RPE), and integrated electromyogram (iEMG) of the vastus lateralis were studied during a sustained static knee extension of single legs in 16 volunteers. The CHO-loading comprised an exhaustive bout of one-legged cycling (73±3% of maximal oxygen uptake for 130–160 min) and consuming a low-CHO diet for 2–3 days and a high-CHO diet for the next 3 days. In the leg that performed the exercise (the experimental leg), the LA concentration after CHO-loading was significantly increased, but the magnitude of MAP, HR, and CO responses during static exercise was significantly decreased in parallel with a significant reduction of RPE and iEMG. In the control leg, there were no changes in the variables before and after CHO-loading. These results suggest that the increased LA concentration resulting from CHO-loading did not affect the cardiovascular adjustment to the sustained exercise. Other mechanisms related to the reduction of RPE and iEMG seem to be responsible for the attenuated cardiovascular responses observed in the experimental leg after CHO-loading.

This study has shown that cyclophosphamide treatment of the insectivore Suncus murinus, causes a down regulation in both muscarinic and P2X receptors, together with a reduced responsiveness to exogenous histamine (0.3 mM) in the urinary bladder. Electrical field stimulation (70 V, 0.3 ms, 0.5–16 Hz, 10 s every 5 min) of bladders from both control and cyclophosphamide-treated animals showed identical responses. Since post-junctional alterations have been revealed by the reduced responsiveness to exogenous carbachol (0.1 μM–3 mM) and β,γ-methylene ATP (0.3–300 μM), it would appear that in the bladders of cyclophosphamide-treated animals there is also a pre-junctional effect, increased transmitter release compensating for the down regulation of the receptors. As the pattern of neurotransmission of the bladder of suncus more closely resembles that of human detrusor than other commonly studied laboratory animals, this insectivore appears to be a useful animal model for the study of bladder neurotransmission in pathophysiological conditions.

In urethane anesthetized, adult male Wistar rats, noxious chemical stimulation of the mid to lower thoracic interspinous tissues, in the form of capsaicin injection, was accompanied by a pronounced increase in gastric sympathetic nerve activity and inhibition of gastric motility. Much weaker effects on gastric sympathetic nerve activity and gastric motility were observed with similar stimulation of the lower lumbar interspinous tissues. The inhibitory response of gastric motility to thoracic stimulation was preserved in spinalized animals, somewhat diminished in vagotomized animals and was abolished in most animals from which the coeliac ganglion had been extirpated. In vagotomized animals, treatment with 1 mg/kg propranolol i.v. did not cause any further attenuation of the inhibitory reflex. However, the inhibitory reflex was extinguished in vagotomized animals which received 1 mg/kg propranolol plus 10 mg/kg phentolamine i.v. These results suggest that noxious chemical stimulation of the interspinous tissues elicits a segmentally organized reflex which is mediated principally at the spinal level and which expresses itself principally, but not exclusively via sympathetic efferents traversing the coeliac ganglion. The expression of the reflex response appears to be largely dependent upon the integrity of alpha adrenergic receptors.

The following experiments examine the role of estrogen as a central modulator of autonomic tone and baroreflex sensitivity in the female rat. Female Sprague–Dawley rats were ovariectomized and then supplemented daily for 7 days with a fixed dose of estrogen (5 μg/kg; sc) to produce a stable level of estrogen similar to that present at proestrous (17 pg/ml). The rats were then anaesthetized with sodium thiobutabarbital (100 mg/kg) and instrumented to record blood pressure, heart rate and both vagal and renal efferent nerve activities. The sensitivity of the cardiac baroreflex was tested using intravenous injection of multiple doses of either phenylephrine hydrochloride or sodium nitroprusside. Estrogen-supplemented female rats exhibited a significantly enhanced BRS as compared to male rats from a previous study (0.78 vs. 0.5). Furthermore, bolus injection of estrogen (1×10⁻² mg/kg; iv) in estrogen-supplemented female rats produced a significant increase in vagal nerve activity and a significant decrease in renal nerve activity which together resulted in a further enhancement of the BRS (0.78 vs. 2.4). Injection of the selective estrogen receptor antagonist, ICI 182,780, into nucleus ambiguus and the intrathecal space of the spinal cord blocked the respective changes in parasympathetic and sympathetic nerve activities indicating that intravenously administered estrogen modulates baseline autonomic tone via the activation of central estrogen receptors.