PubMed · 8753555
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K Matsuzaki. 1995. [Plasma bicarbonate].. https://pubmed.ncbi.nlm.nih.gov/8753555/
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Extracorporeal membrane oxygenation (ECMO) has been used for cardiopulmonary support in neonates, infants, and adults. We report the application of ECMO for critical airway surgery when mechanical ventilation cannot provide adequate gas exchange. Three pediatric patients underwent emergency ECMO establishment because of hypercapnia that could not be managed by conventional mechanical ventilation. The pathology included: (1) left pulmonary artery sling with long-segment tracheal stenosis; (2) absence of the right intermediate bronchus and abnormal origin of the right lower bronchus arising from the left main bronchus; (3) right-lung agenesis with long-segment tracheobronchial stenosis. Venoarterial ECMO was established. Before ECMO, the arterial pH values were 7.28, 7.0, and 7.08, and the PaCO2 values were 111.8, 112.0, and 208.7 mmHg for each patient, respectively. After ECMO support, respiratory acidosis was reversed. The patients then underwent surgical intervention. The surgical procedures included: (1) slide tracheoplasty and reimplantation of the left pulmonary artery; (2) resection of the stenotic tracheal segment and reconstruction of the bronchial tree; (3) tracheal dilatation and stent implantation. The ECMO durations were 11, 5, and 16 h, respectively. All patients were successfully weaned off ECMO without complications. In conclusion, ECMO provided adequate ventilation support for patients undergoing critical tracheobronchial reconstruction when conventional mechanical ventilation could not maintain adequate gas exchange.
A neurosurgical patient who required repeated surgery for intracranial haematoma developed acute respiratory distress syndrome. Raised intracranial pressure proved difficult to manage whilst attempting to maintain optimal gas exchange. The resultant arterial partial pressure of carbon dioxide remained unacceptably high, and treatment by extracorporeal carbon dioxide removal was started. A pumpless arteriovenous interventional lung assist device (Novalung) was connected from the right femoral artery to left femoral vein and reduced the arterial carbon dioxide, corrected the respiratory acidosis and enabled control of the intracranial pressure. Subsequently the requirements for both respiratory and cardiovascular support were reduced. The patient made a complete neurological recovery.
The molecular basis for the renal compensation to respiratory acidosis and specifically the role of pendrin in this condition are unclear. Therefore, we studied the adaptation of the proximal tubule and the collecting duct to respiratory acidosis. Male Wistar-Hannover rats were exposed to either hypercapnia and hypoxia [8% CO(2) and 13% O(2) (hypercapnic, n = 6) or normal air (controls, n = 6)] in an environmental chamber for 10 days and were killed under the same atmosphere. In hypercapnic rats, arterial pH was lower than controls (7.31 +/- 0.01 vs. 7.39 +/- 0.01, P = 0.03), blood HCO(3)(-) concentration was increased (42 +/- 0.9 vs. 32 +/- 0.24 mM, P < 0.001), arterial Pco(2) was increased (10.76 +/- 0.4 vs. 7.20 +/- 0.4 kPa, P < 0.001), and plasma chloride concentration was decreased (92.2 +/- 0.7 vs. 97.2 +/- 0.5 mM, P < 0.001). Plasma aldosterone levels were unchanged. In the proximal tubule, immunoblotting showed an increased expression of sodium/bicarbonate exchanger protein (188 +/- 22 vs. 100 +/- 11%, P = 0.005), confirmed by immunohistochemistry. Total Na/H exchanger protein expression in the cortex was unchanged by immunoblotting (119 +/- 10 vs. 100 +/- 11%, P = 0.27) and immunohistochemistry. In the cortex, the abundance of pendrin was decreased (51 +/- 9 vs. 100 +/- 7%, P = 0.003) by immunoblotting. Immunohistochemistry revealed that this decrease was clear in both cortical collecting ducts (CCDs) and connecting tubules (CNTs). This demonstrates that pendrin expression can be regulated in acidotic animals with no changes in aldosterone levels and no external chloride load. This reduction of pendrin expression may help in redirecting the CNT and CCD toward chloride excretion and bicarbonate reabsorption, contributing to the increased plasma bicarbonate and decreased plasma chloride of chronic respiratory acidosis.