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T H Spaet

Publications and source records attributed to T H Spaet.

14 recordsLinked to original sources
PubMed1979

Hematology.

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Complement System Proteins↗
PubMed1978

Delayed consequences of endothelial removal from rabbit aortae.

One year after de-endothelialization of rabbit aorta by a balloon catheter, the damaged areas show arteriosclerotic thickening. In the study described here, aortae from six rabbits were examined 2 years after the single injury. Three had advanced atherosclerotic lesions. All the animals had been fed standard rabbit chow, and the five tested did not have hypercholesterolemia when they were sacrificed. Apparently vascular injury alone is sufficient basis for development of atherosclerotic disease in the rabbit.

Animals↗
PubMed1978

The influence of the pituitary on arterial intimal proliferation in the rat.

The formation of arteriosclerotic fibromusculoelastic intimal thickening following arterial de-endothelialization is well documented. Recent findings, both in vitro and in vivo, suggest that platelets are a major participant in the pathogenesis of this lesion by releasing a mitogen to medial smooth muscle cells (SMC). This mitogen results in SMC migration to and proliferation within the intima. A similar mitogen has been described as originating in brain and pituitary tissue. We now report that, in hypophysectomized rats with normal platelet counts, intimal hyperplasia is markedly delayed; pair-fed intact controls normally develop lesions. It therefore appears that the pituitary gland plays a significant role in the experimental arteriosclerotic response.

Animals↗
PubMed1977

Intimal healing. The pattern of reendothelialization and intimal thickening.

Studies were undertaken to investigate further the basis of intimal proliferation and the identity of the surface lining cell in rabbit aortas subjected to extensive deendothelialization. Endothelial cells were selectively removed by passage of an inflated balloon catheter through the arterial lumen. The healing response was evaluated at intervals up to 36 weeks by several techniques: 1) permeability to Evans blue, 2) reappearance of endothelial cells as indicated by the specific marker, adsorbed goat anti-rabbit tissue factor-horseradish peroxidase, 3) planimetric measurements of intimal thickness, and 4) electron microscopy. The results indicate that endothelial cell recovery progressed slowly and that it extended only from areas spared denudation. The regions not covered by endothelial cells were lined by cells of smooth muscle cell origin. Such areas were permeable to Evans blue-protein complex, and their luminal smooth muscle cells were associated with connective tissue-like material at their luminal surface; this material apparently acted as a base for platelet accumulation. The present findings indicate that the lumen of the extensively denuded vessel is lined by either endothelial or smooth muscle cells and that intimal healing is related to restoration of endothelial cell cover. In addition, intimal thickening reached a maximum well before reendothelialization was complete.

Animals↗
PubMed1977

Estrogen suppression of surgically induced vascular intimal hyperplasia in rabbits.

Since estrogen has been shown to reduce aortic medial hypertrophy in hypertensive rats, a naturally occurring estrogen compound, estradiol, was studied for its ability to suppress the intimal hyperplasia which follows vessel transection and anastomosis. Suture lines and adjacent abdominal aortas were examined by light and electron microscopy 1 month after surgery, in 23 rabbits. Test animals were given 200 microgram of Depoestradiol I.M. weekly, starting 3 days preoperatively. Control animals were similarly manipulated but received no estrogen. Control animals showed striking intimal thickening over the sutures, in contrast to the estrogen-treated group in which there was significantly less growth of corresponding tissue (p less than 0.01).

Animals↗
PubMed1976

Platelet interaction with human umbilical cord vascular basement membrane.

The basement membrane of the human umbilical vein was studied by electron microscopy with respect to its ultrastructure, susceptibility to digestion by collagenase or trypsin, and reactivity with human platelets. Electron microscopic examination of this vessel showed a continuous reticulated basement membrane which morphologically resembled those of mammalian capillaries and rabbit heart valves. The vascular endothelium was removed by freezing and thawing, thus uncovering the underlying connective tissue. The vessels were sliced into rings which were incubated with collagenase or trypsin. The basement lamella appeared to be susceptible to digestion by either enzyme. Platelet interaction with exposed vascular basement mambrane was studied by rotating frozen-thawed everted and noneverted rings in anticoagulated whole human blood. In heparinized or citrated blood, large aggregates of degranulated platelets adhered to collagenous controls; in contrast, the test rings with exposed basement membrane were partially covered with a monolayer of platelets which appeared to retain discoid or spherical shape and granules. In EDTA-anticoagulated blood, the collagen control rings accumulated a platelet monolayer, whereas little or no adhesion occurred on the basement membrane surface. In this system the basement membrane of the human umbilical vein appears to be a poor platelet reactive surface as compared to collagen.

Basement Membrane↗
PubMed1975

Intimal injury and regrowth in the rabbit aorta; medial smooth muscle cells as a source of neointima.

The present study was undertaken to determine the mechanism of neointima formation in rabbit arteries subjected to extensive endothelial desquamation. Endothelial cells were selectively removed from the abdominal aorta by passing an inflated balloon catheter through the vessel. The healing response was then studied serially for up to a week, when neointima formation had provided a virtually complete cover. In en face preparations, the early neointimal cells appeared in random locations; they did not develop in apposition to residual, healthy endothelium. The possibility of blood cell colonization was explored by inserting killed aortic homografts. Since these homografts showed neointima formation only close to the site of junction with the normal aorta and as a direct extension of healthy endothelium, the likelihood of significant blood cell colonization was deemed small. Histologic and electron microscopic sections provided evidence that the early neointimal cells in the healing aorta were derived from medial smooth muscle cells. Healing of the injured arterial intima was accompanied by thickening instead of prompt restoration to normal, and the thickened intima resembled an arteriosclerotic plaque. The present study thus supports the concept that arteriosclerosis is a disease involving proliferation of medial smooth muscle cells.

Animals↗