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)

Pulmonary pneumatocele is a thin-walled, gas-filled space within the lung that usually occurs in association with bacterial pneumonia and is usually transient. The majority of pneumatoceles resolve spontaneously without active intervention, but in some cases they might lead to pneumothorax with subsequent hemodynamic instability. We report two cases presented to the pediatric intensive care unit at the Royal Hospital, Oman with pneumatoceles. The first was a 14-day-old baby who underwent surgical repair of total anomalous pulmonary venous connection (TAPVC) requiring extracorporeal membrane oxygenation (ECMO) support following surgery. He was initially on conventional mechanical ventilation. Seven days after the surgery, he started to develop bilateral pneumatoceles. The pneumatoceles were not regressing and they did not respond to three weeks of conservative management with high-frequency oscillation ventilation (HFOV). He failed four attempts of weaning from HFOV to conventional ventilation. Each time he was developing tachypnea and carbon dioxide retention. Percutaneous intercostal chest drain (ICD) insertion was needed to evacuate one large pneumatocele. Subsequently, he improved and we were able to wean and extubate him. The second case was a two-month-old male admitted with severe respiratory distress secondary to respiratory syncytial virus (RSV) pneumonitis. After intubation, he required a high conventional ventilation setting and within 24 hours he was on HFOV. Conservative management with HFOV was sufficient to treat the pneumatoceles and no further intervention was needed. Our cases demonstrate two different approaches in the management of pneumatoceles in mechanically ventilated children. Each approach was case dependent and could not be used interchangeably.
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PMID:Two Cases of Pneumatoceles in Mechanically Ventilated Infants. 2636 66

Hypercapnia (HC), elevation of the partial pressure of CO2 in blood and tissues, is a risk factor for mortality in patients with severe acute and chronic lung diseases. We previously showed that HC inhibits multiple macrophage and neutrophil antimicrobial functions and increases the mortality of bacterial pneumonia in mice. In this study, we show that normoxic HC increases viral replication, lung injury, and mortality in mice infected with influenza A virus (IAV). Elevated CO2 increased IAV replication and inhibited antiviral gene and protein expression in macrophages in vivo and in vitro. HC potentiated IAV-induced activation of Akt, whereas specific pharmacologic inhibition or short hairpin RNA knockdown of Akt1 in alveolar macrophages blocked HC's effects on IAV growth and the macrophage antiviral response. Our findings suggest that targeting Akt1 or the downstream pathways through which elevated CO2 signals could enhance macrophage antiviral host defense and improve clinical outcomes in hypercapnic patients with advanced lung disease.
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PMID:Hypercapnia Suppresses Macrophage Antiviral Activity and Increases Mortality of Influenza A Infection via Akt1. 3254 Sep 97