Chemical Vapor Deposition of Organic-Inorganic Bismuth-Based Perovskite Films for Solar Cell Application.

Perovskite solar cells have shown a rapid increase of performance and overcome the threshold of 20% power conversion efficiency (PCE). The main issues hampering commercialization are the lack of deposition methods for large areas, missing long-term device stability and the toxicity of the commonly used Pb-based compounds. In this work, we present a novel chemical vapor deposition (CVD) process for Pb-free air-stable methylammonium bismuth iodide (MBI) layers, which enables large-area production employing close-coupled showerhead technology. We demonstrate the influence of precursor rates on the layer morphology as well as on the optical and crystallographic properties. The impact of substrate temperature and layer thickness on the morphology of MBI crystallites is discussed. We obtain smooth layers with lateral crystallite sizes up to 500 nm. Moreover, the application of CVD-processed MBI layers in non-inverted perovskite solar cells is presented.

Radial arterial pressure measurements may be a poor guide to the beneficial effects of nitroprusside on left ventricular systolic pressure in congestive heart failure.

The effect of nitroprusside on pressure wave transmission from ascending aorta to radial artery was studied in 10 patients with severe congestive heart failure. Nitroprusside resulted in a beneficial increase in cardiac index, reduction of pulmonary wedge pressure and reductions of aortic and radial arterial mean pressures. In 6 patients with an identifiable late systolic peak of aortic pressure (group I), nitroprusside reduced aortic systolic pressure more than radial systolic pressure, resulting in an increase in the difference between aortic and radial systolic arterial pressure (group I control 13 +/- 4, nitroprusside 20 +/- 6 mm Hg; p less than 0.025). Yet in 4 patients in whom no aortic late systolic pressure wave was apparent (group II), nitroprusside did not alter the difference between aortic and radial systolic pressures. Radial arterial pressure is often used to estimate the effect of nitroprusside on the arterial pressure load on the left ventricle. These results indicate that a reduction of radial systolic pressure induced by nitroprusside may underestimate the true reduction of aortic systolic pressure and thus the effect of the vasodilator on the arterial load on the left ventricle. The enhanced difference between aortic and radial arterial systolic pressures appears to be the consequence of nitroprusside on arterial pressure reflections.

Reflected pressure waves in the ascending aorta: effect of glyceryl trinitrate.

Reflected pressure waves returning to the ascending aorta are an important contribution to aortic systolic pressure and thus the load on the left ventricle. The effect of glyceryl trinitrate on pressure wave reflections in the ascending aorta was studied using the transmission of arterial pressure between two high fidelity pressure transducers. Glyceryl trinitrate 0.3 mg sublingually reduced systolic arterial pressure by 11 mmHg owing to a reduction of the late systolic pressure peak. Mean arterial pressure fell 2 mmHg, but heart rate and aortic flow did not change. The aortic input impedance was reduced at the first harmonic (control 18.4(4.1); glyceryl trinitrate 10.8(2.4) kPa.s.litre-1; p less than 0.005) but characteristic impedance was not changed (control 12.7(3.8); glyceryl trinitrate 14.2(3.3) kPa.s.litre-1). The first two harmonics of apparent phase velocity were reduced by glyceryl trinitrate (1.05 Hz: control 3314(798); glyceryl trinitrate 1772(495) cm.s-1; p less than 0.01; 2.1 Hz: control 1246(269); glyceryl trinitrate 754(127) cm.s-1; p less than 0.05), yet the foot to foot wave velocity was unchanged (control 688(112); glyceryl trinitrate 726(112) cm.s-1). There was a significant reduction in the amplitude of the global reflection coefficient at 1.05 Hz (control 0.70(0.09); glyceryl trinitrate 0.48(0.08); p less than 0.001) and at 2.1 Hz (control 0.48(0.07); glyceryl trinitrate 0.23(0.06); p less than 0.005) with no significant change in phase. Glyceryl trinitrate reduces cardiac pulsatile load by diminishing the amplitude of wave reflections arriving back in the aorta during systole yet has no effect on aortic compliance or arteriolar resistance. This study demonstrates a method of evaluating the effect of vasoactive drugs on cardiac pulsatile load.

Effect of nitroglycerin on left ventricular hydraulic load.

It has previously been shown that nitroglycerin increases the compliance of forearm arteries. The present study investigates whether nitroglycerin reduces the hydraulic load on the heart (as measured by aortic input impedance) by a mechanism compatible with an increase in peripheral arterial compliance. In eight subjects, measurements of aortic flow and pressure were made with a catheter tipped probe before and during intravenous nitroglycerin (6 to 30 micrograms/min) administration. The reduction of aortic systolic pressure (129 +/- 5 to 113 +/- 4 mmHg, P less than 0.001) was due to a decrease in the late systolic pressure peak. There was no change in stroke volume, heart rate or systemic vascular resistance. The lower systolic pressure resulted from a decrease in the amplitude of the first harmonic of input impedance (210 +/- 19 to 143 +/- 11 dyne.s.cm-5, P less than 0.005) yet characteristic impedance (a measure of local aortic distensibility) did not change. The ratio of maxima to minima of the impedance spectrum was reduced (1.02 +/- 0.09 to 0.71 +/- 0.11, P less than 0.05) suggesting a decrease in the amplitude of reflected waves contributing to aortic impedance. Nitroglycerin at doses which have no effect on arteriolar resistance vessels, reduces systolic aortic pressure by diminishing the amplitude of wave reflections returning to the ascending aorta in late systole. This mechanism is compatible with the peripheral arterial effects of nitroglycerin.

Respiratory muscle fatigue: a cause of ventilatory failure in septic shock.

The effect of endotoxic shock on the respiratory muscle performance was studied in spontaneously breathing dogs given Escherichia coli endotoxin (Difco Laboratories, 10 mg/kg). Diaphragmatic (Edi) and parasternal intercostal (Eic) electromyograms were recorded using fishhook electrodes. The recorded signals were then rectified and electrically integrated. Pleural, abdominal, and transdiaphragmatic (Pdi) pressures were recorded by a balloon-catheter system. After a short control period, the endotoxin was administered slowly intravenously (within 5 min). Death was secondary to respiratory arrest in all animals. All animals died within 150-270 min after the onset of endotoxic shock. Within 45-80 min of the endotoxin administration, mean blood pressure and cardiac output dropped to 42.1 +/- 4.1 and 40.1 +/- 6.0% (mean +/- SE) of control values, respectively, with little change afterward. Mean inspiratory flow rate and Pdi increased from control values of 0.27 +/- 0.03 l X s-1 and 5.75 +/- 0.7 cmH2O to mean values of 0.44 +/- 0.3 l X s-1 and 8.70 +/- 1.05 cmH2O and then decreased to 0.17 +/- 0.03 l X s-1 and 3.90 +/- 0.30 cmH2O before the death of the animals. There were no major changes in the mechanics of the respiratory system. Edi and Eic increased progressively to mean values of 360 +/- 21 and 263 +/- 22% of control, respectively, before the death of the animals. None of the dogs were hypoxic. Arterial PCO2 decreased from a control value of 42.9 +/- 1.7 Torr to a mean value of 29.9 +/- 2.8 Torr and then increased to 51 +/- 4.3 Torr before the death of the animals.(ABSTRACT TRUNCATED AT 250 WORDS)