Leone Mattioli

Asymmetric septal hypertrophy in childhood: Unreliability of histologic criteria for differentiation of obstructive and nonobstructive forms

Two cases of obstructive asymmetric septal hypertrophy with biventricular outflow obstruction in childhood are presented. Both patients were treated first with propranolol and later by ventriculoseptal myotomy-myectomy. The first patient died two and one-half years following surgery, and the second patient died in the immediate postoperative period. In the first patient the 690 gm. heart had an interventricular septum to posterior left ventricular wall ratio of 1.9, and in the second patient the ratio in the 460 gm. heart was 1.8. In both cases the posterobasal left ventricular free wall was rounded and hypertrophied, as has been reported grossly in obstructive asymmetric septal hypertrophy. However, in both cases, the bizarre disoriented cardiocytes typical of asymmetric septal hypertrophy were present in both ventricular free walls as well as in the interventricular septum, as has been reported in the nonobstructive variety. In these two cases, previously reported morphologic criteria for the differentiation of obstructive and nonobstructive disease are not considered reliable.

The Effect of Chronic Alveolar Hypoxia on Lung and Serum Angiotensin I Converting Enzyme Activity

Summary Mice exposed to chronic alveolar hypoxia showed elevations of serum and lung angiotensin I converting enzyme activity during the second week of exposure. The increment of activity of the lung and serum converting enzyme was of the same order of magnitude and occurred at approximately the same time. An increase in renal renin granules was closely correlated with both lung and serum converting enzyme activity.

Angiotensin-I-converting enzyme activity in idiopathic respiratory distress syndrome of the newborn infant and in experimental alveolar hypoxia in mice*

Serum angiotensin-I-converting enzyme activity was found to be elevated in infants with idiopathic respiratory distress syndrome when compared with healthy premature infants, normal infants, and acutely ill full-term infants. Serum and lung CE activity has been found to be elevated in mice exposed to hypobaric alveolar hypoxia which also stimulated renal renin production. These findings suggest that alveolar hypoxia stimulates the renin-angiotensin-aldosterone system and this system may be involved in the response to the stress of IRDS.

Hepatic artery ligation for cardiac failure due to hepatic hemangioma in the newborn

Summary A 6-wk-old infant born with large hepatic hemangioma underwent successful ligation of the common hepatic artery with marked clinical and hemodynamic improvement of her profound cardiac failure. No alteration of liver enzymes was noted. At 2 yr of age, this infant is clinically normal. We feel on the basis of this case and of two other previously reported cases that ligation of the common hepatic artery is a safe and effective means of therapy for cardiac failure due to diffuse intrahepatic arteriovenous fistulas in the newborn.

Scanning Electron Microscopy of Pulmonary Vascular Endothelium in Rats with Hypoxia-Induced Hypertension

Scanning electron microscopy was used to study the endothelial surface of the pulmonary trunk, artery, and vein in normobaric control rats as well as in rats exposed to hypobaric hypoxia for 7 and 21 days. The individual endothelial cells of the normobaric pulmonary trunk and hilar artery were flat and slightly elongated with elevated nuclear regions, and those of the intermediate-sized artery were more elongated and had more microvilli than the large arteries studied. Their endothelial cell boundaries were outlined by beaded cytoplasmic projections. The surfaces of the normobaric hilar and intermediate-sized veins were smooth and demonstrated numerous longitudinal streaks. These venous endothelial cells were elongated and their cell boundaries were outlined by low discontinuous marginal folds. Exposure to hypobaric hypoxia caused the following changes on the arterial surface: elevation of the endothelial cells; formation of microvilli-rich cell clusters; formation of hollow defects; and the attachment of leukocytes. Hypobaric hypoxia also caused the disappearance of the longitudinal streaks and the occurrence of microvilli-rich cells in the hilar veins. The endothelial surface modifications in the hypobaric rats could be related to thickening of the endothelium, intimal edema, increased intimal connective tissue, luminal invasion of leukocytes, and increased endothelial cell proliferation, known to occur in systemic arteries of hypertensive animals.

Fructose, but Not Dextrose, Induces Leukocyte Adherence to the Mesenteric Venule of the Rat by Oxidative Stress

Recent evidence indicates that fructose is a pro-inflammatory molecule. Oral fructose induces serum and kidney inflammatory intercellular adhesion molecule-1 (ICAM-1) in rats. Fructose also induces ICAM-1 expression in human aortic endothelial cells (HAEC) and monocyte chemoattractant protein-1 in proximal tubular renal cells. It is not known whether fructose may directly promote inflammation on the intestinal microcirculation. Accordingly, using intravital microscopy we studied the effect of topical fructose and dextrose on leukocyte adherence to the mesenteric venule of the rat. Leukocyte adherence was determined during a control period and after fructose was added to the mesentery, in the presence or absence of the NO donor spermine NONO-ate (SNO), and after i.v. injection of the antioxidant lipoic acid (LA). In separate experiments, we examined the effect of topical dextrose on leukocyte adherence to the mesenteric venule. Venular shear rate was calculated. Fructose, but not dextrose, induced significant inflammation independent of shear rate. This effect was completely blocked by SNO and LA, suggesting that fructose induces inflammation via reactive oxygen species (ROS) generation. These results suggest that fructose present in formulas may adversely affect the intestinal microcirculation of premature infants and potentially contribute to the pathogenesis of necrotizing enterocolitis (NEC).

Acetylcholine in the treatment of idiopathic respiratory distress syndrome

Summary This report involved 7 infants with IRDS who were treated with acetylcholine. In 3 of them the drug was infused directly into the pulmonary artery, and a temporary rise in PaO2 was accompanied by fall in pulmonary artery pressure and partial correction of acidosis. However, both pressure and blood-gas tensions reverted to original levels during the course of the infusion, and no lasting beneficial effect was evident.

Effects of Lactose-Containing vs Lactose-Free Infant Formula on Postprandial Superior Mesenteric Artery Flow in Term Infants

BACKGROUND Dietary dextrose and fructose may promote vascular inflammation and endothelial dysfunction. In certain infant populations, altered postprandial mesenteric hyperemia (PPH) may increase risk for feeding intolerance. OBJECTIVE To compare superior mesenteric artery (SMA) PPH following feeds of lactose-containing (LC) formula vs lactose-free (LF; dextrose + sucrose) formula. METHODS In a 2 × 2 crossover study with 6 term newborns, 3 received LC first followed by LF 3 hours later. The remaining 3 received the reverse order. Ultrasound measures of pre- and postprandial SMA flow, diameter, and resistance were taken 5 minutes preprandial and 10, 30, and 40 minutes postprandial. RESULTS Mean ± SD age and weight (n = 6) were 24.1 ± 2.3 hours and 3.1 ± 0.21 kg. Formula intake was similar for LC and LF (22.5 ± 2.8 mL and 25 ± 1.8 mL, respectively; P = .076). Both formulas increased SMA flow at 10 and 30 minutes. However, postprandial flow was greater for LC overall (P = .004) and especially at 30 minutes (LC 103 ml/min, 52% increase vs LF 92.7 ml/min, 31% increase; P = .014). For both formulas, vasodilation was seen at 10 and 30 minutes and was overall significantly greater following LC than following LF (9.1% VS 6.5%; P = .028). Both formulas elicited significant decreases in sma vascular resistance over the 10- to 30-minute period (overall P = .016). However, decreases did not differ across formulas (P = .672). CONCLUSIONS The LC formula elicited a greater SMA PPH response than did LF. SMA flow for both formulas was within normal limits; thus, differences are likely inconsequential for a term newborn. However, in a vulnerable preterm infant, differences may become significant.

Renin-angiotensin system in the llama

Abstract 1. 1. The llama has markedly lower levels of in vitro angiotensin-I (A-I) converting enzyme activity and angiotensin-II (A-II) than nine other species tested. 2. 2. In vivo conversion of A-I to A-II in the llama is similar to that of other species. 3. 3. Resting levels of other components of the renin-angiotensin system, i.e. renal renin granulation, A-I and plasma renin activity, are normal. 4. 4. Acute alveolar hypoxia increased the levels of A-II in four out of five experiments.

Effects of Intragastric Fructose and Dextrose on Mesenteric Microvascular Inflammation and Postprandial Hyperemia in the Rat

OBJECTIVES Fructose superfused on the mesenteric venules of rats induces microvascular inflammation via oxidative stress. It is unknown whether intragastric fructose exerts a similar effect and whether fructose impairs postprandial hyperemia (PPH). The goals were to determine whether intragastric fructose administration promotes leukocyte adherence and whether fructose, owing to its oxidative properties, may also impair nitric oxide-dependent PPH in the mesenteric microcirculation of rats. METHODS Leukocyte adherence to mesenteric venules, arteriolar velocity, and diameter were measured in Sprague-Dawley rats before and 30 minutes after intragastric (1 mL 0.5 M, ~0.3 g/kg) dextrose (n = 5), fructose (n = 6), and fructose after intravenous injection of the antioxidant α-lipoic acid (ALA, n = 6). RESULTS Only fructose increased leukocyte adherence: control 2.3 ± 0.3 per 100 µm; fructose 9.7 ± 1.4 per 100 µm (P < .001). This effect was independent of changes in venular shear rate: control 269 ± 48 s(-1); fructose 181 ± 27 s(-1) (P > .05, r(2) = 0.083 for shear rate vs leukocyte adherence). Dextrose had no effect on leukocyte adherence: control 1.52 ± 0.13 per 100 µm; dextrose 2.0 ± 0.7 per 100 µm (P > .05). ALA prevented fructose-induced leukocyte adherence: control 1.9 ± 0.2 per 100 µm; fructose + ALA 1.8 ± 0.3 per 100 µm (P > .05). Neither fructose nor dextrose induced PPH: arteriolar velocity: control 3.3 ± 0.49 cm/s, fructose 3.06 ± 0.34 cm/s (P > .05); control 3.3 ± 1.0 cm/s, dextrose 3.15 ± 1.1 cm/s (P > .05); arteriolar diameter: control 19.9 ± 1.10 µm, fructose 19.7 ± 1.0 µm (P > .05); control 21.5 ± 2.6, dextrose 20.0 ± 2.7 µm (P > .05). CONCLUSIONS Intragastric fructose induced leukocyte adherence via oxidative stress. Neither dextrose nor fructose induced PPH, likely because of the inhibitory effect of anesthesia on splanchnic vasomotor tone.