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

Abstract

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.

Clostridium perfringens type D epsilon toxin produces a rapid and dose-dependent cytotoxic effect on cerebral microvascular endothelial cells in vitro

“…Control endothelium examined by SEM resembled that reported previously. 6 The crater-like cytoplasmic defects produced by ETX have also been described in these cells in vitro under conditions of hypertension, ischemia, and hypoxia, 5 and after exposure to the neurotoxin, tunicamycin. 1…”

“…Control endothelium examined by SEM resembled that reported previously. 6 The crater-like cytoplasmic defects produced by ETX have also been described in these cells in vitro under conditions of hypertension, ischemia, and hypoxia, 5 and after exposure to the neurotoxin, tunicamycin. 1 Although the endothelial cell line that we used was of human origin, we nevertheless demonstrated that ETX is capable of injuring brain endothelium directly in vitro and it is likely that it would similarly damage cultured cerebral endothelial cells from species known to be susceptible to EXT neurotoxicity, such as ruminant livestock, particularly sheep, and laboratory rodents.…”

Tissue remodeling of rat pulmonary arteries in recovery from hypoxic hypertension

“…The question is whether the processes of hypertrophy and recovery are symmetric. Considerable data on the building up of the lung tissue due to pulmonary hypertension have been obtained (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). Some data on recovery from hypertension are also given in refs.…”

Nonlinear indicial response of complex nonstationary oscillations as pulmonary hypertension responding to step hypoxia

“…As a specific illustration, we consider the changes that occur in the lung when a sea-level dwelling animal is flown to a ski resort at a higher altitude where the partial pressure of oxygen in the gas that the animal breathes is lower. What happens is that the pulmonary arterial blood pressure becomes higher (1-3), the arterial blood vessel wall becomes thicker (3)(4)(5), the different layers of the arteries thicken with different rates and different courses of time (2)(3)(4)(5)(6), the mechanical properties of the blood vessel wall change with specific historical courses (7)(8)(9), cells in the wall modify, grow, proliferate, or move (5,6,(10)(11)(12)(13), intercellular matrix and interstitial space change (14,15), the stress and strain distribution in the vessel wall change with time in a specific way (16), and because of cellular and extracellular changes the zero-stress state of the blood vessel wall changes with time (7)(8)(9). The crucial fact is the blood pressure change, because the blood pressure imposes load on the blood vessel wall, causing stress and strain, and the subsequent tissue and mechanical properties remodeling are believed to be the results of these stress and strain changes.…”