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 ability to maintain alveolar ventilation is compromised by respiratory muscle weakness. To examine the independent role of reflexly mediated neural mechanisms to decreases in the strength of contraction of respiratory muscles, we studied the effects of partial paralysis on the level and pattern of phrenic motor activity in 22 anesthetized spontaneously breathing dogs. Graded weakness induced with succinylcholine decreased tidal volume and prolonged both inspiratory and expiratory time causing hypoventilation and hypercapnia. Phrenic peak activity as well as the rate of rise of the integrated phrenic neurogram increased. However, when studied under isocapnic conditions, increases in the severity of paralysis, as assessed from the ratio of peak diaphragm electromyogram to peak phrenic activity, produced progressive increases in inspiratory time and phrenic peak activity but did not affect its rate of rise. After vagotomy, partial paralysis induced in 11 dogs with succinylcholine also prolonged the inspiratory burst of phrenic activity, indicating that vagal reflexes were not solely responsible for the alterations in respiratory timing. Muscle paresis was also induced with gallamine or dantrolene, causing similar responses of phrenic activity and respiratory timing. Thus, at constant levels of arterial CO2 in anesthetized dogs, respiratory muscle partial paralysis results in a decrease in breathing rate without changing the rate of rise of respiratory motor activity. This is not dependent solely on vagally mediated reflexes and occurs regardless of the pharmacological agent used. These observations in the anesthetized state are qualitatively different from the response to respiratory muscle paralysis or weakness observed in awake subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory response to partial paralysis in anesthetized dogs. 673 17

347 patients with idiopathic respiratory distress syndrome, born 1971 to 1976, were included into a prospective follow-up study. 71 patients (20%) died in the neonatal period, 197 out of 276 survivors (71%) had a complete follow-up for the first year of life, 112 survivors have so far been investigated up to the age of four years. According to neurological findings the patients were classified as normal, doubtful (age 6-12 months) or minimal brain dysfunction (4 years), mild cerebral paresis (CP), or severe cerebral damage, respectively. At the age of one year 3 patients (1.5%) had severe cerebral damage, 14 (7%) showed mild CP and another 56 (28%) had doubtful findings. Very low birth weight of very short period of gestation increased the risk for abnormal neurological findings only slightly. The need for mechanical ventilation, especially for more than 14 days, increases the risk for CP. Serious complications during the neonatal period, particularly implicating cerebral stress, significantly reduces medium-term prognosis. Perinatal asphyxia, neonatal acidosis, hypoxia or hypercapnia did not correlate with impaired cerebral prognosis. Preliminary findings at the age of four years demonstrate good correlation with neurological findings obtained at the age of 12 months. One patient initially classified as normal (2%) and 5 doubtful babies (15%) had developed mild CP. Another initially doubtful baby had severe cerebral damage at the age of four years. 62 out of 78 children tested (79%) showed normal intelligence, 14 (18%) had an IQ of 70--90, and 2 (3%) less than 70.
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PMID:Systematic follow-up of newborns with idiopathic respiratory distress syndrome. Results in 197 patients born 1971 to 1976. 703 Oct 20