The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.
Alloxan diabetic rats failed to show the skin reaction (blue spot) evoked by dextran, whereas the effects produced by histamine and compound 48/80 were not altered. When dextran and glucose were injected simultaneously into the skin the reaction was inhibited. In vitro, mast cell alterations produced by dextran occurred simultaneously with histamine release; both processes were inhibited by glucose, other carbohydrates related to glucose, and inhibitors of anaphylaxis. These experiments suggest that dextran releases histamine by a mechanism similar to that found with 48/80 and anaphylaxis in the rat. The inhibitory effect of carbohydrates may be understood on the basis of a competitive mechanism.
An enzyme presenting kallikrein-like activity (designated sK1) was purified from the supernatant of Schistosoma mansoni adult worm homogenate. The enzyme cleaves bradykinin from purified rat plasma kininogen. Activity was optimal at pH 9.0 and the enzyme showed amidolytic activity, since it hydrolysed the kallikrein synthetic substrate D-Pro-Phe-Arg-p-nitroanilide. The activity of sK1 upon rat plasma kininogen was strongly inhibited by the serine proteinase inhibitors phenylmethanesulfonyl fluoride, aprotinin or soybean trypsin inhibitor, but not by ethylenediaminetetraacetic acid or sodium tetrathionate. The molecular mass of sK1, as determined by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate, was 66 kDa and the pI value, estimated by analytical chromatofocusing, was 4.2. Physical and chemical properties suggest that sK1 is a serine proteinase of the kallikrein family. Evidence is presented which suggests that sK1 is a component of the tegumental surface of the parasite and the levels of its activity in the male adult worm are approximately 21 times higher than those in the female adult worm. The intravenous injection of 3 micrograms of sK1 into an anaesthetized rat induced a drastic reduction in the arterial blood pressure of the animal. This effect lasted for about 1 min, and was followed by a progressive recovery of the arterial pressure. Neither bradycardia nor cardiac arrhythmias were noticed, suggesting a peripheral vasodilation effect. The presence of sK1 on the surface of adult male worms could play an important role in the wandering capacity of coupled worms into the visceral vasculature of the host.
Stimulators of angiogenesis hold potential in promoting the development of collateral circulation in ischaemic tissue and accelerating wound healing, but promote pathological vasoformation in angiogenesis-dependent diseases (solid tumours, atherosclerosis). The renin-angiotensin system is implicated in both beneficial angiogenesis and pathological vascular growth. We investigated the angiogenic activity of angiotensin II (All) in a sponge implant model in mice; this peptide enhanced angiogenesis, as well as glycosaminoglycan (GAG, chondroitin sulfate proteoglycan) and protein synthesis in sponge matrix in mice in a dose-dependent fashion. Extensive angiogenesis was achieved with All (1 µg), which gave no significant increase in wet weight and protein and only a small effect on GAG. In the implants treated with All (2 µg) no further increase in angiogenesis was observed, whereas a marked effect was shown in wet weight (326 ± 15 vs. 424 ± 27 mg), total protein (18 ± 1 vs. 25 ± 1 µg/ww) and GAG(98 ± 10 vs. 160 ± 13 ng/ww). The local blood flow has been determined by measuring the washout rate of 133Xe injected into the implants, correlated with histological evidence of vessel growth. This model of angiogenesis has allowed sequential studies of fibrovascular tissue infiltration simultaneously with histological and biochemical parameters of angiogenesis.
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