Effectiveness of Human Atrial Natriuretic Peptide Supplementation in Pulmonary Edema Patients Using the Pulse Contour Cardiac Output System

PURPOSE: Atrial natriuretic peptide (ANP) has a variety of pharmacologic effects, including natriuresis, diuresis, vasodilatation, and suppression of the renin-angiotensin system. A recent study showed that ANP infusion improved hypoxemia and pulmonary hypertension in a lung injury model. On the other hand, the pulse contour cardiac output (PiCCO(TM)) system (Pulsion Medical Systems, Munich, Germany) allows monitoring of the intravascular volume status and may be used to guide volume therapy in severe sepsis and critically ill patients. MATERIALS AND METHODS: We treated 10 pulmonary edema patients without heart disease with human ANP (HANP). The patients were divided into two groups: a group with normal Intrathoracic Blood Volume (ITBV) (900-1100 mL/m2) (n = 6), and a group with abnormal ITBV (n = 4), as measured by the PiCCOtrade mark device; the extravascular lung water (EVLW) and pulmonary vascular permeability index (PVPI) in the two groups were compared. RESULTS: The average patient age was 63.9 +/- 14.4 years. The normal ITBV group showed significant improvement of the EVLW (before, 16.7 +/- 2.7 mL/kg; after, 10.5 +/- 3.6 mL/kg; p = 0.0020) and PVPI (before, 3.2 +/- 0.3; after, 2.1 +/- 0.7; p = 0.0214) after the treatment. The abnormal ITBV group showed no significant improvement of either the EVLW (before, 16.3 +/- 8.9 mL/kg; after, 18.8 +/- 9.6 mL/kg; p = 0.8387) or PVPI (before, 2.3 +/- 0.8; after, 2.7 +/- 1.3; p = 0.2782) after the treatment. In both groups, the EVLW and PVPI were strongly correlated with the chest X-ray findings. CONCLUSION: We conclude that HANP supplementation may improve the EVLW and PVPI in pulmonary edema patients without heart disease with a normal ITBV. The PiCCO(TM) system seems to be a useful device for the management of pulmonary edema.

Aspects of neural and hormonal control of water and sodium balance

This article reviews some aspects of neural and hormonal control of water and sodium balance. The maintenance of extracellular fluid volume and osmolarity depends on the coordinated action of multiple mechanisms of water and sodium intake and excretion. Different technics for manipulation of the central nervous system, i.e., withdrawing of nervous structures, electrolytic lesion, electrical stimulation and chemical stimulation, have allowed the identification of some brain areas, neural circuits and neurotransmitters that participate in the mechanisms of control of water and sodium intake and excretion. The signals for thirst and actions of angiotension II, cholinergic agents and atrial natriuretic factor upon drinking are discussed. Three possible types of effector mechanism for centrally induced natriuresis are discussed: 1) renal innervation; 2) secretion of a substance by the brain which causes natriuresis through direct or indirect action (antidiuretic hormone and active sodium transport inhibition); 3) CNS control of the secretion of a hormonal substance produced at another site (mineralocorticoid and atrial natriuretic factor). These mechanisms are not mutually exclusive.

Efecto adrenalectomía bilateral sobre la actividad guanililciclasa estimulable por el péptido natriurético auricular en el núcleo paraventricular de la rata / Bi-sided adrenalectomy effects on the natriuretic atrial factor-stimulated guanylcyclase activity on the rat paraventricular nucleus

El Peptido Natriurético Auricular (PNA) o el análogo de la Atriopeptina III (PL 059) estimulan la actividad guanililciclasa particulada en el bulbo olfatorio, la eminencia media , y el núcleo paraventrícular de la rata. El efecto del análogo de la Atripeptina III fue 20-40 por ciento mayor que el del PNA. Se investigó el efecto de la adrenalectomía bilateral (con o sin sustitución con mineral o glucocorticoides), sobre la formación de GMPc estimulada por el PNA en el núcleo paraventricular de la rata. Once días después de la adrenalectomía bilateral se observó una disminución en la capacidad porducción de GMPc inducida por el PNA o por el PL058. Esta acción fue prevenida por la administración de deoxicorticosterona, pero no por dexametasona. Nuestros resultados demuestran la presencia de receptores para el PNA asociados a la actividad guanililciclasa en áreas localizadas del cerebro de la rata; y sugieren que los receptores para el PNA acoplados a la guanililciclasa en el núcleo paraventricular son susceptibles a cambios regulatorios inducidos por la actividad del eje hipotálamo-hipófisis-suprarrenal

Renal vascular and excretory resistance to atrial natriuretic peptide in pre-cirrhotic, bile-duct ligated rats

Renal response to atrial natriuretic peptide in chronic cholestasis was studied in anaesthetized rats and in their isolated perfused kidneys. Cholestasis was induced by bile duct section after ligature, while controls were sham operated. Three weeks after surgery, cholestatic rats showed moderate arterial hypotension, elevated diuresis and no differences in urinary sodium, glomerular filtration rate (GFR) and fractional sodium excretion (FENa), when compared to controls. Isolated kidneys of cholestatic rats had equal basal diuresis and less natriuresis than the controls. Cholestatic rats presented blunted natriuretic and diuretic responses to iv injections of atrial natriuretic peptide (ANP 0.5 microgram), associated with reduced increments in GFR and FENa, when compared with controls. Similarly, the diuretic-natriuretic response of isolated kidneys to ANP (3.5 x 10(-9) M) was greatly attenuated in this group. ANP did not increase perfusion pressure in cholestatic rats, as it did in controls. These results indicate that animals with chronic cholestasis present refractoriness to ANP, which might be mediated by a direct impairment at the renal vascular and tubular sites for ANP action