The Japanese journal of physiology
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Randomized Controlled Trial Comparative Study
Effects of naloxone on respiratory sensation before and after a removal of severe respiratory stress.
Severe respiratory stress causes dyspnea, and a sudden release of this stress frequently accompanies a euphoric sensation. We hypothesized that acute severe respiratory stress may result in an elaboration of endogenous opioids within the central nervous system, and that these opioids may play significant roles in relieving dyspnea and generating euphoric sensation after a sudden removal of the stress. To test this hypothesis, we examined the effects of naloxone (0.04 mg/kg, I. ⋯ Naloxone pretreatment affected neither the ventilation nor the development of dyspneic sensation during loaded breathing. Naloxone pretreatment only slightly attentuated the euphoric sensation developed after the release of severe respiratory stress. These findings suggest a small role of opioids in relieving dyspnea and in generating euphoria before and after a sudden removal of stress.
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Clinical Trial Controlled Clinical Trial
Inhibitory effect of pain-eliciting transcutaneous electrical stimulation on vibration-induced finger flexion reflex in the human upper limb.
We studied the effects of non-pain transcutaneous electrical stimulation (TES) and pain-eliciting TES on vibration-induced finger flexion reflex (VFR) in 12 healthy volunteers. Tonic finger flexion reflex in the upper limb was induced by the application of vibratory stimulation on the volar side of the middle fingertip in the right hand before and after TES. Non-pain TES or pain-eliciting TES was applied on the skin between the bases of the first and second metacarpals in the right hand dorsal area in a crossover design. ⋯ VFRs were reduced approximately to 63.8% and 78.6% of prestimulation flexion force during and after pain-eliciting TES, respectively. Nonpain TES did not inhibit VFR. These results suggest that pain-conducting afferent fibers have inhibitory neuronal connection over the ipsilateral reflex circuits of VFR in the upper limb.
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In previous studies the exhaled nitric oxide (NO) level of asthma patients was investigated only in association with bronchial inflammation, and whether the degree of bronchoconstriction itself influences the exhaled NO level has never been investigated. We therefore evaluated the effect of inhalation of a bronchoconstrictor (methacholine) or a bronchodilator (salbutamol) on the exhaled NO level of healthy volunteers and asthma patients. The exhaled NO level of the healthy volunteers decreased after methacholine inhalation. ⋯ It is suspected that large amounts of NO are trapped in the lung distal to the constricted airway, contributing little to the exhaled NO level at the mouth. However, we expect that the trapped NO is exhaled at a larger fraction after the dilatation of the constricted small airway, thereby increasing the exhaled NO level at the mouth. In conclusion, the results of this study suggest that acute changes in bronchoconstriction themselves influence the exhaled NO level independently of the change in NO synthase activity associated with airway inflammation.
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The effect of acupuncture-like stimulation of various areas (cheek, forepaw, upper arm, chest, back, lower leg, hindpaw, perineum) on cortical cerebral blood flow (CBF) was examined in anesthetized rats. An acupuncture needle (diameter, 340 microm) was inserted into the skin and underlying muscles at a depth of about 5 mm and twisted to the right and left once a second for 1 min. CBF of the cortex was measured using a laser Doppler flowmeter. ⋯ The increase in CBF induced by forepaw stimulation was almost abolished by intravenous administration of muscarinic and nicotinic cholinergic blocking agents (atropine 5 mg/kg and mecamylamine 20 mg/kg), and by bilateral lesions in the nucleus basalis of Meynert. Acupuncture-like stimulation of a forepaw increased acetylcholine release in the cerebral cortex. We concluded that the increase in CBF, independent of systemic blood pressure, elicited by acupuncture stimulation is a reflex response in which the afferent nerve pathway is composed of somatic group III and IV afferent nerves, and efferent nerve pathway includes intrinsic cholinergic vasodilators originating in the nucleus basalis of Meynert.
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An initial analgesia followed by hyperalgesia to phasic noxious stimuli occurs after ingestion of sucrose ad libitum. However, the mechanism underlying hyperalgesia is not known. The present study was designed to explore the role of VMH in the mediation of the hyperalgesic effect of sucrose ingestion. ⋯ However, sucrose feeding to lesioned rats neither potentiated nor attenuated their hyperalgesia. The results suggest that sucrose feeding for 6-48 h ad libitum produces hyperalgesia to phasic noxious and analgesia to tonic noxious stimuli, while VMH lesion produces hyperalgesia to both phasic and tonic noxious stimuli. Secondly, sucrose ingestion by VMH lesion rats does not affect their responses to pain, suggesting the possible role of VMH in the mediation of sucrose-fed nociceptive responses.