scholarly journals EPINEPHRINE SHOCK, ITS RELATION TO PLASMA EPINEPHRINE LEVEL AND THE MECHANISM OF ITS PROTECTION BY GLUCOCORTICOID

1967 ◽  
Vol 17 (6) ◽  
pp. 746-754 ◽  
Author(s):  
Tokuro FUKUDA ◽  
Hiroyuki OKUMA ◽  
Namiyo HATA
2012 ◽  
Vol 167 (1-2) ◽  
pp. 66-69 ◽  
Author(s):  
Xing-Ping Dai ◽  
Zhao-Qian Liu ◽  
Lin-Yong Xu ◽  
Zhi-Cheng Gong ◽  
Qiong Huang ◽  
...  

1996 ◽  
Vol 21 (6) ◽  
pp. 481-491 ◽  
Author(s):  
François Trudeau ◽  
Martin Milot

The purpose of this study was to evaluate the effect of physical training on hemorrhage-induced catecholamine release in rats. The training program consisted of swimming 5 days a week, from 15 min in the first week to 2.5 hours in the 14th week. The rats were divided into four groups. Two groups (one trained and the other untrained) were studied during hemorrhage. The third and fourth groups (one trained and the other untrained) were not subjected to hemorrhage. After 14 weeks, trained rats had a lower heart rate than untrained animals at rest (311.86 ± 8.9 vs. 361.33 ± 12.13 bpm, p <.002) for a similar body weight. The trained and untrained groups had the same blood pressure, hematocrit, and norepinephrine responses following hemorrhage. However, plasma epinephrine concentration was lower in the trained rats 15 and 25 min following hemorrhage. These results suggest a decrease of the hemorrhage-induced epinephrine secretion in trained rats. An alteration of the relationship of arterial baroreflexes and of their hormonal effectors is a potential mechanism for the reduced plasma epinephrine level in trained hemorrhaged rats. Key words: epinephrine, norepinephrine, hypotension, physical training


Hypertension ◽  
1997 ◽  
Vol 30 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Christoph Dodt ◽  
Ulrike Breckling ◽  
Inge Derad ◽  
Horst Lorenz Fehm ◽  
Jan Born

1979 ◽  
Vol 45 (3) ◽  
pp. 219-225 ◽  
Author(s):  
Th. M�ller ◽  
E. Hofschuster ◽  
H. -J. Kuss ◽  
D. Welter

1985 ◽  
Vol 248 (3) ◽  
pp. R302-R307 ◽  
Author(s):  
W. W. Winder ◽  
M. L. Terry ◽  
V. M. Mitchell

We have investigated the physiological role of the marked increase in plasma epinephrine that occurs in fasted exercising rats. Fasted adrenodemedullated (ADM) rats show a marked reduction in endurance run times compared with sham-operated (SO) controls. After running for 30 min at 21 m/min up a 10% grade, ADM rats' blood glucose was 2.9 +/- 0.1 mM vs. 4.3 +/- 0.2 mM in SO rats. At the same time, blood lactate was 3.0 +/- 0.2 mM in SO rats compared with 1.0 +/- 0.1 mM in ADM rats. Glycogenolysis was impaired in ADM rats in the fast-twitch white region of the quadriceps, lateral gastrocnemius, and soleus muscles but not in the fast-twitch red region of the quadriceps muscle. Hepatic adenosine 3',-5'-cyclic monophosphate was increased to the same extent in ADM and SO rats during exercise. Infusion of epinephrine into ADM rats during exercise corrected the hypoglycemia, restored lactate to normal, and stimulated glycogenolysis in soleus, white quadriceps, and lateral gastrocnemius muscles. Epinephrine-dependent glycogenolysis in contracting type I and noncontracting type II muscle fibers apparently provides essential quantities of lactate for hepatic gluconeogenesis in fasted exercising rats.


1998 ◽  
Vol 85 (5) ◽  
pp. 1702-1707 ◽  
Author(s):  
Michael B. Maron

Previously, alveolar liquid clearance (ALC) was observed to increase in a canine model of neurogenic pulmonary edema (NPE) by adrenal epinephrine (S. M. Lane, K. C. Maender, N. E. Awender, and M. B. Maron. Am. J. Respir. Crit. Care Med. 158: 760–768, 1998). In this study the dose-response relationship between plasma epinephrine concentration and ALC was determined in anesthetized dogs by infusing epinephrine to produce plasma concentrations of 256 ± 37, 1,387 ± 51, 15,737 ± 2,161, and 363,997 ± 66,984 (SE) pg/ml ( n = 6 for each concentration) for 4 h and measuring the resultant ALC. The latter was determined by mass balance after instillation of autologous plasma into a lower lung lobe. These plasma concentrations produced ALCs of 14.3 ± 1.2, 20.5 ± 1.9, 30.1 ± 1.5, and 37.9 ± 2.7% of the instilled volume, respectively. ALC after the lowest infusion rate was not different from that previously observed under baseline conditions (14.1 ± 2.1%), whereas in a previous study of NPE, plasma epinephrine concentration increased to 7,683 ± 687 pg/ml and ALC was 30.4 ± 1.6%. These data indicate that, during recovery from canine NPE, ALC is not maximally stimulated and suggest that it might be possible to pharmacologically produce further increases in the rate of resolution of this form of edema.


2006 ◽  
Vol 291 (3) ◽  
pp. E566-E573 ◽  
Author(s):  
Robert S. Lee-Young ◽  
Matthew J. Palmer ◽  
Kelly C. Linden ◽  
Kieran LePlastrier ◽  
Benedict J. Canny ◽  
...  

There is evidence that increasing carbohydrate (CHO) availability during exercise by raising preexercise muscle glycogen levels attenuates the activation of AMPKα2 during exercise in humans. Similarly, increasing glucose levels decreases AMPKα2 activity in rat skeletal muscle in vitro. We examined the effect of CHO ingestion on skeletal muscle AMPK signaling during exercise in nine active male subjects who completed two 120-min bouts of cycling exercise at 65 ± 1% V̇o2 peak. In a randomized, counterbalanced order, subjects ingested either an 8% CHO solution or a placebo solution during exercise. Compared with the placebo trial, CHO ingestion significantly ( P < 0.05) increased plasma glucose levels and tracer-determined glucose disappearance. Exercise-induced increases in muscle-calculated free AMP (17.7- vs. 11.8-fold), muscle lactate (3.3- vs. 1.8-fold), and plasma epinephrine were reduced by CHO ingestion. However, the exercise-induced increases in skeletal muscle AMPKα2 activity, AMPKα2 Thr172 phosphorylation and acetyl-CoA Ser222 phosphorylation, were essentially identical in the two trials. These findings indicate that AMPK activation in skeletal muscle during exercise in humans is not sensitive to changes in plasma glucose levels in the normal range. Furthermore, the rise in plasma epinephrine levels in response to exercise was greatly suppressed by CHO ingestion without altering AMPK signaling, raising the possibility that epinephrine does not directly control AMPK activity during muscle contraction under these conditions in vivo.


2001 ◽  
Vol 91 (4) ◽  
pp. 1708-1712 ◽  
Author(s):  
Adam Steensberg ◽  
Anders Dyhr Toft ◽  
Helle Bruunsgaard ◽  
Marie Sandmand ◽  
Jens Halkjær-Kristensen ◽  
...  

Prolonged strenuous exercise is followed by a temporary functional immune impairment. Low numbers of CD4+T helper (Th) and CD8+ T cytotoxic (Tc) cells are found in the circulation. These cells can be divided according to their cytokine profile into type 1 (Th1 and Tc1), which produce interferon-γ and interleukin (IL)-2, and type 2 (Th2 and Tc2) cells, which produce IL-4. The question addressed in the present study was whether exercise affected the relative balance between the circulating levels of these cytokine-producing T cells. Nine male runners performed treadmill running for 2.5 h at 75% of maximal oxygen consumption. The intracellular expression of cytokines was detected following stimulation with ionomycin and phorbol 12-myristate 13-acetate in blood obtained before, during, and after exercise. The percentage of type 1 T cells in the circulation was suppressed at the end of exercise and 2 h after exercise, whereas no changes were found in the percentage of type 2 T cells. Plasma epinephrine correlated negatively with the percentage of circulating CD8+ T cells producing IL-2, whereas peak IL-6 correlated with the percentage of CD8+ IL-4-producing T cells in the circulation. Peak plasma IL-6 correlated with plasma cortisol postrunning. In conclusion, the postexercise decrease in T lymphocyte number is accompanied by a more pronounced decrease in type 1 T cells, which may be linked to high plasma epinephrine. Furthermore, IL-6 may stimulate type 2 T cells, thereby maintaining a relatively unaltered percentage of these cells in the circulation compared with total circulating lymphocyte number.


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