A collagen-like glycoprotein from elastin-rich tissues.
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Biomedical subjects
Publications and source records attributed to M A Gibson.
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Glycoprotein-containing extracts were obtained from thoracic arteries of embryonic chicks by sequential treatment involving 6 M guanidinium chloride, purified bacterial collagenase, and 6 M guanidinium chloride plus 50 mM dithiothreitol. Two major glycopolypeptides, designated G1 and G2, having apparent mol. wts. of 140,000 and 130,000 respectively were detected by SDS/polyacrylamide gel electrophoresis. Equilibrium density gradient ultracentrifugation demonstrated G1 and G2 to be glycoproteins and not proteoglycans or glycosaminoglycans. Amino acid analysis of a glycoprotein-enriched fraction confirmed the non-collagenous nature of G1 and G2. The highly insoluble nature of these glycoproteins suggests that these species are intimately associated with the extracellular matrix. Glycoproteins of similar size were also extracted from wing tendons indicating that G1 and G2 may be common to the elastic tissues of the chick.
Glucagon concentrations ranging from 1.16 to 300-0 microgram/0.1 ml diluent were injected into the yolk of chick embryos on incubation days 8, 10, and 12. Studies of survival rates, embryo weights, blood sugars, liver and tibiotarsus glycogen histochemistry, and pancreatic alpha and beta tissue histogenesis were undertaken during the 9- to 16-day incubation period. Glucagon dosages of 37.5 and 150.0 microgram/0.1 ml diluent gave the best survival rates. Glucagon caused an increase in embryo weight, increased liver glycogen storage, a chondrocyte glycogen storage pattern which correlated with blood sugar levels, an increase in pancreatic beta tissue and a decrease in pancreatic alpha tissue. Studies of blood sugars following glucagon treatment showed that most concentrations caused an initial (first 16 h) hyperglycemia. Following this, two general patterns were exhibited: (1) the lower glucagon concentrations caused hypoglycemia after about 24 h, and (2) the higher concentrations caused amore prolonged hyperglycemia when administered on incubation day 10 but caused hypoglycemia when administered on incubation day 10 but caused hypoglycemia when administered on days 8 and 12. Interpretation of these results is based on the contribution of three factors to the expression and duration of the glucagon effect: (1) concentration of glucagon administered, (2) insulin secretion, and (3) levels of glycogen storage at the incubation stage of administration.
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Measurements of pH, PCO2, PO2 and total CO2 were recorded simultaneously in samples of chorioallantoic fluid, amnionic fluid and blood of the chorioallantoic artery from chicken embryos on days 8, 10, 12, 14, 16, 17 and 18 of incubation. During the incubation period studied, PCO2 levels similarly increased in the blood and extraembryonic fluids. The pH of the blood and amnionic fluid remained approximately constant while the chorioallantoic fluid became progressively acidic. Increases of amnionic fluid and blood HCO-3 indicated that respiartory compensation processes regulate pH. In addition, the disappearance of chorioallantoic fluid HCO-3 suggested that reabsorptive processes may conserve these ions and contribute them to the amnionic fluid by either a direct transfer through the amnioallantoic membrane or by way of the chorioallantoic vascular system.
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Chickens exhibiting "flip-over" syndrome were found on necropsy to have a blood structure in the heart chamber. Histological studies showed that this structure is formed of erythrocytes, leucocytes, fibrin and serum. Fibroblasts, collagen fibers, and thrombocyte agglutination were not observed. These observations indicate that the structures studied are post-mortem blood clots.
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