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)

Respiratory-related electromyogram (EMG) activities of the middle (MPC) and inferior (IPC) pharyngeal constrictor (PC) muscles were determined simultaneously with up to six additional upper airway abductor and adductor muscles in awake adult goats. Phasic PC activation began in late inspiration and persisted throughout expiration with a steady, an augmenting or a biphasic pattern of activity. Considerable differences were noted in the EMG responses of the MPC and IPC muscles to respiratory-related stimuli. During hypoxia and hypercapnia, phasic MPC activity decreased or was not recruited whereas phasic IPC activity was augmented with increased chemical drive. During spontaneous augmented breaths and peripheral chemoreceptor stimulation with sodium cyanide, the pattern of activation of the MPC was similar to that of the thyroarytenoid muscle (TA), a laryngeal adductor whereas IPC activity was strikingly similar to activity of the laryngeal and pharyngeal dilators. The expiratory portion of an augmented breath was associated with increased phasic MPC and TA but not IPC activities. Dopamine-induced apneas resulted in tonic activation of the MPC and TA at a level equal to or greater than control activity but no recruitment of IPC activity. The marked differences in MPC and IPC responses to respiratory-related stimuli suggests that these muscles may have different mechanical effects on pharyngeal airway caliber in the goat. The results suggest that the MPC may help brake expiratory flow thus helping to control expiratory timing and lung volume. In contrast, the IPC may promote pharyngeal airway patency by stiffening or dilating the pharyngeal airway. The results demonstrate that a variety of stimuli can influence respiratory-related PC activity and suggest that the PC muscles are important in the regulation of breathing and upper airway patency.
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PMID:Respiratory-related pharyngeal constrictor muscle activity in awake goats. 1042 Oct 30

We have investigated whether translocation of constitutive low molecular weight stress proteins (alphaB-crystallin and HSP27) to the myofilament/cytoskeletal compartment occurs during ischemic preconditioning and assessed if this is causally associated with cardioprotection. Triton-insoluble preparations from fresh or aerobically perfused rat hearts (n=4/group) contained relatively little alphaB-crystallin (96 +/- 43 and 43 +/- 36 units respectively) or HSP27 (177 +/- 32 and 101 +/- 26 units respectively). Three preconditioning cycles of (5 min ischemia + 5 min reperfusion) increased the Triton-insoluble crystallin to 864 +/- 61 units (P<0.05) and HSP27 to 1353 +/- 53 units (P<0.05). Two hours of aerobic perfusion following the preconditioning protocol resulted the return of alphaB-crystallin and HSP27 to near control levels (189 +/- 14 units and 252 +/- 24 units, respectively). Stress protein translocation, comparable to that achieved by the IPC protocol was induced by aerobic perfusion with hypercarbic (pH 6.8) perfusion. Thus, three cycles of 5 min hypercarbia + 5 min normocarbia increased alphaB-crystallin to 628 +/- 30 units (P<0.05) and HSP27 to 1353 +/- 53 units. In parallel functional studies, the recovery of LVDP after 35 min ischemia and 60 min of reperfusion was 43 +/- 7% in the ischemic control group, 61 +/- 3% (P<0.05) in the preconditioned group and 42 +/- 6% in the hypercarbic group. Thus, translocation of alphaB-crystallin and/or is not of-itself sufficient to induce cardioprotection. Using a phospho-specific antibody, we have demonstrated that preconditioning not only translocates alphaB-crystallin but also increases its phosphorylation at Ser-59 by 9.7-fold compared to aerobic controls (1616 +/- 402 v 166 +/- 28 units respectively). In contrast, hypercarbia while eliciting a comparable translocation, failed to alter the phosphorylation state of alphaB-crystallin. Preconditioning-induced phosphorylation was significantly attenuated by 50 microM genistein (by 61%), 10 microM SB203580 (by 91%) and 10 microM bisindolylmaleimide (by 68%), but not by 10 microM PD98059 (by 4%). Our findings are consistent with the possibility that ischemic preconditioning may be mediated by phosphorylation and translocation of constitutive low molecular weight stress proteins, particularly alphaB-crystallin.
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PMID:Ischemic preconditioning: a potential role for constitutive low molecular weight stress protein translocation and phosphorylation? 1088 50