Pentobarbital effects on plasma catecholamines: temperature, heart rate, and blood pressure

1985 ◽  
Vol 248 (1) ◽  
pp. E95-E100 ◽  
Author(s):  
D. Baum ◽  
J. B. Halter ◽  
G. J. Taborsky ◽  
D. Porte

The effects of intravenous pentobarbital were studied in dogs. Plasma pentobarbital concentrations were inversely related to epinephrine and norepinephrine concentrations. Plasma catecholamines appeared fully suppressed at pentobarbital levels greater than 25-30 micrograms/ml. Furthermore, pentobarbital levels were negatively related to rectal temperature, heart rate, and mean blood pressure. The methods of pentobarbital administration influenced plasma pentobarbital as well as epinephrine and norepinephrine levels, temperature, heart rate, and blood pressure. These observations suggest the possibility that pentobarbital inhibits the sympathetic nervous system, which in turn may affect temperature, heart rate, and blood pressure. Because pentobarbital anesthesia affects plasma catecholamine concentrations, the regimen used in animal models requires consideration when interpreting data potentially influenced by the sympathetic nervous system.

1992 ◽  
Vol 70 (9) ◽  
pp. 1217-1224 ◽  
Author(s):  
Abdel A. Abdel-Rahman ◽  
Robert G. Carroll ◽  
Mahmoud M. El-Mas

The present study evaluated the contribution of the sympathetic nervous system to the adverse hemodynamic action of ethanol on hypotensive responses in conscious unrestrained spontaneously hypertensive rats. Ethanol caused a dose-related attenuation of the hypotensive effect of guanabenz. An equivalent hypotensive response to sodium nitroprusside was not influenced by ethanol, which indicates a potential specific interaction between ethanol and guanabenz. Alternatively, it is possible that a preexisting high sympathetic nervous system activity, which occurred during nitroprusside infusion, may mask a sympathoexcitatory action of ethanol. Further, ethanol (1 g/kg) failed to reverse the hypotensive effect of the ganglionic blocker hexamethonium. This suggests that a centrally mediated sympathoexcitatory action of ethanol is involved, at least partly, in the reversal of hypotension. In addition, the antagonistic interaction between ethanol and guanabenz seems to take place within the central nervous system and involves opposite effects on central sympathetic tone. Finally, changes in plasma catecholamines provide supportive evidence for the involvement of the sympathetic nervous system in this interaction. In a separate group of conscious spontaneously hypertensive rats, ethanol (1 g/kg) reversed the guanabenz-evoked decreases in blood pressure and plasma catecholamine levels. It is concluded that (i) ethanol adversely interacts with centrally acting antihypertensive drugs through a mechanism that involves a directionally opposite effect on sympathetic activity, and (ii) a sympathetically mediated pressor effect of ethanol is enhanced in the presence of an inhibited central sympathetic tone.Key words: spontaneously hypertensive rats, ethanol, catecholamines, guanabenz, hexamethonium.


2019 ◽  
Vol 133 (9) ◽  
pp. 1097-1113 ◽  
Author(s):  
Ken Chen ◽  
Dongdong Sun ◽  
Shuang Qu ◽  
Yue Chen ◽  
Jialiang Wang ◽  
...  

Abstract Environmental temperature plays a role in the variation of blood pressure. Maternal cold stress could affect the physiological phenotype of the offspring, including blood pressure elevation. In the present study, we found that adult offspring of dams exposed to cold have increased systolic and diastolic blood pressure, and decreased urine volume and sodium excretion, accompanied by increased heart rate and heart rate variability, secondary to increased activity of the sympathetic nervous system. Renal denervation or adrenergic receptor blockade decreased blood pressure and increased sodium excretion. The increase in peripheral sympathetic nerve activity can be ascribed to the central nervous system because administration of clonidine, a centrally acting α2 adrenergic receptor agonist, lowered blood pressure to a greater degree in the prenatal cold-exposed than control offspring. Moreover, these prenatal cold-exposed offspring had hypothalamic paraventricular nucleus (PVN) disorder because magnetic resonance spectroscopy showed decreased N-acetylaspartate and increased choline and creatine ratios in the PVN. Additional studies found that prenatal cold exposure impaired the balance between inhibitory and excitatory neurons. This led to PVN overactivation that was related to enhanced PVN-angiotensin II type 1 (AT1) receptor expression and function. Microinjection of the AT1 receptor antagonist losartan in the PVN lowered blood pressure to a greater extent in prenatal cold-exposed that control offspring. The present study provides evidence for overactive peripheral and central sympathetic nervous systems in the pathogenesis of prenatal cold-induced hypertension. Central AT1 receptor blockade in the PVN may be a key step for treatment of this type hypertension.


1973 ◽  
Vol 44 (6) ◽  
pp. 617-620 ◽  
Author(s):  
L. B. Geffen ◽  
R. A. Rush ◽  
W. J. Louis ◽  
A. E. Doyle

1. Plasma dopamine β-hydroxylase (DβH) amounts were measured by radioimmunoassay in twenty-eight patients, twenty of whom had essential hypertension. There was a positive correlation between resting diastolic blood pressure and plasma DβH concentration. 2. Plasma DβH amounts also correlated significantly with those of plasma noradrenaline (NA) in individual patients. 3. These findings provide further support for the conclusions drawn from studies of plasma catecholamines that the sympathetic nervous system contributes toward the maintenance of the elevated blood pressure in essential hypertension.


2021 ◽  
pp. 026988112199710
Author(s):  
Sophie Metz ◽  
Woo R Chae ◽  
Christian E Deuter ◽  
Christian Otte ◽  
Katja Wingenfeld

Introduction: Facial expressions contain important affective information, and selective attention to facial expression provides an advantage in the face of loss, stress and danger. In addition, the sympathetic nervous system and hypothalamus-pituitary-adrenal axis mediate the organism’s response to loss and danger. Here, we aimed at investigating the influence of sympathetic nervous system and hypothalamus-pituitary-adrenal axis activation on selective attention to affective facial stimuli. Methods and materials: One hundred-and-four healthy men between 18–35 years old (mean (standard deviation) age: 24.1 (3.5) years) participated in the study. We used a randomised, double-blind, placebo-controlled design. Participants received either: (a) yohimbine, (b) hydrocortisone, (c) yohimbine and hydrocortisone or (d) placebo only and participated in a dot-probe task with sad, happy and neutral faces. We collected salivary samples to measure cortisol and alpha amylase activity in addition to measurements of blood pressure and heart rate. Salivary cortisol served as correlate of hypothalamus-pituitary-adrenal axis activation and salivary alpha amylase activity, blood pressure and heart rate as correlates of sympathetic nervous system activation. Measurements were carried out before and after drug administration. Results: We did not find a main effect or interaction effect of hydrocortisone or yohimbine administration on selective attention to happy faces. However, we found an interaction of yohimbine and hydrocortisone on selective attention to sad faces. Post-hoc t-test revealed an attentional bias away from sad stimuli and towards neutral faces in the hydrocortisone-only group. Discussion: Only hydrocortisone administration led to an attentional bias away from sad faces. Future studies should investigate these effects in major depression disorder, as this disorder is characterised by glucocorticoid resistance and increased processing of sad stimuli.


1998 ◽  
Vol 83 (2) ◽  
pp. 515-529 ◽  
Author(s):  
J. H. M. Tulen ◽  
B. J. M. van de Wetering ◽  
F. Boomsma

Cardiovascular and catecholaminergic activity during mental load were studied in patients with Tourette syndrome. Patients and controls performed the Color Word Test, preceded by a baseline period, with continuous measurements of heart rate and blood pressure. Blood samples for assay of plasma catecholamine concentrations were obtained before and during the test. The patients showed higher heart rate and blood pressure during baseline than controls, but no differences regarding plasma catecholamines. The tics corresponded with transient increases in heart rate and blood pressure. Spectral analysis of cardiovascular variability during mental load gave only limited evidence of increased sympathetic activity and no alterations in parasympathetic activity in the patients. Therefore, our findings indicate enhanced cardiovascular activity in the patients but not during mental load. The effects of tics on the cardiovascular parameters illustrate the functional complexity of the autonomic nervous system in Tourette syndrome.


1993 ◽  
Vol 71 (10-11) ◽  
pp. 783-790 ◽  
Author(s):  
Mahmoud M. El-Mas ◽  
Robert G. Carroll ◽  
Abdel A. Abdel-Rahman

This study evaluated the role of sympathetic nervous system (SNS) activity, peripheral hemodynamic changes, and pressure diuresis in blood pressure (BP) normalization in carotid barodenervated rats. The acute and short-term effects of carotid barodenervation or sham operation on blood pressure, heart rate, cardiac output, stroke volume, total peripheral resistance, and plasma catecholamine levels were determined. Changes in plasma volume, urine output, and water and food intakes were also measured. Surgical denervation of the carotid baroreceptors resulted in rapid rises in blood pressure and heart rate in anesthetized rats. These changes were associated with significant increases in plasma catecholamine levels and total peripheral resistance whereas the cardiac index and stroke volume remained unchanged. After recovery from the anesthesia, the blood pressure of carotid barodenervated rats was still significantly higher than that of sham-operated rats at 3 and 24 h after denervation and returned to sham-operated levels by 48 h. Plasma catecholamine levels and total peripheral resistance were higher in carotid barodenervated than in sham-operated rats on the 2 days following surgery. On the other hand, cardiac index (32 ± 1 vs. 40 ± 2 mL∙min−1∙100 g−1 body mass) and stroke volume (205 ± 13 vs. 283 ± 4 μL/beat) were significantly lower on day 2 in carotid barodenervated than in sham-operated rats, which suggests a compensatory role for carotid output in blood pressure normalization after carotid barodenervaton. Both carotid barodenervation and sham operation caused a reduction in water and food intakes but the responses were greater in carotid barodenervated rats. Urine output was drastically reduced for at least 3 days after denervation and so were body masses and water and food intakes. A pressure diuresis that occurred only on the first day after carotid barodenervation when the blood pressure was still elevated may have contributed to blood pressure normalization. Plasma volumes measured 1 and 5 days after carotid barodenervation or sham operation were similar. These findings suggest that blood pressure normalization in carotid-barodenervated rats cannot be accounted for by restoration of the sympathetic nervous system activity to normal levels but rather to a transient pressure diuresis and a reduction in cardiac output which act to offset increases in sympathetic nervous system activity and total peripheral resistance.Key words: carotid barodenervation, blood pressure, sympathetic nervous system, cardiac output, total peripheral resistance, pressure diuresis.


1998 ◽  
Vol 89 (1) ◽  
pp. 30-42 ◽  
Author(s):  
David Amar ◽  
Martin Fleisher ◽  
Carol B. Pantuck ◽  
Harry Shamoon ◽  
Hao Zhang ◽  
...  

Unlabelled BACKGROUND. Changes in the sympathetic nervous system may be a cause of postoperative cardiovascular complications. The authors hypothesized that changes in both beta-adrenergic receptor (betaAR) function (as assessed in lymphocytes) and in sympathetic activity (assessed by plasma catecholamines and by heart rate variability [HRV] measurements obtained from Holter recordings) occur after operation. Methods The HRV parameters were measured in 28 patients having thoracotomy (n = 14) or laparotomy (n = 14) before and for as long as 6 days after operation. Transthoracic echocardiography was performed before and on postoperative day 2. Lymphocytes were also isolated from blood obtained before anesthesia and again on postoperative days 1, 2, 3, and 5 (or 6). They were used to examine betaAR number (Bmax) and cyclic adenosine monophosphate (cAMP) production after stimulation with isoproterenol and prostaglandin E1. In addition, plasma epinephrine, norepinephrine, and cortisol concentrations were determined at similar intervals. Results After abdominal and thoracic surgery, most time and all frequency indices of HRV decreased significantly, as did Bmax and basal and isoproterenol-stimulated cAMP production. The decrements in HRV correlated with those of Bmax and isoproterenol-stimulated cAMP throughout the first postoperative week and inversely correlated with the increase in heart rate. Plasma catecholamine concentrations did not change significantly from baseline values, but plasma cortisol levels did increase after operation in both groups. Left ventricular ejection fraction was normal in both groups and unaffected by surgery. Conclusions Persistent downregulation and desensitization of the lymphocyte betaAR/adenylyl cyclase system correlated with decrements in time and frequency domain indices of HRV throughout the first week after major abdominal or thoracic surgery. These physiologic alterations suggest the continued presence of adaptive autonomic regulatory mechanisms and may explain why the at-risk period after major surgery appears to be about 1 week or more.


2007 ◽  
Vol 113 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Niels P. Riksen ◽  
Marlies Bosselaar ◽  
Stephan J.L. Bakker ◽  
Robert J. Heine ◽  
Gerard A. Rongen ◽  
...  

Plasma NEFA (non-esterified fatty acid) concentrations are elevated in patients with obesity. In the present study we first aimed to provide an integral haemodynamic profile of elevated plasma NEFAs by the simultaneous assessment of blood pressure, pulse wave velocity, FBF (forearm blood flow) and sympathetic nervous system activity during acute elevation of NEFAs. Secondly, we hypothesized that NEFA-induced vasodilation is mediated by adenosine receptor stimulation. In a randomized cross-over trial in healthy subjects, Intralipid® was infused for 2 h to elevate plasma NEFAs. Glycerol was administered as the Control infusion. We assessed blood pressure, pulse wave velocity, FBF (using venous occlusion plethysmography) and sympathetic nervous system activity by measurement of noradrenaline and adrenaline. During the last 15 min of Intralipid®/Control infusion, the adenosine receptor antagonist caffeine (90 μg·min−1·dl−1) was administered into the brachial artery of the non-dominant arm. Compared with Control infusion, Intralipid® increased pulse wave velocity, SBP (systolic blood pressure) and pulse pressure, as well as FBF (from 1.8±0.2 to 2.7±0.6 and from 2.3±0.2 to 2.7±0.6 ml·min−1·dl−1 for Intralipid® compared with Control infusion; P<0.05, n=9). Although in a positive control study caffeine attenuated adenosine-induced forearm vasodilation (P<0.01, n=6), caffeine had no effect on Intralipid®-induced vasodilation (P=0.5). In conclusion, elevation of plasma NEFA levels increased pulse wave velocity, SBP and pulse pressure. FBF was also increased, either by baroreflex-mediated inhibition of the sympathetic nervous system or by a direct vasodilating effect of NEFAs. As the adenosine receptor antagonist caffeine could not antagonize the vasodilator response, this response is not mediated by adenosine receptor stimulation.


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