Impaired transient elevation of blood hemoglobin in response to acute hypoxia in neonates with asplenia.
BACKGROUND
It has been shown that acute hypoxia induces the transient elevation of blood hemoglobin concentration ([Hb]) as a consequence of sympathetic-mediated splenic contraction to maintain the supply of oxygen, and splenectomy abolishes this phenomenon. The purpose of the present paper was to determine, retrospectively, whether the ability of transient elevation of [Hb] against acute hypoxia would be impaired in neonates with asplenia.


METHODS
Eleven neonates who underwent surgery from 1998 to 2003 were enrolled in this retrospective study. They were divided into two groups: (i) five patients with asplenia syndrome with cyanotic congenital heart disease (asplenia group); and (ii) six patients with hypoplastic left heart syndrome who needed nitrogen gas inhalation therapy (HLHS group). In the asplenia group simultaneous data of arterial oxygen saturation (Sao(2)) and [Hb] were obtained before and after the temporary unexpected decrease of percutaneous arterial oxygen saturation. In the HLHS group they were obtained before and after nitrogen gas administration therapy. The arterial oxygen content (Cao(2)) changes and the ratio of Cao(2) change (Cao(2) after hypoxia divided by Cao(2) before hypoxia) were also calculated.


RESULTS
In the asplenia group [Hb] was unchanged (12.9 +/- 1.6 g/dL to 12.8 +/- 1.4, n.s.) and Cao(2) was decreased (14.5 +/- 1.6 mL/dL to 11.9 +/- 1.1, P = 0.018). In the HLHS group [Hb] was increased (14.6 +/- 1.3 g/dL to 15.4 +/- 1.5, P = 0.028), but Cao(2) was changed (18.2 +/- 2.2 mL/dL to 16.7 +/- 3.0, P = 0.043). The ratio of Cao(2) change for the HLHS group was significantly different from that of the asplenia group (0.92 +/- 0.10, 0.83 +/- 0.10, respectively, P = 0.02).


CONCLUSIONS
Patients with asplenia syndrome have some disadvantage regarding this protective mechanism against acute hypoxia.
Department of Pediatrics Cardiology and Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tatsujiro
T
Oka
Toshiyuki
T
Itoi
Kenji
K
Hamaoka
D000015:Abnormalities, Multiple / Q000097:blood*; D000208:Acute Disease; D003490:Cyanosis; D006330:Heart Defects, Congenital / Q000097:blood* / Q000601:surgery; D006454:Hemoglobins / Q000378:metabolism*; D006801:Humans; D018636:Hypoplastic Left Heart Syndrome / Q000097:blood; D000860:Hypoxia / Q000097:blood*; D007231:Infant, Newborn; D010100:Oxygen / Q000097:blood; D012039:Regional Blood Flow; D012189:Retrospective Studies; D013154:Spleen / Q000002:abnormalities*; D013158:Splenic Diseases / Q000097:blood; D013903:Thoracic Surgery
D006454:Hemoglobins; D010100:Oxygen