Background: Contrast-induced nephropathy (CIN) is the third cause of acute deterioration of renal function in hospitalized patients. Hypothesis: The purpose of the study was to compare the efficacy of saline infusion, saline infusion plus N-acetylcysteine (NAC), and sodium bicarbonate (SB) infusion to prevent CIN in patients undergoing coronary angiography and/or percutaneous coronary intervention. Methods: We prospectively studied 156 patients with a baseline creatinine level ≥1.2 mg/dL. The primary endpoint was the development of CIN, defined as an increase in serum creatinine concentration ≥25% over the baseline value within 5 days from contrast exposure. Results: Contrast-induced nephropathy developed in 23 patients (14.7%). Incidence of the primary endpoint was similar in the 3 groups of treatment, occurring in 7 patients (14%) in the saline infusion group, in 9 (17%) in the saline infusion plus NAC group, and in 7 (14%) in the SB infusion group. Conclusions: Our findings suggest that neither the addition of NAC nor the administration of SB add further benefit in CIN prevention, compared to standard hydration with isotonic saline infusion.

Increase in pulmonary artery pressure (PAP), which is common in severe chronic obstructive pulmonary disease (COPD), is a predictor of mortality independent of airflow limitation. beta-agonists might slightly attenuate this increase because they exert a vasodilating effect on pulmonary circulation when systematically administered. We have investigated the acute effects of salmeterol and formoterol on echocardiographic systolic pulmonary artery pressure (sPAP) in 20 patients with COPD and a sPAP greater than 20mmHg at rest. Acute haemodynamic responses to inhaled formoterol or salmeterol were assessed in all patients, in a randomized, double-blind double-dummy fashion. On two consecutive days, patients received, in a randomized order, formoterol 12microg via Turbuhaler plus placebo via Diskus or salmeterol 50microg via Diskus plus placebo via Turbuhaler. Transthoracic Doppler echocardiography measurements of sPAP were made before and 15, 30, 60 and 180min after bronchodilator inhalation. Lung function, pulse oximetry and heart rate were also monitored at the same times. Mean sPAP significantly (p<0.05) decreased in comparison with baseline at 15, 30, and 60min post inhalation but returned towards control levels at 180min after both salmeterol and formoterol. There was no correlation between the maximum increase in FEV(1) and maximum decrease in sPAP either after inhalation of salmeterol (r(2)=0.071) or after that of formoterol (r(2)=0.0006). The increases in FEV(1) in comparison with baseline were always significant (p<0.05) from 15 to 180min post inhalation after either salmeterol or formoterol. Neither pulse oximetry nor heart rate changed in a significant manner (p>0.05). This study demonstrated that salmeterol and formoterol were equally beneficial for pulmonary haemodynamics in patients with COPD. A direct vasodilatation due to the activation of beta-adrenoceptors that are present in pulmonary vessels is a likely mechanism of their action in inducing the decrease in sPAP.

During severe acute respiratory distress syndrome (ARDS), pulmonary hypertension occurs due to obliteration of the pulmonary capillary bed and together with microvascular vasoconstriction, may lead to right ventricular failure 1 . This is a relatively frequent complication of the disease 2 . Inhaled nitric oxide (iNO) may improve oxygenation, reduce pulmonary artery pressure and improve right heart performance 3 . phosphodiesterase (PDE-1) has recently been reported to enhance iNO pulmonary vasodilation effect for a short period in infants after cardiac surgery 4 and in ARDS 5 . No data are available on the prolonged use of PDE inhibitors in adult critically ill patients, although ample literature is now available on chronically ill subjects with pulmonary hypertension 6 . by the FDA for erectile dysfunction. It did not show 7 and the onset and the duration of the two drugs are in patients with prolonged Q-T, although no severe adverse effects have been reported so far. Subsequent studies focused on its potential use in pulmonary PDE-1 8 .There is little data supporting the enteral use of any kind of PDE-1 for the treatment of refractory pulmonary hypertension in the critical care setting. We report a case of right ventricular failure in ARDS due to pulmonary hypertension, in which weaning from iNO and from mechanical ventilation was possible CASE HISTORYAfter seven days of bilateral pnemococcal pneumonia, a 66-year-old woman with septic shock was admitted to our intensive care unit (ICU). She was a heavy smoker with a clinical history of recurrent bronchitis. A CT scan showed bilateral lung consolidation. The P a O 2 /FiO 2 ratio was 97 with 12 cmH 2 O positive end expiratory pressure and the total static lung compliance was 37 ml/cmH 2 O. Fluids and inotropic support (dobutamine and noradrenaline) resulted in cardiac index (CI) 2.9 l/min/m 2 , global end-diastolic volume 859 ml/m 2 and intrathoracic blood volume 1363 ml/m 2 , measured using continuous cardiac output with the PiCCO system SUMMARY We report a 66-year-old patient with refractory pulmonary hypertension secondary to ARDS who was being treated with inhaled nitric oxide. Enteral vardenafil (phosphodiesterase-5 inhibitor) was tried at two different doses (10 mg and 5 mg), in order to wean the patient from nitric oxide. The higher dose decreased pulmonary pressure but caused systemic hypotension and the drug was discontinued. Subsequently, a 5 mg dose of vardenafil decreased pulmonary pressure without hypotension. Pulmonary hypertension was controlled using vardenafil 10-15 mg divided in 2-3 daily doses. This therapy allowed nitric oxide withdrawal, weaning from mechanical ventilation and discharge from ICU.Vardenafil acted in synergy with inhaled nitric oxide, permitted nitric oxide reduction and discontinuation and proved to be effective as a single, long-term treatment for pulmonary hypertension.

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