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  • 1955-1959  (12)
  • Biology  (12)
  • XA 20060  (12)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1956
    In:  American Journal of Physiology-Legacy Content Vol. 185, No. 2 ( 1956-05-01), p. 287-298
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 185, No. 2 ( 1956-05-01), p. 287-298
    Abstract: Skeletal muscle, which has been histochemically characterized by: a) extracellular tissue comprising extracellular fluid plus connective tissue solids, and b) intracellular tissue comprising intracellular water and fiber solids, has provided a method to interpret quantitatively what occurs when skeletal muscle atrophies. Histochemical findings from skeletal muscle (calf and thigh groups) from the legs of puppies following disuse brought about by denervation were compared with those obtained on muscles removed from the opposite weight-bearing leg, the control leg. All tissue data were calculated on a fat-free basis. The calculation of the extracellular tissue mass was based on the chloride space, and the estimation of the connective tissue solids was based on the collagen nitrogen values. The histochemical interpretations indicated that following the denervation of muscle the change of greatest magnitude was in the mass of the extracellular tissue. In a kilogram of control calf muscle the extracellular mass (F) was 295 gm, of which 47 gm were the connective tissue solids. In a kilogram of denervated calf muscle the (F) was 397 gm, of which 57 gm were connective tissue solids. In a kilogram of control thigh muscles the (F) was 249 gm containing 41 gm of connective tissue solids; and there were 378 gm in the (F) of the denervated thigh containing 52 gm of connective tissue solids. After correcting the determined total solids of the muscles for the connective tissue solids, the remaining solids were allotted to the muscle fiber solids. Therefore in atrophied muscle there was a decrease in the muscle fiber solids of 166 gm (control) to 137 gm (denervated). Since histologically a definite shortening of fibers has been found, the histochemical decrease in the fiber weight must be the result of shortening of the muscle fibers. Histochemical evidence that the internal structure of the muscle fibers did not change in denervation was provided by the findings that the calculated concentrations of potassium (156 mEq) and magnesium (30 mEq)/kg of muscle fiber water did not differ from the control values. Likewise, the amount of water per kilogram of muscle fibers remained the same: 77% in the control and denervated calf muscles, and 78% in all of the thigh muscles.
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1956
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1957
    In:  American Journal of Physiology-Legacy Content Vol. 188, No. 2 ( 1957-01-31), p. 399-402
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 188, No. 2 ( 1957-01-31), p. 399-402
    Abstract: When postheparin plasma was incubated with a coconut oil substrate, a decrease in optical density and an increase in unesterified fatty acids occurred. The increase in unesterified acids was prevented by previous intravenous injection of Triton to rats. Addition of post-Triton plasma to a system containing postheparin plasma and coconut oil emulsion inhibited the lipoprotein lipase activity. Incubation of Triton with coconut oil substrate before addition of postheparin plasma caused inhibition of lipoprotein lipase activity. It is concluded that inhibition of lipoprotein lipase activity by Triton is due to modification of the substrate such that the enzyme can no longer act. Further, it is suggested that the chief cause of Triton hyperlipemia is coating of the plasma lipoproteins by Triton resulting in their faulty catabolism.
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1957
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1959
    In:  American Journal of Physiology-Legacy Content Vol. 196, No. 5 ( 1959-05-01), p. 1093-1097
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 196, No. 5 ( 1959-05-01), p. 1093-1097
    Abstract: Qualitative and quantitative distribution of acid-soluble nucleotides in muscle from mice with dystrophia muscularis was compared to normal mouse muscle using filter paper chromatography followed by elution and U.V. spectrophotometry. Qualitatively, no apparent differences were found in the number and types of nucleotides present in both tissues. Similar results were obtained using radioautography with P 32 . Significant amounts of AMP, ADP, ATP, DPN, GTP, GDP were found, while smaller amounts of components tentatively identified as UDP, UTP, CTP and IDP were also observed. The concentrations of AMP, GTP (including UTP), and GDP (including UDP, CTP, and IDP) were significantly higher in the hind limb muscles of dystrophic mice than those obtained for normal mouse muscles, while for ATP the reverse was found. Slight or no significant differences were found in the acid-soluble nucleotides of animals with experimentally induced atrophy of the hind leg when compared to the normal group, while histologically there was a significant decrease of the individual muscle fiber diameter in the atrophic muscle.
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1959
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 1955
    In:  American Journal of Physiology-Legacy Content Vol. 183, No. 3 ( 1955-11-30), p. 395-400
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 183, No. 3 ( 1955-11-30), p. 395-400
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1955
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 1955
    In:  American Journal of Physiology-Legacy Content Vol. 181, No. 3 ( 1955-06-01), p. 661-663
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 181, No. 3 ( 1955-06-01), p. 661-663
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1955
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 1956
    In:  American Journal of Physiology-Legacy Content Vol. 184, No. 3 ( 1956-02-29), p. 505-514
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 184, No. 3 ( 1956-02-29), p. 505-514
    Abstract: In 54 control periods in 15 normal (anesthetized) dogs, the ratios of the clearances of creatinine and ferrocyanide to inulin (Ccr/Cin and Cfer/Cin) differed significantly from unity, averaging 0.936 ± 0.047 and 0.932 ± 0.059, respectively. However, in these animals, clearance ratios did not vary with Cin, or urine flow, provided that Cin exceeded 2.3 ml/min/kg (lower limit of ‘normal’). In these 15 dogs, Cin varied directly with perfusion pressure, when the latter was transiently reduced by either hexamethonium, hemorrhage or aortic occlusion. Values for Cin below 2.3 ml/min/kg were associated with decreased ratios for Ccr/Cin and Cfer/Cin. This phenomenon was uninfluenced by phloridzin or probenecid, was potentiated by urinary concentration, and (at low clearance levels) was obliterated by elevating urine flow relative to Cin. Clearance deficits quickly and permanently disappeared when Cin was elevated above 2.3 ml/min/kg by restoration of perfusion pressure. Aberrant clearance ratios cannot easily be attributed to tubular damage because they were so promptly and permanently reversed, no histological evidence of immediate or delayed tubular necrosis followed their demonstration, and in six dogs with frank tubular necrosis following HgCl 2 , or clamping the renal artery, no clearance deficits accompanied comparable reductions in clearance level. The observed direct relationship between clearance ratios and Cin or urine flow, must therefore reflect partial permeability of the normal renal tubule allowing passive back diffusion of at least creatinine and ferrocyanide. In the normal dog, clearance values should probably be interpreted with caution at levels for Cin below 2.0 ml/min/kg.
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1956
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    American Physiological Society ; 1958
    In:  American Journal of Physiology-Legacy Content Vol. 192, No. 3 ( 1958-02-28), p. 613-619
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 192, No. 3 ( 1958-02-28), p. 613-619
    Abstract: The relationship of pulmonary artery pressure to pulmonary blood flow was studied in the dog by means of occlusive shifting of blood flow within the pulmonary vascular bed. All experiments were performed using the closed-chest preparation. The range of blood flow increases studied was 25–388%. A graphical plot of the percentage change in blood flow versus the percentage change in mean pulmonary artery pressure is presented. A visually estimated curve of this latter data is presented, discussed and compared to four other curves from previous pulmonary vascular studies. A comparison of these curves suggests that the relative maximum capacity of the pulmonary vascular bed of man and dog are similar. These curves plus certain assumptions allow the speculative delineation of a graphical area representing the ‘active’ vasomotor component of exercise at different levels of pulmonary blood flow increase.
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1958
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 8
    Online Resource
    Online Resource
    American Physiological Society ; 1958
    In:  American Journal of Physiology-Legacy Content Vol. 195, No. 3 ( 1958-11-30), p. 579-585
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 195, No. 3 ( 1958-11-30), p. 579-585
    Abstract: Carbon dioxide gas injected intravenously will safely demonstrate experimental interatrial defects using a cinefluorographic technique. Under these experimental conditions gas may be demonstrated in the left atrium and ventricle. At the time gas passes through the defect the systemic pressure rises. In the absence of a defect the systemic pressure falls. Left ventricular systolic pressure levels parallel the changes in systemic blood pressure. The presence of gas in the right atrium elevates pressure in the left atrium only a few millimeters of mercury in controls and in the presence of interatrial defects.
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1958
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 9
    Online Resource
    Online Resource
    American Physiological Society ; 1955
    In:  American Journal of Physiology-Legacy Content Vol. 184, No. 1 ( 1955-12-31), p. 83-90
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 184, No. 1 ( 1955-12-31), p. 83-90
    Abstract: The plasma electrolyte composition and 24-hour urine electrolyte excretion were determined in fasting normal, K-deficient and protein and K-deficient rats following the administration of equal molar quantities of NaCl, KCl, NH 4 Cl and KHCO 3 . An attempt was made to relate any differences in the compositions of the plasma and urine to the levels of renal glutaminase and carbonic anhydrase activities, and, to the chemical compositions of the skeletal muscle and kidneys. Renal glutaminase and carbonic anhydrase activities were found increased in K-deficiency and reduced in protein and K-deficiency. Significant changes from corresponding control levels of renal glutaminase were found in normal and K-deficient animals only after the administration of NH 4 Cl (increased), and, after the administration of KHCO 3 (reduced). The only outstanding change of the carbonic anhydrase activity of the kidneys from these animals was a reduction following NH 4 Cl administration. The doubly deficient rats showed a significant increase in renal glutaminase activity after NH 4 Cl administration; on the other hand, KCl administration resulted in a further reduction of the lowered renal carbonic anhydrase activity. The experimental results supported the contention that a relationship exists between urinary ammonia excretion and the level of renal glutaminase activity, while the transfer of H + to the urine and the level of renal carbonic anhydrase activity could not be related. No clear relationship was found between the K excretion and/or K content of the kidneys and the urine total titratable acidity and ammonia excretion, and urine ph.
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1955
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 10
    Online Resource
    Online Resource
    American Physiological Society ; 1956
    In:  American Journal of Physiology-Legacy Content Vol. 185, No. 2 ( 1956-05-01), p. 275-278
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 185, No. 2 ( 1956-05-01), p. 275-278
    Abstract: Tracings of amino acid patterns obtained chromatographically on the tungstic acid filtrates of skeletal muscle, diaphragm, kidney and liver from normal, and protein- and/or K-deficient rats have been presented. Also presented were the tracings of amino acid patterns of the same tissues from rats maintained on a control and a low-K diet and administered DCA. Evidence was presented indicating that the amino acids lysine and arginine were increased in the skeletal muscle, diaphragm and kidney from rats with K deficiency, with or without DCA administration. Concomitant to these changes, there appeared to be a decreased concentration of the amino acids aspartic acid and glutamic acid. The amino acid pattern of the liver from K-deficient rats remained essentially normal. The administration of a KCl solution by stomach tube during 24 hours to the K-deficient rats resulted in a normalization of the amino acid patterns. The amino acid patterns of skeletal muscle, diaphragm and kidney from protein- and K-deficient rats were found to be normal. However, the amino acid patterns of these tissues were found to have reverted to those observed with the K-depleted rats upon supplementing the diet of the doubly deficient animals with protein for 6 days. The significance of a possible transfer of amino acids along with a shift of H + into muscle cells in exchange for K + in the development of an alkalosis found in K-deficient rats was briefly commented upon.
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1956
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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