natriuretic-peptide--brain and Hyperoxia

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.

Topics: Aged; Aldosterone; Angiotensin II; Atrial Natriuretic Factor; Baroreflex; Case-Control Studies; Endothelin-1; Female; Humans; Hyperoxia; Liver Cirrhosis, Alcoholic; Lung Diseases; Male; Middle Aged; Natriuretic Peptide, Brain; Norepinephrine; Oxygen; Renin

Recent papers discussed include two large, multicentre, high-positive end-expiratory pressure trials in acute lung injury and reflects upon the usefulness of such trial designs. Further papers considered include the emerging story of beta2-agonists for pulmonary oedema, highlights the newly described, iatrogenic demon, of ventilator-induced diaphragm injury, promotes the addition of B-type natriuretic peptide testing to the prediction of extubation success, and muses again over the oxygen debate.

Topics: Adrenergic beta-Agonists; Animals; Critical Illness; Diaphragm; Humans; Hyperoxia; Muscular Atrophy; Natriuretic Peptide, Brain; Oxygen Inhalation Therapy; Positive-Pressure Respiration; Pulmonary Edema; Randomized Controlled Trials as Topic; Respiration, Artificial; Respiratory Distress Syndrome; Sepsis; Ventilator Weaning

B-type natriuretic peptide (BNP) is a cardiac hormone used as a marker of cardiac dysfunction with diuretic and vasodilating properties secreted by the ventricles in response to wall stress. Hyperbaric oxygen (HBO) exposure is known to induce hemodynamic effects in humans which can be complicated by acute pulmonary edema. The aim of this study was to investigate if HBO has any effects on the secretion of BNP in healthy human subjects.. Eight healthy volunteers underwent the following HBO protocol in a hyperbaric chamber: compression to 2.5 atmospheres absolute (ATA); 45 min breathing 100% oxygen; 5 min breathing air; another 45 min in 100% oxygen; then decompression to atmospheric pressure. A venous blood sample was drawn before entering the chamber (To), immediately at the end of the treatment (T1), and at 5 h from To (T2). BNP concentration was determined using a rapid point-of-care immunoassay. Non-parametric statistics were used to analyze data.. No difference in BNP levels was found between T0 and T1 or T2.. The findings of this preliminary study show that in healthy subjects a single HBO exposure does not significantly modify BNP plasma levels. We hypothesize that this can be the net result between the stimulating effect of the HBO-induced vasoconstriction and the direct inhibitory effect on BNP secretion of myocyte hyperoxia. We conclude that HBO does not modify BNP secretion in healthy volunteers and that the direct effect of extreme hyperoxia on BNP secretion deserves further investigation.

Topics: Adult; Atmospheric Pressure; Biomarkers; Decompression; Female; Humans; Hyperbaric Oxygenation; Hyperoxia; Male; Natriuretic Peptide, Brain; Prospective Studies; Vasoconstriction