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Current technologies for measuring plant water status are limited, while recently remote sensing techniques for estimating N status have increased with limited research on the interaction between the two stresses. Because plant water status methods are time-consuming and require numerous observations to characterize a field, managers could benefit from remote sensing techniques to assist in irrigation and N management decisions. A 2-yr experiment was initiated to determine specific wavelengths and/or combinations of wavelengths indicative of water stress and N deficiencies, and to evaluate these wavelengths for estimating in-season biomass and corn (Zea mays L.) grain yield. The experiment was a split-plot design with three replications. The treatment structure had five N rates (0, 45, 90, 134, and 269 kg N ha(-1)) and three water treatments [dryland, 0.5 evapotranspiration (ET), and full ET]. Canopy spectral radiance measurements (350-2500 nm) were taken at various growth stages (V6-V7, V13-V16, and V14-R1). Specific wavelengths for estimating crop biomass, N concentration, grain yield, and chlorophyll meter readings changed with growth stage and sampling date. Changes in total N and biomass in the presence of a water stress were estimated using near-infrared (NIR) reflectance and the water absorption bands. Reflectance in the green and NIR regions were used to estimate total N and biomass without water stress. Reflectance at 510, 705, and 1135 nm were found for estimating chlorophyll meter readings regardless of year or sampling date.

A process of adaptation of the cardiovascular system occurs during pregnancy, entailing physiologic changes. In women with congenital heart disease these changes lay a great burden on the cardiovascular system. Therefore there is an increased risk for mother and fetus, depending on the form of congenital heart disease, preceding operations and the grade of maternal hypoxemia. Overall, the maternal mortality is low, but in certain forms of congenital heart disease the mortality rate can rise to 50%. Infective endocarditis and anticoagulation therapy represent further problems for mother and fetus. It is the duty of the cardiologist, general practitioner and obstetrician to counsel the patient before conception on potential complications and risks of pregnancy, expected physical deterioration of the mother, as well as possible malformations of the child, including the recurrence risk of congenital heart disease. If pregnancy is contraindicated because of the severity of the heart disease, the patient has to be advised about reliable contraceptive methods tailored to her individual needs and their risks, including possible endocarditis, bleeding under anticoagulation therapy, thrombosis, toxic shock syndrome etc.

Clinical experience with long-term nifedipine treatment in 23 patients aged between 1 1/12 and 14 8/12 years is reported. The cardiopulmonary diseases comprised primary pulmonary diseases with pulmonary hypertension (n = 4), congenital heart defects with intracardiac shunts and pulmonary hypertension which either were inoperable as a result of an Eisenmenger reaction (n = 7) or presented a high surgical risk (n = 5), or defects in which pulmonary hypertension did not regress despite corrective (n = 1) or palliative surgery (n = 3), and congenital defects without pulmonary hypertension (n = 3). Subjective improvement with an increase in physical performance was clearly observed in 15 cases. Echocardiography and cardiac catheter examinations showed no progression of the pulmonary arterial diseases, except in 1 patient with severe primary pulmonary hypertension and an 11-year observation period with nifedipine treatment during the last 4 years. No complications occurred during the 4 corrective operations. A patient aged 14 8/12 years with the Down syndrome and atrioventricular septal defect developed easily controllable heart failure during 7-day administration of nifedipine without additional cardiotherapy. 4 children initially suffered from flushed face and scalp, in one case with headache; 2 children reported fatigue. Long-term treatment with nifedipine should begin with strict 7-day supervision in hospital and possibly additional digitalization. Success of the treatment was determined by an improved quality of life in patients with primary pulmonary hypertension and inoperable defects, and by a reduced perioperative risk and postoperative regression of pulmonary hypertension in patients with operable defects.

In children with growth retardation and the typical face, particularly with valvar pulmonary stenosis, the Noonan syndrome is the be suspected. In early infancy, these patients show very severe developmental retardation and muscular hypotony. Mental retardation is frequent but not compulsory. The most important diagnostic tool is the chromosomal analysis. In our patient, the syndrome was diagnosed becaused of the typical appearance and the angiocardiographic findings in connection with a normal chromosomal sequence.

Six out of 14 chronically hemodialysed children with significantly decreased serum carnitine levels were substituted with L-carnitine (15-30 mg/kg/day-Biocarn) up to normal and above normal carnitine levels. None of these patients were digitalised. During the time of investigation plasma carnitine levels were investigated monthly and, simultaneously, three echocardiographic parameters in M-mode were quantitatively und qualitatively determined: shortening fraction (SF-%), ratio of left ventricular pre-ejection/ejection time (LVPT/LVET) and velocity of circumferential fibre shortening (Vcf). Carnitine substitution produced measurable changes in echocardiographic parameters, and a significant quantitative improvement in left ventricular function and performance: after 6 months of carnitine substitution a 24% improvement was seen, after 18 months a 44% mean improvement. No side effects of carnitine were observed; the compatibility was good. Beside these positive effects all patients reported decreased dialysis-associated spasms and polyneuropathic symptoms and increased somatic ability.

About syncopal attacks caused by cardial arrhythmias had been frequently reported. In one family we found female members of three generations affected by characteristical prolongation and alteration of the QT-interval in ECG. All patients suffered from attacks with loss of consciousness which could not be defined as epileptic fits. Ventricular arrhythmias have to be considered as reason for the attacks. This combination of symptoms without additional malformations (i.e. congenital deafness) is well known in literature as Romano Ward Syndrome. Mode of inheritance, pathogenetic mechanisms and possibilities of therapy are discussed. Therapy witha beta blocking medication (propranolol) made our younger patient free of attacks, the other two patients have no complaints since two years without any therapy.

The differentiation between anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) and other causes of cardiomegaly and thereby the decision to operate, as opposed to undertaking conservative therapy is often extremely difficult in clinical practice. Electrocardiographically, signs of myocardial infarction can be missed in ALCAPA, other forms of dilative cardiomyopathy (DCMP) often showing similar clinical features. Up to now aortography alone can make a clear-cut distinction between these two entities. In order to determine the diagnostic value of thallium-201 myocardial scintigraphy in ALCAPA, we investigated 18 children, 7 of them with angiographically or autoptically established ALCAPA and 11 patients with DCMP. The coronary artery anomaly was diagnosed on the basis of the typical myocardial perfusion defects in only 3 of the relevant 7 patients. In 9 of the 11 patients with DCMP ALCAPA was excluded by the homogeneous perfusion pattern or small focal reduction in thallium-201 activity in the left ventricular muscle mass. In view of the overall disappointing results of this method in achieving a specific diagnosis in ALCAPA, all patients with DCMP with or without suspected fibroelastosis should undergo invasive diagnosis with aortography.

The indication and efficacy of mexiletine is described in five patients. In four children the first signs of arrhythmias were seen a short time after viral infection. Two girls had numerous ventricular extrasystoles, which showed very promptly a positive reaction to mexiletine. Two patients had ventricular tachycardias beside ventricular premature beats. Because of signs of cardial insufficiency a 13 year old boy was defibrillated before his cardiac rhythm could be established with mexiletine. Because of ventricular tachycardias the second patient was treated with a combination of mexiletine and propranolol. Seven years after corrective operation of tetralogy of Fallot a nine year old boy showed ventricular extrasystoles. Because of a very low plasma concentration of mexiletine the therapy was without any effect. In all children, a long term ECG over 24 hours was deduced. To control the efficacy of mexiletine in all patients the plasma-concentration was determined. The therapeutic effective plasma concentration of mexiletine lays between 0.5 and 2,5 mcg/ml. This level can be reached by a daily dose of 12.5--16.2 mg/kg body weight.

The outbreak, the progress and the treatment of the anaphylactoid purpura at an 8 months old infant are reported. It is referred to the rare outbreak of this disease at infants younger than one year. The differential diagnosis and the measurement of treatment are discussed.

The postoperative course of 37 children with atrial septal defect primum type with or without a cleft in the septal mitral or tricuspid valve, is traced. The mortality rate, the number of postoperative rhythmic disorders and the success of functional restitution of the mitral valve are emphasized. The number of patients between 1962-1979 was 37. The age was between 3 years and 5 month and 14 years and 9 month. As a parameter of success or failure of the operation the pre- and postoperative symptoms, the ECG and PCG, the X-ray of the chest and the postoperative echocardiogram were considered.

6 children aged 9 months to 13 8/12 years developed reduced physical capacity, failure to thrive, dyspnoea on effort and heart failure after viral infection. Bed rest and anticongestive therapy did not reduce the severe heart failure. Immunosuppressive therapy with prednisolone 2 mg/kg/d and azathioprine 2 mg/kg/d was added on the assumption of chronic myocarditis (n = 4) or endocardial fibrosis (n = 2). 3 of the 6 children showed a considerable improvement in heart size, ECG and systolic heart function. Interruption of immunosuppressive therapy due to side effects in one child led to cardiac deterioration, which was reversed by renewed prednisolone therapy. Two patients died of progressive congestive heart failure. Heart transplantation was successfully performed in the now 14 year-old girl who was suffering from terminal dilated cardiomyopathy. Since there is no specific test for selecting patients who are likely to benefit from immunosuppressive therapy we feel this regimen would be justified in hopeless cases of congestive cardiomyopathy who have not responded to conventional therapy with anti-congestive drugs.

In Pediatric Cardiology for many years the usage of spironolactone (Aldactone) and Canreonat-K+ (Aldactone pro injectione) had been experienced. The efficiency of aldactone was controlled by clinical parameters, electrolytes, discontinuity of the drug and in some cases by radioimmunologic measurement of the plasma aldosterone concentration. The treatment with aldactone in combination with digitalis gave good clinical results in cases with and without signs of secondary hyperaldosteronism. The recommended dosage i. v. and orally was for infancy 2--3 mg/kg/die the first 2--4 days and afterwards 1,5--2 mg/kg/die, for later childhood 4--5 mg/kg/die for 3--5 days and afterwards 2--3 mg/kg/die. Special attention should be paid to hyperkaliemia, over 6 mval serum K+ the aldactone administration was interrupted.

The prevalence and nature of late dysrhythmias following operative repair of transposition of the great arteries were evaluated in 32 children using pre- and postoperative standard electrocardiograms and postoperative Holter monitoring. The Mustard procedure was performed in 17 patients, the Senning procedure in 15 patients. The mean age at operation was 40 +/- 35 months in the Mustard and 9 +/- 6 months in the Senning group. The mean interval between operation and Holter monitoring 7 +/- 2 years in the Mustard and 1.6 +/- 1 years in the Senning group. All patients had sinus rhythm preoperatively. Following operation, the incidence of sinus rhythm increased from 59% in the Mustard and 87% in the Senning group in the first postoperative week to 76% in the Mustard and 100% in the Senning group at the end of follow-up (mean 4.6 +/- 3.5 years). Holter monitoring revealed dysrhythmias or conduction abnormalities in 12 patients (9 Mustard, 3 Senning). A permanent pacemaker had to be inserted in 2 Mustard patients because of complete atrioventricular block and sinus bradycardia with sinus arrest, respectively. Results indicate a prevalence of late postoperative dysrhythmias of 20% in the Senning and of 59% in the Mustard group (p less than 0.05). However, the significantly longer mean follow-up period of the Mustard group precludes a direct comparison between the 2 types of repair.

Under long-term oral treatment with nifedipine (N) 2 of 3 patients (2 children with VSD and Eisenmenger, 1 patient with Truncus I after corrective surgery) showed a remarkable improvement in exercise tolerance and reduction in the total pulmonary resistance. Therefore a single-dose testing with N was performed in 9 patients aged 2 to 20 years with primary pulmonary hypertension (n = 2), secondary pulmonary hypertension because of congenital heart disease with intracardiac shunts (n = 6) and after correction of Truncus Type I (n = 1). Before and after the injection of 0.5 mcg/kg of N into the main pulmonary artery, pulmonary artery pressure, cardiac output and systolic blood pressure were measured at 1 minute intervals during right heart catheterization. The maximal reaction occurred 3 to 4 minutes after the injection. The total pulmonary vascular resistance decreased significantly from 2684.2 +/- 1829.2 to 1300.2 +/- 1117.0 dyn.sec.cm-5.m2 (p less than 0.025), the cardiac index increased significantly from 3.1 +/- 1.65 to 5.73 +/- 1.95 l/min.m2 (p less than 0.01) concomitantly with a mild reduction in the mean pulmonary artery pressure. No significant change in heart rate and systolic blood pressure was seen; no side effects were observed. 4 of the 5 patients with the highest pulmonary vascular resistance showed the best positive reactions. Therefore these 9 patients may benefit from a long-term oral treatment with nifedipine.

In children with congenital heart disease serial noninvasive assessment of the pulmonary vascular bed is desirable in order to determine the appropriate timing of cardiac catheterization and corrective surgery. To assess the value of pulmonary Doppler echocardiography for the estimation of pulmonary arterial pressure we correlated the rightsided systolic time intervals (preejection period, acceleration period, ejection period) derived from pulmonary artery Doppler traces with catheterization data (systolic, mean and diastolic pulmonary arterial pressure, total and vascular pulmonary resistances). 62 children aged from 1 month to 15 years suffering from congenital heart disease (n = 52), from rheumatic heart disease (n = 4), from cardiomyopathy (n = 5) or from primary pulmonary hypertension (n = 1) were investigated. The major finding was a highly significant correlation between the acceleration period and the systolic pulmonary arterial pressure (r = 0.79; p less than or equal to 0.0001). However the acceleration period could not be used for prediction of pulmonary arterial pressure in children with poor myocardial contractility.

A five week old male infant is treated under suspicion of whooping cough because of pertussis like cough, cyanosis, and attacks of reflex apnea. These attacks are seen up to 40 times per day. After exclusion of a cerebral genesis there was found a ventral indentation of the trachea. It was also seen by tracheoscopy, but this part of the trachea was not pulsating. In the angiography the compriming structure was identified as the innominate artery. The genesis of this anatomic variant, the often threatening symptoms in this case without inspiratoric stridor, and the diagnostic and therapeutic steps are discussed.