A maternal warm-reactive autoantibody presenting as a positive direct antiglobulin test in a neonate.

Autoimmune hemolytic anemia in pregnancy is a rare cause of hemolytic disease of the newborn. This report describes a neonate with a mild hemolytic process and a positive direct antiglobulin test (DAT) presenting as the first manifestations of a maternal warm-reactive autoantibody. A full-term male neonate, blood group O, had a strongly positive DAT and laboratory evidence suggestive of a mild hemolytic process. The neonate's mother was also group O and had a negative antibody screen. Umbilical cord blood testing revealed a panreactive eluate though the antibody was not detected in cord serum. The neonate's mother was also found to have a positive DAT. A panagglutinin was identified in an eluate of her red cells, although the autoantibody could not be detected in her serum by a variety of sensitive techniques. There was no clinical or laboratory evidence of maternal hemolysis.

Mechanisms involved in the cardiovascular-renal actions of nitric oxide inhibition.

The roles of the sympathetic nervous system, angiotensin II, and arginine vasopressin in the cardiovascular-renal responses to nitric oxide synthesis inhibition were examined in eight conscious dogs equipped with arterial and venous catheters and a nonoccluding bladder catheter. Nitric oxide inhibition was achieved by intravenous infusion of NG-nitro-L-arginine methyl ester (L-NAME) at 37.1 nmol/kg per minute for 140 minutes in the control group. The same dogs, after a 1-week recovery, were pretreated for 2 days with either prazosin for alpha 1 blockade, prazosin plus propranolol for alpha 1 plus beta blockade, L-158,809 for angiotensin receptor blockade, or d(CH2)Tyr(Me)arginine vasopressin for vasopressin-V1 blockade, and the L-NAME infusion was repeated. After 140 minutes of L-NAME infusion into the control group, mean arterial pressure and renal vascular resistance had increased 16% and 71%, and renal blood flow, glomerular filtration rate, urine flow, and urinary sodium excretion had decreased 33%, 16%, 61%, and 64%, respectively. The decrement in renal blood flow and glomerular filtration during L-NAME administration was unaffected by any of the neurohumoral blockers. During V1 blockade L-NAME resulted in only a 3% increase in arterial pressure, attenuation of the renal vascular resistance response, and almost total elimination of the decrease in urine flow. During angiotensin blockade the L-NAME-induced increase in arterial pressure was markedly attenuated, and the decrease in urinary sodium excretion was attenuated in the alpha 1 plus beta blockade group.(ABSTRACT TRUNCATED AT 250 WORDS)