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 newborn brain, and even more so the brain of the premature child, can be considered as an authentic target organ for numerous pathological conditions, some of which exist outside the central nervous system (changes involving primarily both respiratory function and cardiocirculatory function with serious repercussions at encephalic level). In the premature, this greater "vulnerability" is related to the reduced or absent capacity for self-regulation of the cerebral blood low (mechanism influenced negatively by hypoxia, hypercapnia and metabolic acidosis conditions) and the important role played by numerous factors in protecting newborns from haemorrhagic damage. Of these the most important are the state of prematurity, the presence of vascular, intravascular and extravascular changes, the effects exerted on cerebral haemodynamics by mechanical ventilation and by certain drugs employed in treatment. In mechanically ventilated newborns and premature, prevention of haemorrhagic damage (periendoventricular) is currently based on the application of clear-cut protocols of intensive and rehabilitative treatment. The following form part of these protocols: low damage ventilation techniques (high frequencies, low PJP, low MAP), curarisation (to avoid fluctuations in cerebral blood flow), neuroprotection (phenobarbital), the use of substances and drugs which, by exploiting different mechanisms, go to reduce the extent of the haemorrhage (vitamin E, indomethacin, ethamosylate, tranexamic acid).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevention of hemorrhagic cerebral injury in newborn and premature infants subjected to mechanical ventilation]. 269 3

Chronic lung disease (CLD) or bronchopulmonary dysplasia is a recognized sequel of preterm birth. With improving survival of infants at lower gestational ages, the incidence is on the rise. Pathological features of CLD include alveolar maldevelopment, with or without areas of pulmonary fibrosis. Assisted ventilation, infection/inflammation, oxygen administration, and fluid overload are the major risk factors in the evolution of CLD.Interventions, including the treatment of maternal infection, administration of prenatal glucocorticoids, and postnatal surfactant replacement therapy, improve the survival of preterm infants; however, their effect on CLD is difficult to determine. Strategies that have been effective in reducing CLD are the administration of retinol (vitamin A), high frequency oscillatory ventilation, and administration of glucocorticoids. Previous concerns regarding neurological problems associated with high frequency ventilation have not been substantiated in recent studies. Current recommendations do not advise the routine use of glucocorticoids due to concerns regarding long-term neurodevelopment. Therapies that were found to be ineffective in reducing the incidence of CLD include prenatal thyrotropin, cromolyn sodium (sodium cromoglycate), alpha-1 antitrypsin, superoxide dismutase, tocopherol (vitamin E), ascorbic acid (vitamin C), allopurinol, ambroxol, inositol, inhaled bronchodilators, and fluid restriction. Strategies that may be effective in reducing lung injury and subsequent CLD include avoiding assisted ventilation, lung protective ventilatory maneuvers, permissive hypercapnia, prevention of infection, early aggressive nutrition, and the treatment of a patent ductus arteriosus. The use of inhaled glucocorticoids improves pulmonary dynamics but long-term effects are unknown. The management of infants with established CLD has not been studied adequately, and the role of various ventilatory strategies for infants with established CLD is not clear. Adequate oxygenation should be maintained to prevent hypoxic episodes. Diuretics are helpful during acute decompensation; however, their long-term impact has not been well studied. Provision of adequate nutrition, immunization (routine and against respiratory syncytial virus), follow-up, and monitoring are the key elements in the long-term management of infants with CLD. Future research priorities should be to identify strategies to prevent/treat inflammation and promote the healing processes in the injured lung. The long-term effects of lung-protective ventilation strategies need to be studied.
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PMID:Current perspectives on the prevention and management of chronic lung disease in preterm infants. 1283 19

The hypnotic agent propofol has pharmacokinetic characteristics that allow for rapid onset and offset of drug effect and fast elimination from the body. Elderly patients show a greater sensitivity to the hypnotic effect of propofol. The drug is extensively metabolized in the liver through the cytochrome P450 system and glucuronidation, with potential for drug interaction. Propofol does not cause significant inotropic depression at clinically relevant concentrations. But in vitro, propofol impairs isotonic relaxation of the heart and decreases free cytosolic Ca(2+) concentrations in myocardial cells. In animal models, the cardioprotective effects of propofol derive in part from its antioxidant and free radical scavenging properties. Propofol decreases cerebral blood flow and cerebral metabolic rate dose-dependently. The neuroprotective effect of propofol in animal models is attributed to its antioxidant property, the potentiation of gamma-aminobutyric acid type A (GABA(A))-mediated inhibition of synaptic transmission, and the inhibition of glutamate release. Subhypnotic doses of propofol induce sedative, amnestic, and anxiolytic effects in a dose-dependent fashion. Propofol impairs ventilation with a considerable effect on the control of ventilation and central chemoreceptor sensitivity. Propofol reduces the ventilatory response to hypercapnia and the ventilatory adaptation to hypoxia, even at subanesthetic doses. The drug potentiates hypoxic pulmonary vasoconstriction, an effect caused by inhibition of K(+) (ATP)-mediated pulmonary vasodilatation. Most of the pharmacological actions of propofol result from interaction with the GABA(A) receptor or with calcium channels. Propofol prolongs inhibitory postsynaptic currents mediated by GABA(A) receptors, indicating that its effects are associated with enhanced inhibitory synaptic transmission, but propofol also influences presynaptic mechanisms of GABAergic transmission. Propofol modulates various aspects of the host's inflammatory response. It decreases secretion of proinflammatory cytokines, alters the expression of nitric oxide, impairs monocyte and neutrophil functions, and has potent, dose-dependent radical scavenging activity similar to the endogenous antioxidant vitamin E.
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PMID:Propofol. 1817 94