Acoustic phenomena in the latent period of skeletal muscle: a simple method for in-vivo measurement of the electro-mechanic latency (EML)

1985 ◽  
Vol 404 (2) ◽  
pp. 162-165 ◽  
Author(s):  
A. Hufschmidt
Keyword(s):  
Skeletal Muscle ◽  
Latent Period ◽  
Simple Method ◽  
In Vivo Measurement

Effect of insulin on rat heart and skeletal muscle phenylalanyl-tRNA labeling and protein synthesis in vivo

1994 ◽  
Vol 267 (2) ◽  
pp. E337-E342 ◽  
Author(s):  
L. H. Young ◽  
W. Stirewalt ◽  
P. H. McNulty ◽  
J. H. Revkin ◽  
E. J. Barrett
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Hormonal Regulation ◽  
Specific Activity ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
In Vivo Measurement ◽  
Arterial Plasma ◽  
Kinetics Of

In vivo measurement of muscle protein synthesis and its hormonal regulation is limited by the difficulty of measuring aminoacyl-tRNA specific activity (SA). We assessed the kinetics of heart and skeletal muscle phenylalanyl-tRNA labeling during continuous infusion of L-[ring-2,6-3H]phenylalanine (Phe) to fasted anesthetized rats. We measured Phe SA in arterial and femoral venous plasma, the tissue acid-soluble pool and muscle protein hydrolysates after 5 min (n = 7), 30 min (n = 6), and 90 min (n = 7). We also assessed insulin's effect on labeling of the tRNA pool and muscle protein synthesis during a hyperinsulinemic clamp (2 mU.kg-1.min-1; n = 7). Labeling of tRNA in heart reached 59 +/- 5, 67 +/- 3, and 83 +/- 3% of arterial SA at 5, 30, and 90 min of saline infusion, respectively, but only 10 +/- 5, 34 +/- 2, and 48 +/- 2% in skeletal muscle at those times (P < 0.01 vs. heart). The tRNA SA was intermediate between SA in the acid-soluble pool and arterial plasma. Femoral venous SA was 32 +/- 2% lower (P < 0.001) than arterial SA. Skeletal muscle tRNA SA was also 29 +/- 3% lower (P < 0.001) than femoral venous SA. Insulin did not alter tRNA labeling and neither heart (9.8 +/- 1.1%/day for saline vs. 8.4 +/- 1.0%/day for insulin) nor skeletal muscle (6.7 +/- 1.5%/day vs. 4.2 +/- 0.4%/day) protein synthesis. Thus labeling of phenylalanyl-tRNA occurs more rapidly in heart than in skeletal muscle and is unaffected by insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

In-Vivo Measurement of Skeletal Muscle Tissue Oxygen Tension and Perfusion during Mild Ischemia

2002 ◽  
Vol 96 (Sup 2) ◽  
pp. A655
Author(s):  
Michael Williams ◽  
Natarajan Aravindan ◽  
Zheng Li ◽  
Andrew Shaw
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Tension ◽  
Muscle Tissue ◽  
Skeletal Muscle Tissue ◽  
Tissue Oxygen Tension ◽  
Tissue Oxygen ◽  
In Vivo Measurement

In vivo measurement of structural changes in the microcirculation of the skeletal muscle under long term blood flow loading

Biorheology ◽  
1996 ◽  
Vol 33 (1) ◽  
pp. 84-84
Author(s):  
K KOSAKI ◽  
S ICHIOKA ◽  
M SHIBATA ◽  
A KAWARADA ◽  
A KAMIYA
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Structural Changes ◽  
In Vivo Measurement

The Filter Loop Technique as a Method of Measuring Platelet Aggregation in the Flowing Blood of the Rat; the Inhibitory Activity of 5-oxo-l-cyclopentene-l-heptanoic Acid (AY-16,804) on Platelet Aggregation

1973 ◽  
Vol 30 (01) ◽  
pp. 138-147 ◽  
Author(s):  
Christopher R. Muirhead
Keyword(s):  
Platelet Aggregation ◽  
Prostaglandin E1 ◽  
Suitable Model ◽  
Heptanoic Acid ◽  
Simple Method ◽  
Loop Technique ◽  
Flowing Blood ◽  
Filter Loop

SummaryThe filter loop technique which measures platelet aggregation in vivo in the flowing-blood of the rat was compared to the optical density technique of Born which is carried out in vitro with platelet rich plasma. Using these two experimental models the effect on platelet aggregation of three known inhibitors sulfinpyrazone, dipyridamole and prostaglandin E1, and a novel compound 5-oxo-l-cyclopentene-l-heptanoic acid (AY-16, 804) was determined.The effects on platelet aggregation of the known inhibitors were consistent with information in the literature. Prostaglandin E1 was the most potent inhibitor in both techniques; sulfinpyrazone inhibited aggregation in both models but was less potent than prostaglandin E1. AY-16, 804 exhibited activity in vitro and in vivo similar to that of sulfinpyrazone. Dipyridamole did not inhibit platelet aggregation in vivo and did not inhibit aggregation in vitro in concentrations at which it remained soluble.The filter loop technique is a suitable model for measuring platelet aggregation in the flowing blood of the rat. It is a relatively simple method of determining aggregation and easily adapted to other species.

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