The first demonstration of chromatic dispersion monitoring in optical networks having employed all-optical wavelength conversion is described. Experimental results confirm that dispersion monitoring based on an in-band subcarrier tone combined with wavelength conversion based on four-wave mixing (FWM) render dispersion monitoring possible in an optical network utilising wavelength conversion.
Introduction: In former studies an elevation of hydrogen peroxide and/or lactate in breath condensate due to pulmonary inflammation has been reported. A reduction of H2O2 due to anti inflammatory treatment in exacerbated COPD was also observed.
The effect of sustained converting enzyme (CE) inhibition on modest levels of exercise performance was investigated using German Shepherds. The dogs were trained to run on an inclined treadmill and to tolerate repeated jugular venous puncture. The effects of exercise were assessed by monitoring heart rate and respiratory rate and plasma catecholamine- and serum electrolyte concentrations on each of two control runs. Plasma CE- and renin activity were also determined. Inhibition of CE-activity was established thereafter by high dose treatment with 10 mg/kg Hoe 498 p.o. once daily for one week and the run repeated. These large doses of Hoe 498 were well tolerated. Neither running performance nor cardiorespiratory responses were altered by CE-inhibition. Plasma K+ and catecholamines were taken as measures of peripheral sympathetic activity, and CE-inhibition did not alter the increase in either of these in response to exercise. It is concluded that converting enzyme inhibition with Hoe 498 does not impair exercise performance despite any direct effects the loss of angiotensin II may have on reflex sympathetic functions.
Subchronic bolus administration of the angiotensin-converting-enzyme inhibitor ramipril caused a dose-dependent (0.1 to 10 mg.kg-1.d-1), yet each in his own way 24-hour sustained, reduction in arterial blood pressure in conscious unrestrained spontaneously hypertensive rats with tele-metric recording, and 0.01 mg.kg-1.d-1 was a no-effect dose. This was accompanied by dose-dependent attenuation of heart rate lowering during periods of low locomotor activity. Neither effect persisted for more than a few days after cessation of the medication with full restoration of pre-treatment levels. No dosage altered the circadian rhythm of blood pressure, heart rate and locomotor activity of the rats.
Two days before admission a 22-year-old woman developed general fatigue, nausea, headache and retrosternal pain. Physical examination was unremarkable.Erythrocyte sedimentation rate was increased to 20/48, C-reactive protein to 3.3 mg/dl, and there was evidence of myocardial damage (creatine kinase 609 U/l, creatine kinase-MB 42 U/l, troponine T 8.39 ng/ml); ST-segment elevations in I, II, III, aVF and V-V6 of the ECG. Echocardiography revealed clearly thickened myocardium, moderate but haemodynamically not significant pericardial effusion, as well as impaired left ventricular function. Antimyosin scintigraphy was very abnormal. Cardiac catheterization confirmed the left ventricular dysfunction, rise of left ventricular enddiastolic pressure to 17 mm Hg, and a markedly reduced cardiac output of 2.4 l/min. Myocardial biopsy showed severe myocarditis with marked myocytolysis and considerable lymphocytic infiltrations. Enteroviral RNA was demonstrated in the myocardium by polymerase chain reaction.The haemodynamics became normal within only 3 days. Myocardial biopsy after 6 months was unremarkable histologically and immunohistologically, and left ventricular function was also normal. However, while after a further 12 months myocardial biopsy remained normal and no virus was demonstrated, there was definite, though moderate, impairment in left ventricular function, indicating a dilated cardiomyopathy.Even when histological and immunohistological evidence of healing of an acute viral myocarditis has been achieved, with complete normalization of left ventricular function, a dilated cardiomyopathy may subsequently develop. The pathophysiological mechanism of this occurrence remains unknown.
