Vasodilator Effect of Glucagon: Receptorial Crosstalk Among Glucagon, GLP-1, and Receptor for Glucagon and GLP-1.

Glucagon is known for its insulin-antagonist effect in the blood glucose homeostasis, while it also reduces vascular resistance. The mechanism of the vasoactive effect of glucagon has not been studied before; thereby we aimed to investigate the mediators involved in the vasodilatation induced by glucagon. The vasoactive effect of glucagon, insulin, and glucagon-like peptide-1 was studied on isolated rat thoracic aortic rings using a wire myograph. To investigate the mechanism of the vasodilatation caused by glucagon, we determined the role of the receptor for glucagon and the receptor for GLP-1, and studied also the effect of various inhibitors of gasotransmitters, inhibitors of reactive oxygen species formation, NADPH oxidase, prostaglandin synthesis, protein kinases, potassium channels, and an inhibitor of the Na(+)/Ca(2+)-exchanger. Glucagon causes dose-dependent relaxation in the rat thoracic aorta, which is as potent as that of insulin but greater than that of GLP-1 (7-36) amide. Vasodilatation by GLP-1 is partially mediated by the glucagon receptor. The vasodilatation due to glucagon evokes via the glucagon-receptor, but also via the receptor for GLP-1, and it is endothelium-independent. Contribution of gasotransmitters, prostaglandins, the NADPH oxidase enzyme, free radicals, potassium channels, and the Na(+)/Ca(2+)-exchanger is also significant. Glucagon causes dose-dependent relaxation of rat thoracic aorta in vitro, via the receptor for glucagon and the receptor for GLP-1, while the vasodilatation evoked by GLP-1 also evolves partially via the receptor for glucagon, thereby, a possible crosstalk between the 2 hormones and receptors could occur.

Running intensity as determined by heart rate is the same in fast and slow runners in both the 10- and 21-km races.

The aims of this study were to determine (1) whether running speed is directly proportional to heart rate (HR) during field testing and during 10- and 21-km races, and (2) whether running intensity, as estimated from HR measurements, differs in 10- and 21-km races and between slow and fast runners at those running distances. Male runners were divided into a fast (65-80 min for 21 km; n = 8) or slow (85-110 min for 21 km; n = 8) group. They then competed in 10- and 21-km races while wearing HR monitors. All subjects also ran in a field test in which HR was measured while they ran at predetermined speeds. The 10-km time was significantly less in the fast compared with the slow group (33:15 +/- 1:42 vs 40:07 +/- 3:01 min:s; mean +/- S.D.), as was 21-km time (74:19 +/- 4:30 vs 94:13 +/- 9:54 min:s) (P < 0.01). Despite the differences in running speed, the average running intensity (%HRmax) for the fast and slow groups in the 10-km race was 90 +/- 1 vs 89 +/- 3% and in the 21-km race 91 +/- 1 vs 89 +/- 2%, respectively. In addition, %HRmax was consistently lower in the field test at the comparative average running speeds sustained in the 10-km (P < 0.01) and 21-km (P < 0.001) races. Hence, factors in addition to work rate or running speed influence the HR response during competitive racing. This finding must be considered when running intensity for competitive events is prescribed on the basis of field testing performed under non-competitive conditions in fast and slow runners.

The relationship between critical power and running performance.

Critical power is a theoretical concept that presumes there is a certain work-rate which may be maintained without exhaustion. The extent to which critical power predicts running performance over varying distances has not been determined, and so the aim of this study was to correlate measurements of critical power in the laboratory to running performances in the field at 40 m and 1, 10 and 21.1 km in a group of .17 male long-distance runners (mean +/- S.D. age = 31.7 +/- 7.3 years). Each subject ran to exhaustion on the treadmill in the laboratory at six different speeds, ranging from 17 to 25 km h-1. Least squares analyses were used to fit an exponential decay to the relationship between the running speed (y) versus time to exhaustion (x). Critical power was calculated as the running speed (y) coinciding with the asymptote or C parameter of the y = A.e(-Bx) + C relationship. The VO2 max was also measured in all subjects. For the data in the field, each subject was timed over 40 m and 1 km and participated in 10- and 21.1-km races. The mean critical power of the subjects in this study was 18.5 +/- 1.6 km h-1. The test-retest correlation coefficient for the determination of critical power was r = 0.99. The mean VO2 max, measured in a progressive exercise protocol starting at 13 km h-1 and increasing by 1 km h-1 every minute, was 59.2 +/- 4.6 ml O2 kg-1 min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Modified enzyme-linked immunosorbent assay for detecting enteroinvasive Escherichia coli and virulent Shigella strains.

Immune sera were produced in rabbits with living cells of an enteroinvasive O143 strain of Escherichia coli. To remove O and K antibodies, sera were absorbed with an avirulent derivative of the same strain. In the enzyme-linked immunosorbent assay, absorbed sera reacted specifically with only virulent Shigella strains and enteroinvasive E. coli strains of different geographical origin, regardless of species or serogroups. The investigation of 83 strains indicated complete agreement between enzyme-linked immunosorbent assay results and those of the keratoconjunctivitis test. It is assumed that the absorbed immune sera reacted with a possible virulence marker antigen. This inexpensive and simple method provides an alternative to other virulence tests. It has a definite advantage for screening large number of isolates within 24 h.

Microbiological findings and protein concentration in gastric juice.

From 17 patients subjected to pentagastrin test, 136 samples of gastric juice (fasting sample, basal secretion, fractions after stimulation) were collected. The concentration of the protein components (IgG, IgA, IgM, C3 and albumin) in the fasting samples were in excess of those found in the basal secretion, but protein output (volume X concentration) was nearly identical in the two samples. The protein concentration of the fractions obtained in response to pentagastrin stimulation were too low to be measurable. According to correlation analysis, protein concentration in the gastric juice is primarily the function of the microbiological finding. The allergic effect of microorganisms in the gastric juice may give rise to an increase in its immunoglobulin and albumin concentrations.