SummaryNewborn rats were exposed to air or hyperoxic conditions for the first 6 days of life. Resulting effects on the pulmonary vascular bed were determined by analy& of barium angiograms; scanning electron microscopv of methvlmethacrvlate corrosion casts and -" whole lung, morphometric estimations of pulmonary arteries/area and capillary number/area, and arterial blood gas measurements. Similar studies were also performed on the lungs of animals allowed to recover in air for 1 and 2 wk. Although the general pattern of the pulmonary arterial bed by barium angiograms appeared similar, diminished branching or underfilling of the distal arterial segments was more frequently encountered in hyperoxicexposed animals. Morphometric examination and corrosion casts revealed differences in vascular pattern and density between hyperoxia and air-exposed animals. The number of capillaries/mm2 of lung tissue was less in hyperoxic-exposed pups than controls after 6 days of exposure to hyperoxia but markedly increased to slightly above control levels by 2 wk of air recovery. The number of 20-50 pm size vessels/mm2 followed a similar pattern of change. Corrosion casts of lungs exposed to 6 days of hyperoxia revealed less microvascular densitv com~ared to air controls. but after 1 wk recovery in air, hyperoxic-exposed animals had a more extensive network of microvessels. Maximum P a o~ attained bv animals in the various groups closely resembled the patterns of change in microvessel density. These findings support the thesis that a major alteration of lung vascular growth and development occurs subsequent to exposure of the newborn to hyperoxia.Retarded lung growth and maturation have been demonstrated to result from early neonatal exposure of rats to concentrations of normobaric hyperoxia as low as Fio:! = 0.4 (3). This earlier work from our laboratory demonstrated the potential that exposure to hyperoxia may have in contributing to many of the lung changes previously reported in infants who have developed manifestations of chronic lung disease. A serious functional abnormality which is common to most of these infants is an altered ventilationperfusion distribution. This has been documented in infants with bronchopulmonary dysplasia (19), Mikity-Wilson disease (18) and chronic pulmonary insufficiency of prematurity (12), all diseases which require, or stem directly from periods of hyperoxic therapy. Swyer et al. (18) have reported fewer and smaller capillaries in the lungs of infants who died from Mikity-Wilson disease than were found in the lungs of infants who died from non-respiratory causes. On the other hand, Pratt (16) has shown that pulmonary capillary proliferation occurred in a number of adult humans who succumbed after receiving prolonged periods of hyperoxic therapy for respiratory distress.The objective of this study was to determine if alterations in pulmonary vascular development occur during, or after exposure of newborn rats to hyperoxia. We therefore examined the effect of exposure to hyperoxia on the pulmonary v...

Twenty long-term survivors of childhood cancer underwent exercise echocardiography to evaluate possible late anthracycline-induced cardiac toxicity. Ten patients ages 10 to 20 years had received anthracyclines, and ten patients ages 8 to 27 years had not received anthracyclines as part of their medical regimen. Both groups had normal cardiac function at rest. Patients who had not received anthracyclines had a greater increase in M-mode shortening fraction (P less than 0.005), velocity of circumferential fiber shortening (P = 0.05), and Doppler aortic peak flow velocity (P = 0.01) than patients receiving anthracyclines. There were no significant differences in work performed, or increase in heart rate or blood pressure with exercise between the groups. These results suggest that subtle abnormalities in myocardial function exist which become apparent only after exercise in survivors of childhood cancer who have received anthracyclines and have normal resting cardiac function.

Persistent fifth aortic arch manifested as a double-lumen aortic arch (DLAA) is a rare anomaly. We present such a case with transposition of the great arteries, ventricular septal defect (VSD), and pulmonary atresia. Review of the eight previously published cases indicates relatively frequent association of DLAA with preductal coarctation of the aorta. We attempt to explain the coexistence of this lesion with DLAA. We also discuss evidence supporting derivation of the inferior channel of the DLAA from the embryologic fifth aortic arch.

No abstract

o VER-THE-COUNTER preparations containing combinations of phenylpropanolamine HCL, ephedrine, and caffeine are highly publicized and readily available in many parts of the United State. I Recently these preparations have become major abuse items for adolescents who obtain them from paraphernalia shops as &dquo;legal&dquo; stimulants or illicitly on the street in the form of &dquo;look-alikes&dquo; marketed as &dquo;speed.&dquo;These over-the-counter preparations have been reported to cause psychosis, severe hypertension, and even cerebral hemorrhage.2-4 The purpose of this report is to discuss our experience with an adolescent who presented with complex cardiac arrhythmias, including ventricular tachycardia, following ingestion of such a combination stimulant and to emphasize the potential dangers of these drugs. Case ReportThe patient, a 14-year-old white female, ingested 15 to 18 capsules called R~JB~ (ephedrine 25 mg, caffeine 200 mg, phenylpropanolamine 50 mg) in a suicide gesture following expulsion from school. Approximately 1.5 hours after the ingestion she complained of blurred vision, nervousness, tremor, and inability to walk. Her mother, at that time, leamed of the ingestion and took her to a local hospital where she was given ipecac and activated charcoal. On admission her blood pressure was 104/62 mm Hg, with a heart rate of 180 and frequent aberrant beats. An electrocardiogram demonstrated premature ventricular contractions, junctional beats and premature atrial contractions as well as short of ventricular tachycardia. The remainder of the physical examination was remarkable. Because of the serious nature of the arrhythmias, lidocaine therapy (50 mg/kg intravenous bolus, followed by a constant infusion of 20 >g/kg/min) was instituted.This treatment did not alter the appearance of the arrhythmias. The patient was subsequently transported to the University of Iowa Hospitals for further treatment.Upon arrival the patient remained alert and responsive but complained of palpitations, nervousness, and blurred vision. Examination revealed a pulse of 140 beats/min which was irregular; a blood pressure of 135/68 mm Hg; pupils that were 3 mm, equal, and reacted slowly to light; and generalized hyperrenexia. The lidocaine infusion was continued for 15 minutes after admission. Continuous ECG monitoring was remarkable for numerous ventricular premature contractions (Fig I A). Due to the lack of response to lidocaine, the patient received I mg propranolol as an intravenous infusion over three minutes, during which the heart rate converted to a normal sinus rhythm at a rate of 86 beats per minute (Fig 1B and C). The lidocaine infusion was discontinued, and the patient's recovery was uneventful with oral administration of propranolol without further arrhythmias. Discussion

The clinical course of 19 infants with severe respiratory symptoms associated with the presence of both congenital heart disease and gastroesophageal reflux is described. Down Syndrome or central nervous system disease was present in 12 of the 19 infants. The identification of reflux as a major or additional cause of the respiratory complications was often overlooked. Medical therapy alone was successful in only one of the 19 patients. Early repair or palliation of the cardiac malformation with or without subsequent antireflux surgical procedure was associated with relief of the symptoms in 13 patients.

No abstract

Left ventricular (LV) apical aneurysms were observed in 16 of 50 (32%) children (average age 8 years) consecutively catheterized after surgical repair of congenital heart disease. The LV apex was vented by a sump during cardiopulmonary bypass in each. The aneurysms varied in size, but were generally small. Average dimensions were 7.5 X 6.8 mm in the anteroposterior projection and 8.9 X 5.7 mm in the left anterior oblique projection. The LV apex wall was thinner in patients with aneurysms than in age- and lesion-matched controls. All of the LV aneurysm patients were asymptomatic during average follow-up of 4 years. Nevertheless, such aneurysms are anticipated to represent a potential source of cardiovascular complications and, when possible, alternate methods for venting the left ventricle are recommended.