Data are reported which show significant regional capillary differences in left ventricular endocardium and epicardium of normal rats and of rats with hyperthyroid-induced cardiac hypertrophy. The epicardial region of control rats has 38% more capillaries than the endocardial region. Control endocardial myocytes are 62% larger in cross-sectional area than epicardial myocytes. Hypertrophic hearts exhibit regional differences in capillary density similar to those in the normal hearts, but there is an overall reduction of 12 and 17.5% in capillary density in both regions. The average cross-sectional area of myocytes increases 34.5% in the epicardium and 22.5% in the endocardium.

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Chronic hyperthyroidism was induced in radiothyroidectomized adult albino rats by feeding a diet of 0.3-0.4% desiccated thyroid for four to ten weeks. The left ventricle from control and hyperthyroid animals was examined with the electron microscope after perfusion fixation with 3% phosphate buffered glutaraldehyde and postfixation in 1 % osmium tetroxide. No differences were discerned in the appearance of the Golgi zone, glycogen, lipid, lysosomes, sarcoplasmic reticulum, or the sarcomere ultrastructure of the ventricle from hyperthyroid animals compared with untreated animals. Changes were noted in the mitochondria. These included marked hypertrophy without increase in numbers and localized areas of vacuolization and disorientation of the cristae.Apparently these changes are reversible since the ventricular mitochondria of previously hyperthyroid animals allowed to return to a euthyroid state were indistinguishable from those seen in the control group.

Pressure-volume characteristics of whole lungs were measured in euthyroid rats and in rats fed 0.4% desiccated thyroid for eight weeks. The lungs were degassed by incising the diaphragm after the animals had breathed 100% oxygen for ten minutes. The pressure-volume characteristics were measured by inflating and deflating the lungs at a rate of 3.5 cc/min. Total lung capacity (TLC) was considered to be that volume of air required to produce a transpulmonary pressure of 30 cm H2O. At TLC there was 35% greater lung volume in the thyroid-treated animals than in their littermate controls. Similar results were observed in saline-filled lungs. Alveolar surface are (Sa) increased from 0.28m2 in the lungs of control animals to 0.75m2 in lungs of thyroid-treated animals. There was an 85% increase in the alveolar surface density (SVa) in the thyroid-treated animals. These results, obtained by morphometric analysis, suggest that greater lung volume in the thyroid-treated animals resulted from alveolar hyperplasia or "partitioning."