Myocardial microvasculature in fetuses and neonates of rat. Stereological study.

The myocardial development is anchored on the development of the blood vessels. We studied 5 fetuses in each 18.5 and 20.5 day of gestation and 5 neonates in each 2 and 7 day postnatal. Only one animal randomly selected per litter was used. Fragments of the ventricular myocardium were embedded in paraffin with random orientation, sectioned with 5 microns thickness and stained with routine methods. Myocardial capillaries were counted into the test-area and test-points were considered when falling over capillaries since these did not cut the forbidden line. The length and volume densities of the myocardial capillaries were determined (Lv[cap] and Vv[cap], respectively). The absolute length and volume of the myocardial capillaries (L[cap] and V[cap], respectively) were estimated by the product of the Lv[cap] and Vv[cap] by the volume of the heart (V[heart]). The Lv[cap] decreased greatly after birth (from 1,752.4 to 684.2/mm2). These changes were significant only between the two age groups of fetuses (days 18.5 and 20.5) and neonates of age day + 7. The Vv[cap], equal to Lv[cap], was practically unchangeable during fetal period but decreased greatly after birth. The Vv[cap] was different between early fetuses and early and late neonates. Difference was significant also between late fetuses and late neonates when the Vv[cap] decreased from 8.2 to 2.1%. Both L[cap] and V[cap] presented a tendency of increase during the fetal and neonatal periods. These absolute parameters had a significant grow-up between fetuses of age 18.5 and 20.5 days, decrease immediately after birth but improved its magnitude in late neonates. These results suggest that the relative extension and volume of the capillary bed are greater in fetal period than in early postnatal period. However, the continuous growth of the cardiac myocardium improves the absolute length and volume of the capillaries.

On the factors which contribute to thinning of the villous membrane in human placentae at high altitude. II. An increase in the degree of peripheralization of fetal capillaries.

The contribution made by fetal capillary peripheralization to the thinning of the villous membrane seen in human placentae from high-altitude pregnancies is examined by stereological methods. Variables characterizing the shape of the villous core and the spatial relationships between trophoblast and capillaries are quantified. They shed light on the relative importance of dynamic versus mechanistic processes of villous membrane attenuation. Highland villi differ from lowland villi in several ways. On average, they possess a thinner barrier due to closer approximation of capillaries to overlying trophoblast; in consequence, the villous core is more irregular in outline and its surface (that of the inner aspect of the trophoblast) exceeds in area that of the outer aspect of the trophoblast. These results suggest that the dynamic process (protoplasmic streaming within syncytiotrophoblast) cannot alone explain thinning of the villous membrane. A mechanistic process (capillary peripheralization and obtrusion into the trophoblastic epithelium) is sufficient to account for the differences observed, although the possibility that both processes operate concurrently cannot be discounted. This report completes a study into factors contributing to villous membrane thinning at high altitude.

Vascular pathogenesis of limb defects. I. Radial artery anatomy in radial aplasia.

Twelve human fetuses with radial aplasia were dissected to evaluate the vasculature of the arm. Three types of vascular patterns were found. In type I there was a single midline superficial vessel with no radial or ulnar artery. This pattern occurred in four perfused twins (acardia) with twins reversed arterial perfusion sequence, one fetus with clinical trisomy 18, and one with an unknown disorder with multiple field defects. In type II there was absence of the radial artery with or without persistence of the embryonic median artery; the other vessels were normal. This pattern was seen in three fetuses with unknown disorders associated with multiple malformations. In type III the radial artery was present but had an abnormal course. This pattern was found in three fetuses with thrombocytopenia-absent radius syndrome. From these dissections and the results of animal experiments on the embryology of the vasculature, the following conclusions can be drawn. Vasculogenesis precedes differentiation of mesenchyme into muscle and bone. The embryonic capillary net determines the adult vascular anatomy of the limb. Failure to form, malformations, or disruption of the capillary net results in anomalies of the adult vasculature and may lead to musculoskeletal defects. Failure to chondrogenesis does not disturb the capillary net, and normal arteries will develop. Absence of the radial artery found in association with radial aplasia implies that there was abnormal vasculogenesis or disruption of developing vessels, or both. Either can lead to this congenital musculoskeletal defect.