Our 20-year experience with 1239 very low birth weight infants suggests strongly that the late-onset, slow, continuous drip feeding protocol and avoidance of indomethacin and early dexamethasone treatment contribute to the prevention of necrotizing enterocolitis.

To determine the therapeutic range of plasma indomethacin levels for ductus closure, we evaluated the ductus response and renal side effects on two therapeutic regimens using different dosage; regimen I received 0.3 mg/kg q 24 h for a maximum of 3 doses, and regimen II received 0.1, 0.2 and 0.3 mg/kg at 24-hour intervals, for a maximum of 3 doses if needed. Infants in regimen I had significantly higher plasma indomethacin and higher ductus response rate than infants in regimen II. Urine output (U/O) was comparable between the regimens, but serum sodium was lower in regimen I than in regimen II. In both regimens, U/O and serum sodium returned to normal by 72 h. The plasma indomethacin levels at 12 h after 1 dose correlated significantly with ductus response and hyponatremia. There appeared to be a minimal level of plasma indomethacin above which U/O decreased; with a plasma level > 170 ng/ml the majority (>97%) of infants showed a decrease in U/O. While there was a 50% or greater chance that ductus would close when the plasma levels reached 600 ng/ml or more, a great proportion of infants would also develop renal side effects. Thus, a safe therapeutic range of plasma indomethacin appeared to be very narrow. However, when the dose of indomethacin is increased to optimize constrictive response, there is no significant increase in incidence and severity of renal adverse effects. In view of the transient nature of renal side effects, they should not hinder indomethacin therapy if ductus closure is indicated.

The ccmbination o f a m p i c i l l i n w i t h an a m i n q l y c o s i d e i s the conventional a n t i m i c r o b i a l therapy f o r pramture i n f a n t s admitted

. o f P e d i a t r i c s , U n i v e r s i t y o f New Mexico. Albuaueraue. NM. We p r e v i o u s l y described t h a t a c t i o n p o t e n t i a l CAP) parameters from neonatal ( N ) v e n t r i c u l a r myocardium a r e more r e s i s t a n t than a d u l t (A) APs t o acute hypoxia (H). I n t h i s study, we used standard microelectrode techniques t o evaluate t h e e f f e c t s o f acute H (p02=30 t o r r ) on A (n=10) and N (3-12 days o l d ) ( n = l l ) canine PF APs and PF arrhythmogenesis. PFs were paced a t 1 Hz. Compared t o A, c o n t r o l AP from N PF had s i g n i f i c a n t l y (s)(p<0.05) lower values f o r AP amplitude (APA), Vmax, AP d u r a t i o n a t 50% r e p o l a ri z a t i o n (APD50), APD90 and e f f e c t i v e r e f r a c t o r y p e r i o d (ERP) .A f t e r 30 min. o f acute hypoxic superfusion, N PF showed s g r e a te r r e d u c t i o n s than A PF i n Vmax (-20% vs -9%), APDSO (-18% vs -8%) and APD90 (-13% vs -4%). Changes i n APA, maximum d i a s t o l i c p o t e n t i a l (MDP) and ERP d i d n o t d i f f e r . A l l N AP parameters (except MDP) were s reduced a f t e r H. Reoxygenation f o r 30 min. p a r t i a l l y r e s t o r e d N AP i n d i c e s . When pacing was stopped d u r i n g c o n t r o l , no A o r N PF had spontaneous a c t i v i t y (sa) f o r 15 sec. H produced sa i n 0 o f 10 A and 2 o f 11 N PF. The sa increased d u r i n g e a r l y reoxygenation ( 1 o f 10 i n A; 4 o f 11 i n N) b u t was abolished i n a l l a f t e r 30 min. The H and reoxygenation r e l a t e d e c t o p i c sa was due t o both enhanced a u t o m a t i c i t y and r e e n t r y , t h e l a t t e r probably induced by t h e decreases i n Vmax (conducti o n v e l o c i t y ) , APD and ERP. I n summary, N PF have an enhanced s e n s i t i v i t y t o acute H. The arrhythmogenic e f f e c t s o f H i n -v i t r o may e x p l a i n t h e H and r e p e r f u s i o n r e l a t e d arrhythmias seen c l i n i c a l l y i n some c h i l d r e n . AMIODARONE (AM) ADVERSELY AFFECTS SINUS NODE (SN)t 158 E Ẽ : ; : . AM is being used more frequently to control "resistant" childhood arrhythmias. As a Class I11 agent, AM supposedly acts by uniformly prolonging action potential (AP) duration and refractoriness. Because sinus slowing is observed clinically, we evaluated the acute effects of 0.68-34ugIml AM on SN pacemaker activity using rabbit SN preparations and standard microelectrode techniques. Data were collected only from true SN pacemaker cells impaled continuously throughout the study. AM produced significant (p