title: Reduced baroreflex sensitivity and pulmonary dysfunction in alcoholic cirrhosis: effect of hyperoxia.
abstract: Patients with cirrhosis exhibit impaired regulation of the arterial blood pressure, reduced baroreflex sensitivity (BRS), and prolonged QT interval. In addition, a considerable number of patients have a pulmonary dysfunction with hypoxemia, impaired lung diffusing capacity (Dl(CO)), and presence of hepatopulmonary syndrome (HPS). BRS is reduced at exposure to chronic hypoxia such as during sojourn in high altitudes. In this study, we assessed the relation of BRS to pulmonary dysfunction and cardiovascular characteristics and the effects of hyperoxia. Forty-three patients with cirrhosis and 12 healthy matched controls underwent hemodynamic and pulmonary investigations. BRS was assessed by cross-spectral analysis of variabilities between blood pressure and heart rate time series. A 100% oxygen test was performed with the assessment of arterial oxygen tensions (Pa(O(2))) and alveolar-arterial oxygen gradient. Baseline BRS was significantly reduced in the cirrhotic patients compared with the controls (4.7 +/- 0.8 vs. 10.3 +/- 2.0 ms/mmHg; P < 0.001). The frequency-corrected QT interval was significantly prolonged in the cirrhotic patients (P < 0.05). There was no significant difference in BRS according to presence of HPS, Pa(O(2)), Dl(CO), or Child-Turcotte score, but BRS correlated with metabolic and hemodynamic characteristics. After 100% oxygen inhalation, BRS and the QT interval remained unchanged in the cirrhotic patients. In conclusion, BRS is significantly reduced in patients with cirrhosis compared with controls, but it is unrelated to the degree of pulmonary dysfunction and portal hypertension. Acute hyperoxia does not significantly revert the low BRS or the prolonged QT interval in cirrhosis.
authors.affiliation: Dept. of Clinical Physiology, Hvidovre Hospital, Denmark. soeren.moeller@hvh.regionh.dk
authors.forename: Søren
authors.initials: S
authors.lastname: Møller
authors.forename: Jens S
authors.initials: JS
authors.lastname: Iversen
authors.forename: Aleksander
authors.initials: A
authors.lastname: Krag
authors.forename: Peter
authors.initials: P
authors.lastname: Bie
authors.forename: Andreas
authors.initials: A
authors.lastname: Kjaer
authors.forename: Flemming
authors.initials: F
authors.lastname: Bendtsen
mesh_terms: D000368:Aged; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000378:metabolism; D009320:Atrial Natriuretic Factor / Q000097:blood; D017704:Baroreflex / Q000502:physiology*; D016022:Case-Control Studies; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D006801:Humans; D018496:Hyperoxia; D008104:Liver Cirrhosis, Alcoholic / Q000150:complications*; D008171:Lung Diseases / Q000209:etiology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D010100:Oxygen / Q000627:therapeutic use*; D012083:Renin / Q000097:blood
chemical_list: D019332:Endothelin-1; D000804:Angiotensin II; D020097:Natriuretic Peptide, Brain; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012083:Renin; D010100:Oxygen; D009638:Norepinephrine