Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pattern of respiration in infants during anaesthesia is not well documented. In this study, minute ventilation (MV) during elective mask halothane anaesthesia (HA) was measured during spontaneous ventilation in infants (Group I) and children (Group II). Airflow was measured with pneumotachography (#0 Fleisch in Group I and #1 Fleisch in Group II). Analogue signals of pressure and flow were recorded on magnetic tape for off-line playback. The flow signal was mathematically integrated to volume. The surgical procedure was divided into three stages: A, B and C representing HA, surgical stimulation and emergence respectively. The pattern of respiration during spontaneous ventilation was described as tidal volume (VTx), respiratory frequency (fx), mean inspiratory flow (VT/TIx), inspiratory duty cycle (TI/TTotx) where the subscript x denoted the stage. Seven infants (2.7 +/- 0.5 mo, 5.8 +/- 0.5 kg) and five children (3.1 +/- 1.1 yr, 15.8 +/- 1.7 kg) were studied. There was no difference in MV between Groups I and II. Halothane anaesthesia in both groups was characterized by rapid shallow breathing: VTA was lower in Group I (2.90 +/- 0.8 ml.kg-1) than in Group II (3.74 +/- 0.40 ml.kg-1) (P < 0.05). Tidal volume was lower during anaesthesia than emergence in both groups (P < 0.05). There was no difference in VT/TIx between groups. The VT/TIA was lower than VT/TIC in Group I (P < 0.05) but not in Group II. There was no intra or intergroup difference in TI/TTot between stages. We suggest that during HA infants have a greater reduction in VT than children, which may predispose infants to hypercarbia during HA.
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PMID:Minute ventilation during mask halothane anaesthesia in infants and children. 844 48

Evidence suggests both opioid mu and delta receptors may participate in the regulation of respiration at different central nervous system sites. In the past, the overlapping receptor specificity of various opioid drugs has made it difficult to dissect the receptor subtype-specific activities involved in respiratory regulation. The new family of delta receptor selective agents such as cyclic[D-Pen2, 5]enkephalin, deltorphins, (+)-4-((alpha-R)-alpha-((2S,5R)-4-allyl-2, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide, naltrindole and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH have now made it feasible to more clearly define the role of delta receptors in respiratory control. In a series of experiments we observed that systemic infusion of rats with the highly mu receptor-specific opioid alfentanil induced antinociception and hypercapnia, and both of these effects were antagonized by the mu antagonist D-Phe-Cys-Tyr-Orn-Thr-Pen-Thr-NH2. However, peripheral administration of the delta receptor antagonist naltrindole reverses the hypercapnia but not the antinociceptive activity of alfentanil. This differential effect of naltrindole on antinociception and hypercapnia could also be produced with the delta agonist (+)-4-((alpha-R)-alpha-((2S,5R)-4-allyl-2, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide. In addition, intracerebroventricular delivery of a number of peptide delta ligands cyclic[D-Pen2,5]enkephalin, deltorpnin II and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH also produced the same differential reversal of hypercapnia without affecting antinociception. Thus, both the traditional delta agonists and antagonists are able to reverse the alfentanil-induced hypercapnia without affecting antinociception. The reversal of alfentanil-induced hypercapnia by these delta ligands was antagonized by a novel synthetic delta antagonist cis-4-(alpha-(4-((Z)-2-butenyl)-3, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide. We propose that in this experimental respiration model, the delta antagonists naltrindole and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH behave like delta agonists with low but sufficient intrinsic activities to reverse alfentanil-induced hypercapnia in rats. The results suggest that a function of the delta receptor is to modulate or counteract the respiratory depression induced by the mu receptor.
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PMID:Delta-opioid ligands reverse alfentanil-induced respiratory depression but not antinociception. 986 59