Journal of applied physiology
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Clinical experience and laboratory studies suggest that neonates are more sensitive than adults to the ventilatory depressant effects of morphine. Similar sensitivity has been cited, but not demonstrated, for fentanyl. To examine this issue, we determined ventilatory pharmacodynamics of morphine and fentanyl in 28 dogs aged 2-35 days. ⋯ For fentanyl, there was a small maturational increase in C50 and no change in keo. We conclude that there are marked maturational changes in the ventilatory depressant effects of morphine resulting from maturational changes in sensitivity rather than in equilibration. Maturational changes in the ventilatory effects of fentanyl are much smaller in magnitude than those for morphine.
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Acidic solutions mimick many of the effects of capsaicin (Cap), including pain, bronchoconstriction, cough, and sensory neuropeptide release. Evidence from the use of the Cap antagonist capsazepine suggests that in some cases protons act at the Cap receptor. In the present study, we have investigated whether cough evoked by Cap and citric acid (CA) is mediated specifically via the Cap receptor on airway sensory nerves. ⋯ This inhibitory effect of capsazepine did not appear to reflect a nonspecific suppression of the cough reflex, since cough evoked by exposure to hypertonic (7%) saline for 10 min was unaffected by pretreatment with capsazepine (100 microM). These data show that capsazepine is a specific inhibitor of Cap- and CA-induced cough in guinea pigs. Moreover, they suggest that low pH stimuli evoke cough and nasal irritation by an action at the Cap receptor, either directly or through the release of an intermediate agent.
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We studied the effects of ventilation and pleural effusion on measurements of airway thermal volume (ATV) and pulmonary blood flow (PBF) by using the airway gas thermometry method of V. B. Serikov, M. ⋯ The coefficient of lung thermal conductivity, a practical index of the rate of heat conduction through tissue from lung vessels, was related to the ratio of the decrease in expired air temperature to VE, and estimated PBF was consistent with the thermodilution cardiac output. Pleural effusion had little effect on measurements of ATV and PBF. However, ATV and PBF showed increased variation in dogs with dextran-induced lung edema.
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Clinical Trial
Reactive hyperemia unmasks reduced compliance of cutaneous arteries in essential hypertension.
To evaluate changes in distal cutaneous arteries during hypertension, we used a noninvasive method to assess the compliance and vascular resistance of the hand radial arteries, mainly distributed to the skin, in 10 normotensive and 10 hypertensive (HT) men. Radial artery diameter and blood velocity were measured by means of pulsed Doppler concomitantly with measurements of finger arterial pressure by photoplethysmography. Hand radial vascular resistance was calculated as the ratio of mean arterial pressure to mean radial blood flow. ⋯ During hyperemia, the only difference between the groups, except for pressure, was lower compliance in HT subjects (P < 0.01). Moreover, compliance during hyperemia negatively correlated with baseline mean pressure (P = 0.001). Thus hyperemia unmasked reduced compliance in the HT patients but did not show abnormal resistance, suggesting that the elastic properties of the hand skin radial arteries might be more sensitive than their resistive properties to high blood pressure.
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The rate of recovery from diaphragmatic fatigue beyond 1 h is unknown. To investigate this question, we studied 12 healthy subjects and measured transdiaphragmatic twitch pressure (Pditw) using magnetic stimulation of the phrenic nerves. Measurements were obtained at baseline and after a fatigue protocol consisting of inspiratory resistive loading in which the subjects generated 60% of maximal transdiaphragmatic pressure until task failure. ⋯ The nadir in Pditw after the protocol was delayed by 10 min. In separate experiments, we showed that this delay was probably due to the development of twitch potentiation as a result of forceful diaphragmatic contractions during the fatigue protocol. In conclusion, induction of diaphragmatic fatigue with this experimental protocol produced a marked decrease in diaphragmatic contractility that persisted for at least 24 h.