Exercise plasma catecholamines in dogs: role of adrenals and cardiac nerve endings

1981 ◽  
Vol 241 (2) ◽  
pp. H243-H247 ◽  
Author(s):  
F. Peronnet ◽  
R. A. Nadeau ◽  
J. de Champlain ◽  
P. Magrassi ◽  
C. Chatrand
Keyword(s):  
Adrenal Medulla ◽  
Species Difference ◽  
Plasma Catecholamines ◽  
Vena Cava ◽  
Moderate Intensity ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Moderate Exercise ◽  
Norepinephrine Concentration ◽  
Severe Exercise

The plasma norepinephrine concentration (NE, ng . ml-1) in the pulmonary artery of dogs increased above resting values (0.22 +/- 0.04) for moderate (0.53 +/- 0.06) and severe exercise (1.45 +/- 0.23) and during prolonged exercise of moderate intensity (2.06 +/- 0.14). The plasma epinephrine concentration (E) increased above resting values (0.14 +/- 0.04) for severe exercise only (0.76 +/- 0.10) or when moderate exercise was prolonged (1.81 +/- 0.24). The E response, which appeared greater than that found in humans, is probably related to the species difference in the vasomotor response to exercise between humans and dogs, the latter not being subjected to compensatory vasoconstriction in nonworking areas. The activity of the adrenal medulla is confirmed by the plasma catecholamine (CA) gradient between proximal and distal posterior vena cava at rest (0.20 +/- 0.09) and during short- (0.35 +/- 0.08) and long-duration exercise (1.37 +/- 0.23). On the contrary, the heart is not a source of plasma CA in dogs: coronary sinus CA did not exceed aortic CA at rest and for moderate exercise and was lower than aortic CA for severe exercise (4.80 +/- 0.25 vs. 6.55 +/- 0.76 ng . ml-1).. The sources of plasma NE remain unclear in exercising dogs. Significant amounts of NE may be released by the adrenal medulla.

Effect of hypoxemia on plasma catecholamines in intact and immunosympathectomized fetal lambs

1986 ◽  
Vol 251 (5) ◽  
pp. R893-R900 ◽  
Author(s):  
J. A. Schuijers ◽  
D. W. Walker ◽  
C. A. Browne ◽  
G. D. Thorburn
Keyword(s):  
Arterial Pressure ◽  
Adrenal Medulla ◽  
Cardiovascular Response ◽  
Plasma Catecholamines ◽  
Reversed Phase ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Sympathetic Function ◽  
Significant Change ◽  
Arterial Po2

Fetal lambs treated with sheep anti-mouse nerve growth factor antibodies (anti-NGF) at 80 days gestation subsequently showed a diminished cardiovascular response to intravenous infusion of tyramine (1 mg/min over 10 min) and no significant change in plasma norepinephrine concentrations as measured by reversed-phase high-pressure liquid chromatography and electrochemical detection. At autopsy at 135 days gestation, catecholamine content of the heart, thyroid, kidney, and ileum was reduced by greater than 70% compared with age-matched control fetuses. The anti-NGF-treated fetuses were thus judged to have impaired sympathetic function. When made hypoxemic (arterial PO2 12-14 Torr) for 1 h at 120 or 130 days gestation, anti-NGF-treated fetuses showed no significant change of arterial pressure, heart rate, or plasma catecholamines, whereas control fetuses showed bradycardia, a 28% increase in arterial pressure, and a 670% increase of plasma norepinephrine concentrations. These results suggest that the increase of arterial pressure that occurs during hypoxemia in fetal lambs between 120 and 135 days gestation is attributable to increased activity of the peripheral sympathetic nervous system. The adrenal medulla appears to contribute to the plasma catecholamine pool at rest, but the lack of increased plasma catecholamines during hypoxia after anti-NGF implies that the adrenal medulla was unable to release catecholamines. Possible reasons for this are discussed.

Catecholamine-fuel interrelationships during exercise in fasting men

1980 ◽  
Vol 48 (1) ◽  
pp. 109-113 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
G. Peres
Keyword(s):  
Maximal Oxygen Consumption ◽  
Plasma Catecholamines ◽  
Plasma Free Fatty Acid ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Adrenergic Response ◽  
Response To Exercise

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.

Endurance run increases circulating IL-6 and IL-1ra but downregulates ex vivo TNF-alpha and IL-1 beta production

1995 ◽  
Vol 79 (5) ◽  
pp. 1497-1503 ◽  
Author(s):  
J. P. Drenth ◽  
S. H. Van Uum ◽  
M. Van Deuren ◽  
G. J. Pesman ◽  
J. Van der Ven-Jongekrijg ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Ex Vivo ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
O2 Consumption ◽  
Esophageal Temperature ◽  
Trained Subjects ◽  
Norepinephrine Concentration ◽  
Fluid Losses ◽  
Cutaneous Vascular Resistance

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

Dehydration reduces cardiac output and increases systemic and cutaneous vascular resistance during exercise

1995 ◽  
Vol 79 (5) ◽  
pp. 1487-1496 ◽  
Author(s):  
J. Gonzalez-Alonso ◽  
R. Mora-Rodriguez ◽  
P. R. Below ◽  
E. F. Coyle
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
O2 Consumption ◽  
Esophageal Temperature ◽  
Trained Subjects ◽  
Norepinephrine Concentration ◽  
Fluid Losses ◽  
Cutaneous Vascular Resistance

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

Sympathoadrenal activation in sinoaortic-denervated rats following endotoxin

1991 ◽  
Vol 260 (4) ◽  
pp. R739-R746 ◽  
Author(s):  
Z. Z. Zhou ◽  
R. D. Wurster ◽  
M. Qi ◽  
S. B. Jones
Keyword(s):  
Sham Group ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
Sham Operation ◽  
Plasma Catecholamine ◽  
Induced Hypotension ◽  
The Third ◽  
Sympathoadrenal Activation ◽  
Alpha Chloralose

We evaluated the role of the baroreceptor reflex in mediating the sympathoadrenal activation during endotoxicosis, using acutely as well as chronically denervated rats. Three groups of experiments were conducted. In the first experiment, hemodynamic and plasma catecholamine responses following endotoxin (5 mg/kg iv) were measured in alpha-chloralose-anesthetized rats with acute sinoaortic baroreceptor denervation (SAD) or sham operation. In the second experiment, chronically sinoaortic-denervated rats and sham controls were used and experiments were conducted as in acute preparations. In the third experiment hydralazine (1 mg/kg iv) was given to chronically denervated rats and sham controls to evaluate the singular contribution of hypotension-evoked baroreflex disinhibition in the absence of endotoxin. In both acute and chronic preparations, endotoxin induced marked elevation of plasma norepinephrine and epinephrine in the presence as well as the absence of arterial baroreceptors (P greater than 0.05). Plasma catecholamines were significantly increased by hydralazine-induced hypotension in the sham group, but this elevation was far less than that induced by endotoxin. Hypotension alone did not significantly increase plasma catecholamines in SAD rats. These results suggest that the baroreflex is not the major factor in mediating sympathoadrenal activation during endotoxicosis and that non-baroreflex mechanisms may be involved in stimulating such activation.

Epinephrine infusion during moderate intensity exercise increases glucose production and uptake

2000 ◽  
Vol 278 (5) ◽  
pp. E949-E957 ◽  
Author(s):  
Stuart H. Kreisman ◽  
Nicholas Ah Mew ◽  
Mylène Arsenault ◽  
Sharon J. Nessim ◽  
Jeffrey B. Halter ◽  
...  
Keyword(s):  
Plasma Catecholamines ◽  
Glucose Production ◽  
Cycle Ergometer ◽  
Moderate Intensity ◽  
Metabolic Clearance ◽  
Moderate Exercise ◽  
Moderate Intensity Exercise ◽  
Epinephrine Infusion ◽  
Ergometer Exercise ◽  
Male Subjects

The glucoregulatory response to intense exercise [IE, >80% maximum O2 uptake (V˙o 2 max)] comprises a marked increment in glucose production (Ra) and a lesser increment in glucose uptake (Rd), resulting in hyperglycemia. The Ra correlates with plasma catecholamines but not with the glucagon-to-insulin (IRG/IRI) ratio. If epinephrine (Epi) infusion during moderate exercise were able to markedly stimulate Ra, this would support an important role for the catecholamines' response in IE. Seven fit male subjects (26 ± 2 yr, body mass index 23 ± 0.5 kg/m2,V˙o 2 max 65 ± 5 ml ⋅ kg− 1 ⋅ min− 1) underwent 40 min of postabsorptive cycle ergometer exercise (145 ± 14 W) once without [control (CON)] and once with Epi infusion [EPI (0.1 μg ⋅ kg− 1 ⋅ min− 1)] from 30 to 40 min. Epi levels reached 9.4 ± 0.8 nM (20× rest, 10× CON). Ra increased ∼70% to 3.75 ± 0.53 in CON but to 8.57 ± 0.58 mg ⋅ kg− 1 ⋅ min− 1in EPI ( P < 0.001). Increments in Ra and Epi correlated ( r 2 = 0.923, P ≤ 0.01). In EPI, peak Rd (5.55 ± 0.54 vs. 3.38 ± 0.46 mg ⋅ kg− 1 ⋅ min− 1, P = 0.006) and glucose metabolic clearance rate (MCR, P= 0.018) were higher. The Ra-to-Rdimbalance in EPI caused hyperglycemia (7.12 ± 0.22 vs. 5.59 ± 0.22 mM, P = 0.001) until minute 60 of recovery. A small and late IRG/IRI increase ( P = 0.015 vs. CON) could not account for the Ra increase. Norepinephrine (∼4× increase at peak) did not differ between EPI and CON. Thus Epi infusion during moderate exercise led to increments in Ra and Rd and caused rises of plasma glucose, lactate, and respiratory exchange ratio in fit individuals, supporting a regulatory role for Epi in IE. Epi's effects on Rd and MCR during exercise may differ from its effects at rest.

Blood pressure and plasma catecholamines in acute and prolonged hypoxia: effects of local hypothermia

1999 ◽  
Vol 87 (6) ◽  
pp. 2053-2058 ◽  
Author(s):  
Inge-Lis Kanstrup ◽  
Troels Dirch Poulsen ◽  
Jesper Melchior Hansen ◽  
Lars Juel Andersen ◽  
Morten Heiberg Bestle ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sea Level ◽  
High Pressures ◽  
Acute Mountain Sickness ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Local Cooling ◽  
Local Hypothermia

This study measured the pressor and plasma catecholamine response to local hypothermia during adaptation to hypobaric hypoxia. Eight healthy men were studied at rest and after 10 and 45 min of local cooling of one hand and forearm as well as after 30 min of rewarming at sea level and again 24 h and 5 days after rapid, passive transport to high altitude (4,559 m). Acute mountain sickness scores ranged from 5 to 16 (maximal attainable score: 20) on the first day but were reduced to 0–8 by the fifth day. Systolic blood pressure, heart rate, and plasma epinephrine increased on day 1 at altitude compared with sea level but declined again on day 5, whereas diastolic and mean blood pressures continued to rise in parallel with plasma norepinephrine. With local cooling, an increased vasoactive response was seen on the fifth day at altitude. Very high pressures were obtained, and the pressure elevation was prolonged. Heart rate increased twice as much on day 5 compared with the other two occasions. Thoracic fluid index increased with cooling on day 5, suggesting an increase in pulmonary vascular resistance. In conclusion, prolonged hypoxia seems to elicit an augmented pressor response to local cooling in the systemic and most likely also the pulmonary circulation.

Fetal adrenal medulla catecholamine response to hypoxia-direct and neural components

1990 ◽  
Vol 258 (6) ◽  
pp. R1340-R1346 ◽  
Author(s):  
C. Y. Cheung
Keyword(s):  
Adrenal Medulla ◽  
Plasma Catecholamines ◽  
Neural Mechanisms ◽  
Plasma Norepinephrine ◽  
Direct Response ◽  
Neural Input ◽  
Catecholamine Response ◽  
Ovine Fetal ◽  
Arterial Po2

In the fetus, the adrenal medullary catecholamine responses to hypoxia are mediated by direct and neural mechanisms. The present study determined the maturation of these responses in unanesthetized ovine fetuses from 109 to 136 days gestation. In intact fetuses at 109-119 days gestation, hypoxia lowered arterial PO2 from 23.4 +/- 0.9 to 9.5 +/- 0.4 mmHg and induced acute increases in plasma norepinephrine (P less than 10(-5)) and epinephrine (P less than 10(-5)) concentrations. Fetuses at 130-136 days gestation showed similar changes in PO2 and plasma catecholamines as in younger fetuses. Blockade of neural input to the adrenal by hexamethonium (25 mg/kg) reduced but did not eliminate the increases in plasma norepinephrine and epinephrine concentrations in fetuses at 109-119 days gestation, while it completely abolished these responses in fetuses at 130-136 days gestation. These results suggest that in unanesthetized ovine fetuses a direct response of the adrenal medulla to hypoxia is present at 110 days gestation. In contrast, at 130 days gestation the response to hypoxia is entirely neurally mediated. Thus neural innervation to the ovine fetal adrenal medulla matures before 110 days gestation, much earlier than previously reported.

Role of adrenal medulla in hemodynamic response to hemorrhage and naloxone

1988 ◽  
Vol 254 (3) ◽  
pp. R559-R565 ◽  
Author(s):  
J. C. Schadt ◽  
R. R. Gaddis
Keyword(s):  
Adrenal Medulla ◽  
Pressor Response ◽  
Sympathetic Nerves ◽  
Hemodynamic Response ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Intact Group ◽  
New Zealand White Rabbits ◽  
Possible Cause

We tested the hypothesis that enkephalins or some other compound(s) released by the adrenal medulla during hemorrhage were responsible for the resultant hypotension. We compared the hemodynamic and plasma catecholamine responses to hemorrhage and subsequent opioid receptor blockade with naloxone in intact, adrenal-denervated (ADD), and adrenalectomized (ADX) rabbits. The studies were done in conscious, chronically prepared, male New Zealand White rabbits. The hemodynamic response to hemorrhage was not different among the three groups. Plasma norepinephrine (NE) increased early in hemorrhage in all groups. In the ADD and ADX animals, NE decreased significantly at the transition to hypotension, suggesting decreased release of NE by peripheral sympathetic nerves as a possible cause of the decrease in pressure. In the intact group, NE did not decrease but reached a plateau possibly due to the release of some NE by the adrenal medulla, which obscured the decreased release by sympathetic nerves. The pressor response to naloxone, though present in all groups, was attenuated by adrenalectomy or adrenal denervation. The plasma NE response to naloxone was similar in all groups and involved a two- to threefold increase after naloxone. We conclude that enkephalins or any other compounds released by the adrenal gland are not responsible for the acute hemodynamic changes during hemorrhage in the conscious rabbit. However, some substance(s) released by the adrenal medulla, perhaps epinephrine, does play a role in naloxone's pressor effect, since this is reduced by adrenalectomy or adrenal denervation.

Morphine suppresses plasma catecholamine responses to laparotomy but not to 2-deoxyglucose

1982 ◽  
Vol 242 (5) ◽  
pp. E317-E322 ◽  
Author(s):  
G. J. Taborsky ◽  
J. B. Halter ◽  
D. Porte
Keyword(s):  
Specific Interaction ◽  
Plasma Catecholamines ◽  
Opiate Receptor ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Base Line ◽  
Midline Laparotomy ◽  
Morphine Administration ◽  
Catecholamine Response ◽  
Anesthetized Dogs

The increase of plasma catecholamines that occurs during surgery can be reduced by administration of morphine. To test the hypothesis that morphine specifically blocks nociceptive stimulation during surgery, we compared the effects of morphine administration on the plasma catecholamine response to a laparotomy in pentobarbital-anesthetized dogs with the effect of morphine on the plasma catecholamine response to the neuroglucopenic agent, 2-deoxy-D-glucose (2DG, 300 mg/kg iv). In control dogs, plasma epinephrine (Epi) and plasma norepinephrine (NE) both increased progressively with time following a midline laparotomy (delta Epi by 50 min, +133 +/- 42 pg/ml, P less than 0.01 and delta NE by 50 min, +108 +/- 38 pg/ml, P less than 0.01, mean +/- SE, n = 12). 2-Deoxy-D-glucose produced a similar increase of both plasma NE and Epi. In dogs that received the anesthesia alone, plasma catecholamines did not increase from base line during the experiment. The analgesic morphine (15 mg iv), given 15 min after the completion of laparotomy, not only prevented the progressive rise of plasma catecholamines after laparotomy, but also caused a small but significant decline (P less than 0.05). Naloxone (0.4 mg iv) totally reversed the suppressive effects of morphine, restoring both catecholamines to the levels of their time-related control. In marked contrast, neither morphine nor naloxone affected the plasma NE and Epi increases following the administration of 2DG. These data suggest that morphine suppression of plasma catecholamines during surgery is not due to a generalized attenuation of sympathetic outflow, but rather to a specific interaction with an opiate receptor that either mediates analgesia or lies within the neural pathway stimulated by laparotomy but not by 2DG.

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