naloxone and Hyperventilation

After hyperventilation, systolic and diastolic blood pressure (BP) significantly decreased in 14 hypertensive patients (group 1), did not change in 9 (group 2) and increased in 8 (group 3). Basal BP, norepinephrine and dynorphin B levels were higher in group 1 than in groups 2 and 3. The decrease in BP after hyperventilation was associated with a decrease in plasma norepinephrine, Met-enkephalin and dynorphin B and an increase in beta-endorphin. Naloxone abolished the hyperventilation-induced BP and norepinephrine decreases. Our findings indicate that hyperventilation may select hypertensive patients with different sympatho-adrenergic activity and that the increase in beta-endorphin reduces BP response to hyperventilation in patients with high sympatho-adrenergic tone.

Topics: Aged; beta-Endorphin; Blood Pressure; Cross-Over Studies; Dynorphins; Enkephalin, Methionine; Female; Heart Rate; Humans; Hypertension; Hyperventilation; Male; Middle Aged; Naloxone; Norepinephrine; Time Factors

Topics: Adult; Anesthesia, General; Clinical Trials as Topic; Drug Evaluation; Humans; Hyperventilation; Intraoperative Complications; Isoflurane; Male; Naloxone; Premedication; Spinal Cord Injuries; Thiopental

Although respiratory heat loss with cooling of the tracheobronchial mucosa is responsible for the airway obstruction that develops after inhalation of subfreezing air in asthmatics, the mechanism by which airway cooling results in bronchoconstriction is not known. In order to test whether release of endogenous opiate peptides might play a role in mediating this response, asthmatic subjects were studied before and after isocapnic hyperventilation of subfreezing air after the administration of placebo or naloxone, given in a double-blind fashion. Five asthmatic subjects were tested with low-dose (0.8 mg) and 5 with high-dose (10 mg) naloxone given intravenously. Pretreatment with naloxone at either dose did not attenuate the decrease in FVC, FEV1, or FEF25--75 after cold air in comparison with placebo pretreatment. A slightly greater decrease in FEV1 and FEF25--75 after low-dose naloxone than placebo pretreatment can be partially explained by a difference in the temperature achieved during cold air inhalation. We conclude that endogenous opiate peptides are not involved in mediating the bronchoconstrictor response to cold air inhalation in asthmatics.

Topics: Adult; Asthma; Bronchi; Bronchial Spasm; Cold Temperature; Endorphins; Female; Humans; Hyperventilation; Lung Volume Measurements; Male; Naloxone; Premedication; Pulmonary Ventilation; Spirometry

After hyperventilation, systolic blood pressure (SBP) significantly decreased in 10 subjects (group 1), did not change in eight (group 2) and increased in 15 (group 3). Diastolic blood pressure and heart rate increased in all groups. The decrease in SBP was associated with a decrease in plasma catecholamines and increase in beta-endorphin, whereas the increase in SBP was accompanied by an increase in catecholamine and Met-enkephalin levels. Naloxone abolished the hyperventilation-induced SBP and catecholamine decrease only in group 1. These findings show an activation of the endogenous opioid system after hyperventilation and the role of beta-endorphin in reducing SBP in response to the test.

Topics: Adult; Analysis of Variance; beta-Endorphin; Blood Pressure; Catecholamines; Enkephalin, Methionine; Female; Heart Rate; Humans; Hydrogen-Ion Concentration; Hyperventilation; Male; Naloxone; Opioid Peptides; Time Factors

The adjuvant arthritic rat model has been utilized for the study of chronic pain, as polyarthritic rats present a variety of symptoms similar to those seen in human chronic pain conditions. In particular, hyperventilatory responses are notable in both and may more accurately reflect basal ongoing pain than do evoked noxious stimuli. To assess whether adrenal medullary transplants in the spinal subarachnoid space can alleviate basal arthritic pain, respiratory parameters were determined using whole body plesthmography in polyarthritic rats. Arthritis was induced by inoculation with an intradermal injection of complete Freund's adjuvant. Steady-state ventilation was monitored at weekly intervals in arthritic animals with adrenal medullary or control striated muscle transplants. Results revealed that adjuvant arthritis produced significant hyperventilation in animals with control transplants, as indicated by increased tidal volumes and minute ventilation, which paralleled the progression of the inflammatory process. In contrast, this hyperventilation was eliminated by adrenal medullary transplants. A role for catecholamines and opioid peptides released from the transplants was suggested by the reversal of these effects with phentolamine and naloxone. In addition, the retardation in weight gain normally observed in polyarthritic animals was markedly attenuated by adrenal medullary, but not control transplants. These findings indicate that adrenal medullary transplants in the spinal subarachnoid space can alleviate basal chronic pain as assessed in adjuvant arthritis.

Topics: Adrenal Medulla; Adrenergic alpha-Antagonists; Animals; Arthritis, Experimental; Catecholamines; Chronic Disease; Hyperventilation; Naloxone; Narcotic Antagonists; Opioid Peptides; Pain; Pain Management; Phentolamine; Rats; Rats, Sprague-Dawley; Respiratory Mechanics; Subarachnoid Space; Weight Gain

The purpose of this study is to investigate the effect of hyperventilation on the spinal pain modulating system by using naloxone. Under enflurane anaesthesia, cats were prepared with midcollicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells, responding primarily to noxious peripheral stimuli, were sampled with a microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period, ventilation was adjusted to produce hypocapnia of PCO2 20-25 mmHg. After activities of WDR cells were well suppressed, naloxone 0.1 mg.kg-1 was given intravenously. Changes of firings of WDR cells were investigated. Returning to normocapnia, recovery of firings was followed. Hypocapnia of PCO2 20-25 mmHg significantly suppressed the activities of WDR cells. Naloxone significantly antagonized the suppressive effects of hyperventilation upon the activity of WDR cell. Our results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell and the mechanisms of those suppressive effects are related to pain modulating system by endogenous opiates.

Topics: Action Potentials; Animals; Cats; Decerebrate State; Evoked Potentials; Female; Hyperventilation; Male; Naloxone; Pain; Spinal Cord

Recent work from this laboratory (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55:483-488, 1983) has shown that the biphasic respiratory response to hypoxia in piglets is due to changing central neural respiratory output. To test the hypothesis that either adenosine or opiatelike neurotransmitters mediate the failure to sustain hyperpnea in response to hypoxia, 12 piglets were studied at a mean age of 2.9 +/- 0.4 days (range 2-6 days). Animals were anesthetized, paralyzed, and ventilated using a servo-controlled system that maintained end-tidal CO2 constant. Electrical activity of the phrenic nerve was recorded as the index of breathing. An initial experimental trial of 6 min ventilation with 15% O2 was performed in all 12 piglets. Thereafter all 12 piglets were treated with aminophylline (n = 6), naloxone (n = 3), or naltrexone (n = 3) and again subjected to 15% O2. During initial exposure to hypoxia there was an initial increase in phrenic activity that was not sustained. During recovery ventilation with 100% O2, phrenic activity transiently declined below the base-line level and then gradually returned. Subsequent intravenous administration of aminophylline, naloxone, or naltrexone caused base-line phrenic activity to increase. Thereafter repeat exposures to 15% O2 were carried out. During these posttreatment trials of hypoxia, phrenic activity further increased, but the hyperventilation was again not sustained. These findings suggest it is unlikely that either adenosine or mu-endorphin neurotransmitters are the primary mediators of the biphasic response to hypoxia in newborns.

Topics: Adenosine; Aminophylline; Animals; Animals, Newborn; Endorphins; Hyperventilation; Hypoxia; Naloxone; Naltrexone; Neurotransmitter Agents; Phrenic Nerve; Respiration; Swine