One hundred goitrous school children received 475 mg iodized oil by mouth, while 100 controls received mineral oil, on a double-blind basis. On follow-up 22 months later the urinary iodine had increased and goiter size had decreased in both groups, more strikingly in the iodine-treated children. There were no consistent differences between the two treatment groups in rate of somatic growth or performance on the Stanford-Binet and Bender tests. Because of the complexities introduced by increases in urinary iodine in the controls, we compared goiter reduction with improvement in IQ score in all children, regardless of group, and found a significant relationship (p = 0.014), particularly in girls (p = 0.029). We conclude that oral iodized oil is an attractive alternative to its injection but we recommend an approximate doubling of the dose used here for more effective control. Also, while our data are not conclusive, they support the possibility that correction of iodine deficiency may improve mental performance in school age children, particularly girls.

To systemically evaluate the effects of acute hypoxemia and hypercapnic acidosis on the sympathetic nervous system, five unanesthetized mongrel dogs were studied during acute hypoxemia [arterial O2 tension (PaO2) 33 +/- 2 Torr], acute hypercapnic acidosis [arterial CO2 tension (PaCO2) 53 +/- 1 Torr; pH, 7.19 +/- 0.02], and combined acute hypoxemia and hypercapnic acidosis (PaO2, 36 +/- 1 Torr; PaCO2, 52 +/- 1 Torr; pH, 7.18 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis resulted in increased mean arterial pressure, cardiac output, and heart rate. Moreover, combining acute hypoxemia and hypercapnic acidosis acted synergistically to increase circulating norepinephrine and epinephrine. Acute hypoxemia alone and acute hypercapnic acidosis alone resulted in reversible increases in mean arterial pressure, cardiac output, heart rate, and circulating norepinephrine. Although plasma epinephrine concentrations increased during acute hypoxemia, circulating epinephrine was unchanged during acute hypercapnic acidosis. These data indicate that acute hypoxemia and hypercapnic acidosis result in synergistic increase in circulating catecholamines.

SUMMARY. The effects of acute hypoxemia and hypercapnic acidosis were examined in five unanesthetized dogs in which sodium intake was controlled at 80 mEq/24 hours for 4 days prior to study. Each animal was studied during combined acute hypoxemia and hypercapnic acidosis (Pac>2 = 36 ± 1 mm Hg, Paco? = 52 ± 1 mm Hg, pH = 7.18 ± 0.02), acute hypoxemia alone (Pac>2 = 32 ± 1 mm Hg, Pacch = 32 ± 1 mm Hg, pH = 7.34 ± 0.01), and acute hypercapnic acidosis alone (Paoj = 82 ± 2 mm Hg, Paco? = 51 ± 1 mm Hg, pH = 7.18 ± 0.02). Although mean arterial pressure, cardiac output, and heart rate increased during combined hypoxemia and hypercapnic acidosis, effective renal plasma flow and glomerular filtration rate decreased. In addition, filtered sodium load and urinary sodium excretion decreased during combined hypoxemia and hypercapnic acidosis. Either acute hypoxemia or hypercapnic acidosis alone resulted in increased mean arterial pressure, cardiac output, and heart rate. However, in contrast to their combined effects, renal hemodynamic function was unchanged and natriuresis was observed. Measurement of plasma renin activity and angiotensin II concentrations indicated that hypoxemia or hypercapnic acidosis alone resulted in moderate activation of the renin-angiotensin system. Moreover, combined hypoxemia and hypercapnic acidosis acted synergistically resulting in major renin-angiotensin activation. Systemic angiotensin II blockade using 1-sarcosine, 8-alanine, angiotensin II (2 Mg/kg per min) during combined acute hypoxemia and hypercapnic acidosis resulted in decreased renal hemodynamic function. We conclude that acute hypoxemia and hypercapnic acidosis act synergistically to increase mean arterial pressure, diminish renal hemodynamic function and activate the renin-angiotensin system. Systemic angiotensin inhibition studies suggest activation of the renin-angiotensin system maintains renal hemodynamic function during combined hypoxemia and hypercapnic acidosis, instead of mediating the renal vasoconsrriction. (Circ Res 53: 202-213, 1983)

No abstract

SUMMARY. Since heart failure may occur in the setting of lung dysfunction and CO2 retention with only modest increases in cardiac work load, we questioned whether myocardial function is impaired by hypercapnic acidosis. To determine the influence of hypercapnic acidosis on right ventricular function, we measured the effects of acute (2 hours) and chronic (2 weeks) hypercapnic acidosis on right ventricular performance during normal and increased right ventricular afterload in five conscious dogs. Systemic hemodynamic and right ventricular functions were unaltered during normal right ventricular afterload by acute hypercapnic acidosis (Paco2 = 49 ± 3 mm Hg, pH = 7.27 ± 0.003). As right ventricular afterload was increased by progressive balloon occlusion of the right ventricular outflow tract during acute hypercapnic acidosis, the rise (slope) in right ventricular enddiastolic pressure was increased 4-fold (P < 0.01) over that observed in normocapnic control. Maximum isovolumic right ventricular dP/dt rose (P < 0.05) comparably with increasing right ventricular afterload during normocapnic control and acute hypercapnic acidosis. Chronic hypercapnic acidosis (Paco2 = 55 ± 2 mm Hg, pH = 7.28 ± 0.01) resulted in systemic vasodilation and increased (P < 0.05) heart rate and cardiac output during normal right ventricular afterload. As right ventricular afterload was increased during chronic hypercapnic acidosis, the rate of rise in right ventricular end-diastolic pressure was 2-fold (P < 0.01) above normocapnic control but maximum isovolumic right ventricular dP/dt was unchanged in contrast to normocapnic control and acute hypercapnic acidosis. Moreover, cardiac output fell and stroke work was unchanged with increasing afterload during chronic hypercapnic acidosis. /?-Adrenergic blockade resulted in an increased (P < 0.01) rate of rise in right ventricular end-diastolic pressure with afterload during normocapnic control and chronic hypercapnic acidosis. We conclude that hypercapnic acidosis results in diminished right ventricular performance during increased right ventricular afterload, evidenced by accentuated rise in right ventricular end-diastolic pressure, and may contribute to the congestive heart failure and edema observed in patients with pulmonary hypertension and CO2 retention.