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.

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.

scholarly journals Role of adenosine in dialysis-induced hypotension.

1994 ◽  
Vol 4 (12) ◽  
pp. 1987-1994 ◽  
Author(s):  
T Shinzato ◽  
M Miwa ◽  
S Nakai ◽  
H Morita ◽  
H Odani ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Adenosine Receptor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Induced Hypotension ◽  
Adenosine Receptor Antagonist ◽  
Hemodialysis Session

First, this investigation showed that plasma levels of inosine, hypoxanthine, and xanthine, which are metabolites of adenosine, rose sharply when blood pressure dropped suddenly along with symptoms during a hemodialysis session (sudden hypotension), but not when it decreased gradually with eventual symptoms (gradual hypotension). Because adenosine has an action to dilate vessels, this result indicates the possibility that the increased release of adenosine would be a cause of sudden hypotension. Second, it was found that the frequency of sudden hypotension decreases with the administration of caffeine, which is an adenosine-receptor antagonist, whereas the frequency of gradual hypotension did not change. This result supports the above-mentioned hypothesis that adenosine may well be a mediator of sudden hypotension, but not of gradual hypotension. Third, our investigation demonstrated no significant differences in plasma norepinephrine level, in plasma renin activity, or in mean blood pressure between the hemodialysis session in which caffeine was administered and the session in which a placebo was given. These findings suggest that the effect of caffeine administration to prevent sudden hypotension is not mediated by the stimulation of the sympathetic nervous system or activation of the renin-angiotensin system, but by the adenosine-receptor antagonism.

Effects of nonhypotensive endotoxemia in conscious rats: role of prostaglandins

1988 ◽  
Vol 254 (3) ◽  
pp. H509-H516 ◽  
Author(s):  
M. Burnier ◽  
B. Waeber ◽  
J. F. Aubert ◽  
J. Nussberger ◽  
H. R. Brunner
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Conscious Rats

A nonhypotensive dose of endotoxin was administered to normal conscious rats to evaluate the vascular and humoral effects of endotoxemia per se. Mean blood pressure and heart rate remained stable during the 45 min infusion of Escherichia coli endotoxin (0.01 mg/min). However, a marked increase in plasma renin activity (4.2 +/- 0.48 vs. 30.2 +/- 6 ng.ml-1.h-1, mean +/- SE, P less than 0.01), plasma epinephrine (0.112 +/- 0.04 vs. 1.71 +/- 0.5 ng/ml, P less than 0.01), and plasma norepinephrine (0.269 +/- 0.028 vs. 1.3 +/- 0.2 ng/ml, P less than 0.001) was observed during infusion in endotoxin-treated rats when compared with the vehicle-treated animals. In addition, the blood pressure response to exogenous norepinephrine was significantly reduced during nonhypotensive endotoxemia. Significant changes in regional blood flow distribution, as assessed by radiolabeled microspheres, were observed in endotoxemic rats; in particular a decrease in renal blood flow (7.39 +/- 0.43 vs. 5.97 +/- 0.4 ml.min-1.g-1, P less than 0.05) and an increase in coronary blood flow (5.01 +/- 0.38 vs. 6.44 +/- 0.33 ml.min-1.g-1, P less than 0.01) were found. The role of prostaglandins in the vascular and humoral alterations induced by nonhypotensive endotoxemia was also examined. Pretreatment with indomethacin (5 mg) prevented the increase in plasma renin activity as well as plasma catecholamine levels. On the contrary, the decreased vascular reactivity and the reduction in renal blood flow observed during endotoxemia were not affected by prostaglandin synthesis inhibition. Thus significant vascular and humoral changes have been found during endotoxemia even in absence of hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

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.

Cardiovascular and hormonal response to hemorrhage in conscious rats

1988 ◽  
Vol 254 (5) ◽  
pp. H947-H953 ◽  
Author(s):  
G. Fejes-Toth ◽  
T. Brinck-Johnsen ◽  
A. Naray-Fejes-Toth
Keyword(s):  
Plasma Concentrations ◽  
Ascending Aorta ◽  
Plasma Catecholamine ◽  
Adrenergic Blockade ◽  
Compensatory Mechanisms ◽  
Compensatory Response ◽  
The Third ◽  
Converting Enzyme Inhibition ◽  
Freely Moving

The effect of arginine vasopressin (AVP) pressor blockade on the response to graded hemorrhage was investigated on conscious, unstressed, freely moving rats. The parameters studied were mean arterial pressure (MAP), heart rate (HR), blood velocity in the ascending aorta (ABV), and plasma concentrations of AVP (pAVP), renin (PRC), corticosterone (pCS), and catecholamines. After the first hemorrhage (0.75% of body wt over 5 min), MAP remained unchanged while ABV declined and HR increased. The two subsequent hemorrhages brought about significant reduction in MAP, HR, and ABV. pAVP, pCS, and PRC increased gradually during the experiment, while plasma catecholamine levels remained unchanged except for epinephrine, which increased after the third hemorrhage. After pretreatment with the AVP-pressor antagonist, [d(CH2)5Tyr(Me)]AVP, the hemorrhage-induced cardiovascular changes were practically identical to those seen in control animals. Results with AVP blockade performed after the third hemorrhage were also negative. A pressor role of AVP after hypotensive hemorrhage could only be revealed in the presence of converting-enzyme inhibition and alpha-adrenergic blockade. In addition, [d(CH2)5Tyr(Me)]AVP did not modify the effect of hemorrhage on pCS and catecholamines and caused only a slight enhancement of the increase in PRC. It is concluded that conscious, nonstressed rats, if all compensatory mechanisms are allowed full expression, exhibit a normal cardiovascular compensatory response to hemorrhage in the absence of functional AVP pressor receptors.

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.

scholarly journals Adenosine receptor blockade and hypoxia-tolerance in rainbow trout and Pacific hagfish. II. Effects on plasma catecholamines and erythrocytes

1996 ◽  
Vol 199 (2) ◽  
pp. 497-507
Author(s):  
N Bernier ◽  
J Fuentes ◽  
D Randall
Keyword(s):  
Rainbow Trout ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Sham Group ◽  
Plasma Catecholamines ◽  
Hypoxia Tolerance ◽  
Hypoxic Exposure ◽  
Plasma Adrenaline ◽  
Hb Concentration

The purpose of this study was to examine the role of adenosine receptors (ARs) in (1) the regulation of catecholamine secretion and (2) the modulation of blood oxygen capacitance by catecholamines. To this end, we assessed the response of rainbow trout and Pacific hagfish treated with either an AR blocker, theophylline, or saline under hypoxic and normoxic conditions. Compared with the control hypoxic rainbow trout, AR blockade resulted in a smaller increase in haematocrit and haemoglobin (Hb) concentration of the blood, smaller red blood cell transmembrane pH differences and mean cellular [Hb] (MCHC), as well as a 16-fold higher plasma adrenaline concentration after only 10 min of acute hypoxic exposure. In hypoxic hagfish, AR blockade had no effect on the [Hb] of the blood, and there was no regulation of red blood cell pH or changes in MCHC. However, whereas plasma [adrenaline] did not change following exposure to a PwO2 of 1.33 kPa in the hypoxic sham group, the concentration increased 3.8-fold within 10 min in the theophylline-injected group. These results suggest that adenosine modulates the circulating level of catecholamines in both hypoxic rainbow trout and hypoxic Pacific hagfish.

Age-related augmentation of plasma catecholamines during dynamic exercise in healthy males

1985 ◽  
Vol 59 (4) ◽  
pp. 1033-1039 ◽  
Author(s):  
J. L. Fleg ◽  
S. P. Tzankoff ◽  
E. G. Lakatta
Keyword(s):  
Statistical Significance ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Group Iii ◽  
Peak Vo2 ◽  
Age Related ◽  
Group I ◽  
Submaximal Work ◽  
Male Subjects

Although plasma norepinephrine (NE) increases with age in response to a variety of submaximal adrenergic stimuli, the effect of age on plasma catecholamine levels during maximal aerobic effort and during submaximal work at a fixed percent of peak O2 consumption (VO2) is unknown. We therefore measured NE, epinephrine (E), and VO2 at rest and during graded maximal treadmill exercise in 24 healthy male volunteers (ages 22–77 yr) from the Baltimore Longitudinal Study of Aging who were rigorously screened to exclude the presence of cardiovascular disease. At rest neither heart rate (HR) nor VO2 were age related. Resting NE (pg/ml) was not age related, but resting E (pg/ml) was higher in male subjects 68–77 yr old (group III) than in those aged 22–37 (group I) or 44–55 yr (group II), P less than 0.01. Maximal HR (beats/min) showed a strong inverse relationship to age (203.5 - 0.65 age, r = -0.80, P less than 0.001). Peak VO2 in milliliters per kilogram total body weight per minute decreased with age (47.7 - 0.23 age, r = -0.71, P less than 0.001). At maximal effort both NE (P less than 0.01) and E (P less than 0.05) were higher in group III than in either of the younger groups. At submaximal work levels NE and E also increased with age, and when normalized for relative effort at loads between 45 and 80% of peak VO2 both NE and E were higher in the group III male subjects, although statistical significance was reached for NE (P less than 0.01) but not for E (P = 0.09).

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