Pulmonary regurgitation in large atrial shunts without pulmonary hypertension

Seven patients with pulmonary regurgitation (PR), normal pulmonary artery (PA) pressures and large left-to-right atrial shunts are reported. Six had secundum atrial septal defects (ASD) and one had anomalous pulmonary venous drainage. These comprised 4% of 180 patients with atrial shunts and normal PA pressures. Pulmonary regurgitation was diagnosed clinically by mid-frequency diastolic decrescendo murmurs beginning after the pulmonic component of the second heart sound, and diagnoses were confirmed by catheterization. In two patients who had serial preoperative catheterizations over 8 and 16 years, PR progressed in one and was present only on the second study in the other. All patients underwent shunt correction, at which time the pulmonic anulus and artery appeared dilated, but the pulmonic valves were normal and did not require revision. In all patients the PR murmur disappeared after shunt correction alone, and on chest X-ray both PA and overall heart size decreased. Although it is known that pulmonary regurgitation occurs with atrial septal defects and pulmonary hypertension, the present study demonstrates that it also occurs with high flow atrial shunts, in which setting it has different implications and is reversible with shunt correction alone.     

On the metabolism of prostaglandins by rat brain homogenate

Using radio-immuno assays for prostaglandins and prostaglandin metabolites, three prostaglandin metabolizing enzymes were found in the 100,000 X g supernatant of rat brain, 15-hydroxy-prostaglandin-dehydrogenase, delta13-reductase and prostaglandin E-9-keto-reductase. Specific activity of the latter enzyme was highest in striatum and midbrain and lowest in cortex, cerebellum and spinal cord.     

Cryoimmunoglobulin IgGk with microtubular ultrastructure associated with pyoderma gangrenosum

Based on the hitherto published population data of the human red cell PGM1 and acid phosphatase polymorphisms, the geographical distributions of their gene frequencies were analyzed. As far as the acid phosphatase alleles are concerned, a marked geographical gradient was found as the Pa and Pb alleles showed significant correlations with the mean annual temperatures of the various human biotopes (Pa:r = -0.706; Pb:r = +0.812). Against that, the world distribution of the PGM1 alleles did not show a comparable correlation (PGM1 1:R = +0.063; PGM2 1:R = -0.063). The possible reasons for the distribution pattern of the acid phosphatase alleles are discussed.     

Splenic imaging with 99mTc-labeled erythrocytes: a comparative study of cell-damaging methods

Several methods of damaging red blood cells (RBCs) for splenic imaging were compared to determine the optimum approach. The RBCs from donor animals were labeled with 99mTcO4- and damaged by heat, excess acid citrate dextrose (ACD), excess Sn(II) ion, or the sulfhydryl inhibitors N-ethylmaleimide (NEM) or p-hydroxymercuribenzoate (PMB). The organ distributions of undamaged and damaged RBCs were determined in rats, and splenic imaging studies were performed in rabbits. Splenic deposition and spleen-to-liver ratios with heat- or sulfhydryl-damaged 99mTc-RBCs were significantly greater (p less than 0.001) than the values obtained using ACD or Sn(II) ion. Heat-damaging produces good splenic localization of 99mTc-RBCs but requires rigidly controlled incubation conditions. NEM-damaging provides an excellent and predictable alternative approach.     

The erythropoietin response to the anemia of thermal injury

Erythropoietin excretion was persistently increased following major thermal injury in 4 of 5 patients. A good correlation was found between erythropoietin excretion and red cell mass but not between erythropoietin excretion and hematocrit. In spite of the increased erythropoietin, erythropoiesis in these thermally injured patients was inadequate to compensate for erythrocyte deficits as judged by bone marrow morphology, reticulocyte counts, and transfusion requirements.     

Effects of zinc and vitamin A deficient diets on the hepatic mobilization and urinary excretion of vitamin A in rats

Weanling rats were fed diets deficient in zinc (ZD), vitamin A (AD), or both (ZAD) for 3 weeks. Each then received 20 mug of 11,12-3H-retinyl acetate. Plasma retinol was monitored for radioactivity for 5 hours and urine for 6 days. Rats were killed and measurements made of plasma and liver vitamin A and plasma zinc. Plasma vitamin A was depressed but growth was not affected in AD rats compared to pair-fed controls. Radioactivity appeared most rapidly in the plasma retinol fractions of the two vitamin A-depleted groups (AD and ZAD) and was excreted most rapidly in the urine of these same groups. Zinc-deficient diets (ZD and ZAD) caused depressed plasma levels of zinc and vitamin A and growth retardation greater than in pair-fed controls. However zinc deficiency had no effect on mobilization of newly-ingested vitamin A or urinary excretion of labeled metabolites. Liver stores of vitamin A were lower for ZD rats than for controls. The data indicate that zinc deficiency is not a limiting factor in hepatic vitamin A release except as it influences growth and body demand for the vitamin. The data also suggest that newly-absorbed vitamin A is mobilized and utilized in preference to that previously stored in the liver.     

Aldosterone secretion during high sodium cerebrospinal fluid perfusion of the brain ventricles

Conscious sheep with permanent indwelling cannulae in the lateral ventricles and the cisterna magna were Na depleted and then perfused for 9 h with an artificial CSF solution. There were 3 experimental groups: Group I (n=5) received perfusion with aritifical CSF containing NA 170 MEq./1, Group II (n=7) received perfusion with artificial CSF containing Na 145 mEq./1, Group III (n=7) received no perfusion. In Group I the blood aldosterone level fell from 26.4 +/- 7.4 to 8.6 +/- 2.3 ng/100 ml by 9 h after perfusion. There was no significant change in plasma [Na] or [K], blood angiotensin II or plasma renin concentration. Blood cortisol and corticosterone levels rose. There was also a fall in post-perfusion. Group III showed no significant change in blood aldosterone concentration. Multivariate statistical analysis showed that the fall in aldosterone levels during 170 mEq./l Na perfusion could not be accounted for by changes, either alone or together, of ACTH as evidenced by alteration in blood cortisol or corticosterone, or by change of plasma [Na], [K] or renin concentrations. This data supports the hypothesis of an additional factor which may be of CNS origin being involved in the control of aldosterone secretion.     

Nitrous oxide "analgesia": resemblance to opiate action

Nitrous oxide produced a dose-related "analgesia" in mice (median effective dose, 55 percent). The analgesia was evaluated by means of a phenylquinone writhing test. Narcotic antagonists or chronic morphinization reduced nitrous oxide analgesia. Either nitrous oxide releases an endogenous analgesic or narcotic antagonists have analgesic antagonist properties heretofore unappreciated.     

Neisseria lactamica meningitis

Neisseria lactamica was recovered from the blood and cerebrospinal fluid of a 7-month-old girl with acute purulent meningitis. The isolate was identified initially as N meningitidis. However, additional biochemical testing at the Center for Disease Control showed that the organism fermented lactose and produced beta-D-galactosidase, thereby confirming its identity as N lactamica.     

A statistical note on the association of colorectal cancer and lymphoma

The degradation and excretion of 2-14C-uric acid were examined in three adult woolly monkeys (Lagothrix lagothrichia) to determine the basis for the relatively high serum and urinary uric acid concentrations previously reported in this species. Like man and the great apes which lack uricase, but in distinction to most other mammals, these animals converted very little urate to allantoin. Uric acid turnover, as has been reported for other New World monkeys, was several times that of normal man. Renal urate excretion as well as disposition by extrarenal mechanisms may protect Lagothrix vrom hyperuricemia. The capacity to convert urate to allantoin appears to have been lost late in the evolution of New World monkeys. The woolly monkey deserves further study as a primate model for investigations of enzyme replacement strategies.