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The hypertensive synergism of A-II and urea was studied in anesthetized cats. Femoral arterial pressure was measured while test substances were infused in a femoral vein. Dose-response analysis of the A-II + urea interaction suggested that A-II pressor effects and A-II + urea potentiation involve a common mechanism. Methylurea and mannitol + A-II also induce a similar potentiation. While plasma osmolality and plasma volume indicated no systemic changes, intracellular osmotic shifts may be a factor in the synergism. Since inhibition of the potentiation by indomethacin was not replicated, prostaglandins can no longer be considered important. No effect of ganglionic blockade also eliminated CNS influences as a factor. Dual infusion suggested urea-induced A-II changes were not important for the synergism. Since a synergism of A-II with amino acids occurred, alteration of A-II receptors was indicated. Thus, the A-II + urea pressor synergism may involve either intracellular osmotic shifts or a receptor modification so A-II is more accessible.

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Nine patients with univentricular heart 17 years of age or older were followed up for a mean duration of 13 years (range 5 to 26 years). Five patients had type A and four patients had type C univentricular heart. Pulmonary stenosis was present in eight of nine patients. Palliative shunt surgery was performed in seven patients, ventricular septation was performed in one patient, and no surgical intervention was performed in one patient. Eight patients were in New York Heart Association functional class II and one patient was in New York Heart Association functional class III. Long term follow-up of these patients suggests that a selected group of adults with univentricular heart may achieve a relatively long survival and good functional class with conservative management.

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In this retrospective study, we reviewed the records of patients who had coarctectomies at the University of Virginia Hospital after 1 year of age. Follow-up data for 5 years or more after surgery were available for 52 patients. Data from 23 similar patients from the Medical College of Virginia brought the total postoperative sample size to 75. The blood pressure of this group of patients did not differ significantly from that of the population at large. We conclude that successful repair of coarctation of the aorta in childhood or early adolescence does not lead to a higher-than-expected incidence of resting hypertension in childhood.

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The blood pressure of 3,166 adolescents was measured periodically in Richmond during the period 1974-1977. The subjects were students in public and private schools and ranged in age from 14 to 18 years. Analysis of the readings showed minimal differences relating to age, sex, school and race but a strong correlation with obesity. Only two organic renal causes of hypertension were discovered. A 3 1/2-year followup of 902 students indicated significant tracking, with a correlation coefficient of .385 for systolic and .305 for diastolic pressure. At the conclusion of the study, 340 students (10.7%) were identified as needing followup for hypertension.

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Surgical repair of the Taussig-Bing deformity has been successful in 2 children weighting 7.7 and 11.1 kg, respectively. In the first case the right ventricular patch divered left ventricular blood to the pulmonary arter, thus creating a physiologically complete transposition which was then corrected by an interatrial Mustard baffle. In the second case a right ventricular tunnel diverted left ventricular blood to the aorta, and right ventricular blood was directed to the distal pulmonary artery by means of an external conduit bypassing a subpulmonic stenosis. These patients represent the seventh and eighth successful corrections of the Taussig-Bing anomaly. One case (Patient 2) is the youngest to undergo repair and the first to receive an external conduit for bypass of an associated subpulmonic stenosis.

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A case of transposition of the great arteries without a significant ventricular septal defect or patent ductus arteriosus was treated when the patient was 5 months of age by retransposition of the great arteries and coronary arterial supply to the appropriate ventricle. The patient has done well for 13 months, despite the late occurrence of aortic regurgitation.

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Stimulation of the midbrain during acute combined arterial hypoxia and hypercapnea produces serious cardiac dysrhythmias which are not evoked when stimulation is elicited either with normal arterial blood gas tensions or with isolated mild hypercapnea. The cardiac dysrhythmias are mediated by both enhanced sympathetic and parasympathetic efferent discharge. The results support the concept that increased autonomic activity in combination with acute arterial hypoxia and hypercapnea contribute significantly to the exhibition of serious cardiac rhythm disturbances. Acute hypoxia appears to be the major determinant of such dysrhythmias.

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