scholarly journals Perioperative Supplemental Oxygen and Plasma Catecholamine Concentrations After Major Abdominal Surgery – a Substudy of a Randomized Clinical Trial

2021 ◽  
Author(s):  
Alexander Taschner ◽  
Barbara Kabon ◽  
Markus Falkner von Sonnenburg ◽  
Alexandra Graf ◽  
Nikolas Adamowitsch ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Supplemental Oxygen ◽  
Cardiovascular Complications ◽  
Plasma Catecholamine ◽  
Nerve Activity ◽  
Significant Difference ◽  
Patients At Risk ◽  
Plasma Catecholamine Concentrations

Abstract BackgroundIncreased sympathetic nerve activity due to perioperative stress is associated with higher plasma catecholamine concentrations that lead to an increase in heart rate and blood pressure. This fact plays a pivotal role in the development of perioperative myocardial ischemia. A previous study in healthy volunteers has shown that the administration of supplemental oxygen attenuated sympathetic nerve activity, which was associated with lower plasma catecholamine concentrations. However, in patients undergoing surgery evidence is still lacking. We therefore tested the hypothesis that perioperative supplemental oxygen attenuates sympathetic nerve activity estimated by plasma catecholamines in patients at risk for cardiovascular complications undergoing major abdominal surgery.MethodsWe randomly assigned 81 patients to receive either 80% versus 30% inspired oxygen concentration throughout surgery and for the first two postoperative hours. We assessed noradrenaline, adrenaline and dopamine plasma concentrations as surrogate parameters for sympathetic nerve activity before induction of anesthesia, two hours after surgery and on the third postoperative day.Results41 patients received 80% oxygen and 40 patients received 30% oxygen. There was no significant difference in postoperative noradrenaline (effect estimated:-41.5 ng.L-1, 95%CI -134.3, 51.2; p=0.38), adrenaline (effect estimated:11.2 ng.L-1, 95%CI -7.6, 30.1; p=0.24) and dopamine (effect estimated:-1.61 ng.L-1, 95%CI -7.2, 3.9; p=0.57) concentrations between both groups. ConclusionsWe found no significant difference in postoperative plasma catecholamine concentration between the 80% and 30% oxygen group in patients at risk for cardiovascular complications undergoing major abdominal surgery. Based on our results, it seems likely that supplemental oxygen did not influence sympathetic nerve activity in the perioperative setting.Trial RegistrationClinicalTrials.gov (NCT 03366857)European Clinical Trial Database (EudraCT 2017-003714-68)

Neurohumoral interactions in conscious dehydrated rabbit

1988 ◽  
Vol 254 (2) ◽  
pp. R338-R347 ◽  
Author(s):  
A. J. Trapani ◽  
K. P. Undesser ◽  
T. K. Keeton ◽  
V. S. Bishop
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Regional Hemodynamics ◽  
Plasma Catecholamine Concentrations

The purpose of this study was to examine the role of angiotensin II (ANG II), arginine vasopressin (AVP), and neurogenic mechanisms in maintaining arterial pressure (MAP) in conscious water-deprived rabbits. Water deprivation produced marked increases in plasma renin activity and the concentration of AVP; however, plasma catecholamine concentrations were unchanged. Arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) was similar in water-replete and dehydrated animals. Administration of an ANG II receptor antagonist (ANG IIX) to water-deprived animals produced a small decrease in MAP but no significant changes in HR or mesenteric and hindquarters vascular resistances. Similarly, there was no significant effect on MAP, HR, or regional hemodynamics when dehydrated animals received an AVP-V1 antagonist (AVPX). RSNA increased by maximums of 61 and 43% in response to ANG IIX and AVPX, respectively. Combined administration of ANG IIX and AVPX produced significant decreases in MAP (-9 mmHg) and hindquarters resistance (-24%) and 117% and 23 beat/min increases in RSNA and HR, respectively. The effect on mesenteric resistance was variable; however, the response was generally a decrease. We conclude that ANG II and AVP pressor mechanisms are activated to sustain MAP in the dehydrated state. In contrast, the basal level and baroreflex control of sympathetic nervous system activity are unchanged from the water-replete state. However, activation of sympathetic nerve activity may become important in maintaining peripheral resistance when ANG II and AVP receptors are blocked in water-deprived animals.

Abstract 529: Muscle Sympathetic Nerve Activity is Higher in Winter than Other Seasons

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Jian Cui ◽  
Matthew D Muller ◽  
Allen R Kunselman ◽  
Cheryl Blaha ◽  
Lawrence I Sinoway
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Epidemiological Data ◽  
Repeated Measurements ◽  
Nerve Activity ◽  
Cardiovascular Morbidity And Mortality ◽  
Significant Difference

Epidemiological data suggest that blood pressure tends to be higher in winter and lower in summer, particularly in the elderly. Moreover, hospitalization and mortality rates due to cardiovascular disease have higher rates in winter than summer. Whether autonomic adjustment including muscle sympathetic nerve activity (MSNA) varies with season is unclear. To test the hypothesis that resting MSNA varies along the seasons, we retrospectively analyzed the supine baseline (6 min) MSNA and heart rate (from ECG) of 57 healthy subjects (33M, 24F, 29 ± 1 yrs, range 22-64 yrs) from studies in our laboratory (room temperature ~23 °C). Each of these subjects from central Pennsylvania was studied during 2 or more seasons (total 231 visits). A linear-mixed effects model, which is an extension of the analysis of variance model accounting for repeated measurements (i.e. season) per subject, was used to assess the association of season with the cardiovascular outcomes. The Tukey-Kramer procedure was used to account for multiple comparisons testing between the seasons. MSNA burst rate in winter (21.3 ± 1.0 burst/min) was significantly greater than in summer (13.7 ± 1.0 burst/min, P < 0.001), spring (17.5 ± 1.6 burst/min, P = 0.04) and fall (17.0 ± 1.2 burst/min, P < 0.002). There was no significant difference in MSNA in other comparisons (spring vs. summer, P = 0.12; spring vs. fall, P = 0.99; summer vs. fall, P = 0.054). Heart rate (63.6 ± 1.1 vs. 60.8 ± 1.2 beats/min, P = 0.048) was significantly greater in winter compared to summer. Blood pressure (automated sphygmomanometry of the brachial artery) was not significantly different between seasons. The results suggest that baseline sympathetic nerve activity varies along the seasons, with peak levels evident in winter. We speculate that the seasonal MSNA variation may contribute to seasonal variations in cardiovascular morbidity and mortality.

Pulse-synchronous sympathetic burst power as a new index of sympathoexcitation in patients with heart failure

2004 ◽  
Vol 287 (4) ◽  
pp. H1821-H1827 ◽  
Author(s):  
Yoshitaka Oda ◽  
Hidetsugu Asanoi ◽  
Hiroshi Ueno ◽  
Kunihiro Yamada ◽  
Shuji Joho ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Class Ii ◽  
Plasma Norepinephrine ◽  
Class Iii ◽  
Nerve Activity ◽  
Significant Difference ◽  
Patients With Heart Failure

The upper limit of incidence of muscle sympathetic neural bursts can lead to underestimation of sympathetic activity in patients with severe heart failure. This study aimed to evaluate the pulse-synchronous burst power of muscle sympathetic nerve activity (MSNA) as a more specific indicator that could discriminate sympathetic activity in patients with heart failure. In 54 patients with heart failure, the pulse-synchronous burst power at the mean heart rate was quantified by spectral analysis of MSNA. Thirteen patients received a central sympatholytic agent (guanfacine) for 5 days to validate the feasibility of this new index. Both burst incidence and plasma norepinephrine level showed no significant difference between patients in New York Heart Association functional class III (94 ± 6 per 100 heartbeats and 477 ± 219 pg/ml, respectively) and class II (79 ± 14 per 100 heartbeats and 424 ± 268 pg/ml, respectively). In contrast, the burst power was useful for discriminating patients in class III from those in class II (61 ± 8% vs. 39 ± 10%; P < 0.05). Inhibition of sympathetic nerve activity by guanfacine was more sensitively reflected by the change of burst power (−36 ± 25%) than by that of burst incidence (−12 ± 14%; P < 0.001). The sympathetic burst power reflects both burst frequency and amplitude independently of the absolute values and provides a sensitive new index for interindividual comparisons of sympathetic activity in patients with heart failure.

scholarly journals Sympathetic and cardiovascular actions of orexins in conscious rats

1999 ◽  
Vol 277 (6) ◽  
pp. R1780-R1785 ◽  
Author(s):  
Tetsuro Shirasaka ◽  
Masamitsu Nakazato ◽  
Shigeru Matsukura ◽  
Mayumi Takasaki ◽  
Hiroshi Kannan
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Nerves ◽  
Plasma Norepinephrine ◽  
High Dose ◽  
Plasma Catecholamine ◽  
Nerve Activity ◽  
Orexin A ◽  
Conscious Rats ◽  
Renal Sympathetic

The novel hypothalamic peptides orexin-A and orexin-B are known to induce feeding behavior when administered intracerebroventricularly, but little is known about other physiological functions. The renal sympathetic nerves play important roles in the homeostasis of body fluids and the circulatory system. We examined the effects of intracerebroventricularly administered orexins on mean arterial pressure (MAP), heart rate (HR), renal sympathetic nerve activity (RSNA), and plasma catecholamine in conscious rats. Orexin-A (0.3, 3.0 nmol) provoked an increase in MAP (94.3 ± 0.7 to 101.9 ± 0.7 mmHg and 93.1 ± 1.1 to 108.3 ± 0.8 mmHg, respectively) and RSNA (28.0 ± 7.0 and 57.9 ± 12.3%, respectively). Similarly, orexin-B (0.3, 3.0 nmol) increased MAP (93.9 ± 0.9 to 97.9 ± 0.9 mmHg and 94.5 ± 1.1 to 105.3 ± 1.7 mmHg, respectively). Orexin-A and -B at 3.0 nmol also increased HR. In other conscious rats, a high dose of orexin-A and -B increased plasma norepinephrine. Plasma epinephrine only increased with a high dose of orexin-A. These results indicate that central orexins regulate sympathetic nerve activity and affect cardiovascular functions.

Frequency domain characteristics of muscle sympathetic nerve activity in heart failure and healthy humans

1997 ◽  
Vol 273 (1) ◽  
pp. R205-R212 ◽  
Author(s):  
S. Ando ◽  
H. R. Dajani ◽  
J. S. Floras
Keyword(s):  
Heart Failure ◽  
Frequency Domain ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Power ◽  
Breathing Frequency ◽  
Nerve Activity ◽  
Significant Difference

The purpose of this study was to characterize oscillations in muscle sympathetic nerve activity (MSNA) in the frequency domain in healthy subjects and patients with congestive heart failure (CHF) and to relate these to blood pressure (BP), heart rate (HR), and breathing frequency. MSNA burst frequency was significantly greater in CHF [52 +/- 21 (n = 12) vs. 35 +/- 11 (n = 19) bursts/min, P < 0.05], whereas breathing frequency and HR were similar. There was no significant difference between CHF and healthy subjects in total power, harmonic power, and nonharmonic power in the MSNA spectrum from 0 to 0.5 Hz, but low frequency power (LF, 0.05-0.15 Hz, P < 0.05) was reduced in heart failure patients. There was less coherence between BP and MSNA in the LF range, but similar spectral power in both groups in the very LF (VLF, 0-0.05 Hz) and high frequency (0.15-0.5 Hz) ranges. The transfer of MSNA oscillations into BP in the VLF (P < 0.05) and LF (P < 0.02) ranges was significantly lower in CHF, but gains in the transfer function and in the coherence between BP and MSNA and in the coherence between respiration and MSNA were similar in the two groups. These observations indicate that modulation of MSNA by the arterial baroreflex and respiration is preserved in CHF. The loss of LF power in the MSNA signal may be due to impaired neuroeffector transduction. The higher sympathetic nerve firing rate in CHF would therefore appear to be caused by factors other than the loss of regulation by these two inhibitory influences.

scholarly journals Neck movement but not neck position modulates skin sympathetic nerve activity supplying the lower limbs of humans

2018 ◽  
Vol 119 (4) ◽  
pp. 1283-1290
Author(s):  
Philip S. Bolton ◽  
Elie Hammam ◽  
Vaughan G. Macefield
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
The Body ◽  
Respiratory Frequency ◽  
Lower Limbs ◽  
Neck Movement ◽  
Nerve Activity ◽  
Skin Sympathetic Nerve Activity ◽  
Cross Correlation Analysis ◽  
Significant Difference

We previously showed that dynamic, but not static, neck displacement modulates muscle sympathetic nerve activity (MSNA) to lower limbs of humans. However, it is not known whether dynamic neck displacement modulates skin sympathetic nerve activity (SSNA). Tungsten microelectrodes inserted into the common peroneal nerve were used to record SSNA in 5 female and 4 male subjects lying supine on a table that fixed their head in space but allowed trapezoidal ramp (8.1 ± 1.2°/s) and hold (17.5° for 53 s) or sinusoidal (35° peak to peak at 0.33–0.46 Hz) horizontal displacement of the body about the head. SSNA recordings were made before, during, and after trapezoidal and sinusoidal displacements of the body. Spike frequency analysis of trapezoidal displacements and cross-correlation analysis during sinusoidal displacements revealed that SSNA was not changed by trapezoid body-only displacement but was cyclically modulated during sinusoidal angular displacements (median, 95% CI: 27.9%, 19.6–48.0%). The magnitude of this modulation was not statistically ( P > 0.05) different from that of cardiac and respiratory modulation at rest (47.1%, 18.7–56.3% and 48.6%, 28.4–59.3%, respectively) or during sinusoidal displacement (10.3%, 6.2–32.1% and 26.9%, 13.6–43.3%, respectively). Respiratory frequency was entrained above its resting rate (0.26 Hz, 0.2–0.29 Hz) during sinusoidal neck displacement; there was no significant difference ( P > 0.05) between respiratory frequency (0.38 Hz, 0.25–0.49 Hz) and sinusoidal displacement frequency (0.39 Hz, 0.35–0.42 Hz). This study provides evidence that SSNA is modulated during neck movement, raising the possibility that neck mechanoreceptors may contribute to the cutaneous vasoconstriction and sweat release associated with motion sickness. NEW & NOTEWORTHY This study demonstrates that dynamic, but not static, stretching of the neck modulates skin sympathetic nerve activity in the lower limbs.

scholarly journals Sympathetic nerve activity changes following acute exposures to electronic and tobacco cigarette smoking in humans

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
K Dimitriadis ◽  
K Narkiewicz ◽  
I Leontsinis ◽  
D Konstantinidis ◽  
C Mihas ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cigarette Smoking ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Tobacco Cigarette ◽  
Significant Difference ◽  
The Impact

Abstract Background/Introduction Tobacco cigarette (TC) smoking acutely increases blood pressure and sympathetic nerve activity, whereas there are scarce data on the impact of electronic cigarette (EC). Purpose The aim of the study was to assess the acute effects of TC, EC and sham smoking on blood pressure, heart rate and sympathetic nervous system in healthy subjects. Methods We studied 12 normotensive male habitual smokers (mean age 33 years) free of cardiovascular disease. The study design was randomized and placebo controlled with 3 experimental sessions (sham smoking, tobacco cigarette smoking, and e-cigarette smoking) in random order, each session on a separate day. Subjects smoked 2 tobacco cigarettes containing 1.1 mg nicotine or simulate smoking (sham smoking) with the 2 cigarettes separated by 5 minutes. Additionally, participants smoked e-cigarettes for a period of 5 and 30 minutes. In all occasions, sympathetic drive was assessed by muscle sympathetic nerve activity (MSNA) (baroreflex-dependent) and skin sympathetic nerve activity (SSNA) (baroreflex-independent) based on established methodology (microneurography). Results After the first and second TC smoking, there was significant increase in mean arterial pressure (MAP) (by 6 and 8 mmHg, respectively, overall p&lt;0.001) and heart rate (by 8 and 12 beats/minute, respectively, overall p&lt;0.001) compared to baseline. Similarly, EC smoking at 5 and 30 minutes compared to baseline was accompanied by augmentation of MAP (by 6 and 10 mmHg, respectively, overall p&lt;0.001) and heart rate (by 5 and 9 beats/minute, respectively, overall p&lt;0.001). Sham smoking was accompanied by a reduction in MAP after the first and second cigarette compared to baseline (by 2 and 4 mmHg, respectively, p=0.001), whereas there was no significant difference in heart rate (p=NS). The first and second TC smoking was characterized by lower muscle MSNA (by 6 and 6 bursts/minute, respectively, overall p&lt;0.001) compared to baseline, whereas SSNA was increased (by 9 and 10 bursts/minute respectively, overall p&lt;0.001). Additionally, EC smoking at 5 and 30 minutes caused a decrease in MSNA (by 8 and 8 bursts/minute, respectively, overall p&lt;0.00) and an augmentation in SSNA (by 7 and 9 bursts per minute, respectively, overall p&lt;0.001) compared to baseline. Sham smoking had no significant effect on MSNA and SSNA (p=NS for both). Conclusions Sympathetic, pressor and heart rate unfavorable responses to EC smoking are similar to those elicited by TC in healthy subjects. Our findings provide novel insights into the negative impact of EC on cardiovascular system and support opinions recommending great caution concerning EC use. FUNDunding Acknowledgement Type of funding sources: None.

Catecholamine response during 12 days of high-altitude exposure (4,300 m) in women

1998 ◽  
Vol 84 (4) ◽  
pp. 1151-1157 ◽  
Author(s):  
Robert S. Mazzeo ◽  
Avon Child ◽  
Gail E. Butterfield ◽  
Jacinda T. Mawson ◽  
Stacy Zamudio ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Altitude ◽  
Sea Level ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cycle Phase ◽  
Plasma Catecholamine ◽  
Nerve Activity ◽  
Altitude Exposure ◽  
Excretion Rates

We have previously demonstrated that acclimatization to high altitude elicits increased sympathetic nerve activity in men. The purpose of this investigation was to determine 1) whether women respond in a similar manner as found previously in men and 2) the extent to which menstrual cycle phase influences this response. Sixteen eumenorrheic women (age, 23.6 ± 1.2 yr; weight, 56.2 ± 4.3 kg) were studied at sea level and during 12 days of high-altitude exposure (4,300 m) in either their follicular (F; n = 11) or luteal (L; n = 5) phase. Twenty-four-hour urine samples were collected at sea level and during each day at altitude. Catecholamines were determined by high-performance liquid chromatography with electrochemical detection. Compared with sea-level values, urinary norepinephrine excretion increased significantly during altitude exposure, peaking on days 4–6. Thereafter, levels remained constant throughout the duration of altitude exposure. The magnitude of this increase was similar between the F (138%) and L (93%) phase. Urinary epinephrine levels were elevated on day 2 of altitude exposure compared with sea-level values for both F and L subjects (93%). Thereafter, urinary epinephrine excretion returned to sea-level values, and no differences were found between F and L subjects. Plasma catecholamine content was consistent with urinary values and supports the concept of an elevation in sympathetic activity over time at altitude. Mean and diastolic blood pressure as well as heart rate adjustments to high altitude correlated significantly with urinary norepinephrine excretion rates. It was concluded that 1) urinary and plasma catecholamine responses to 12 days of high-altitude exposure in women are similar to those previously documented to occur for men; 2) whereas no differences in catecholamine levels were observed between F- and L-phase assignments, for a given urinary norepinephrine excretion rate, blood pressure and heart rates were lower for F vs. L subjects; and 3) several cardiovascular adaptations associated with high-altitude exposure correlated with 24-h urinary norepinephrine excretion rates and thus sympathetic nerve activity.

P3559Renal sympathetic nerve activity, assessed by renal 123-iodine metaiodobenzylguanidine scintigraphy, reflects disease severity in heart failure with reduced ejection fraction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Yoshitaka ◽  
H Murai ◽  
H Tokuhisa ◽  
M Takamura
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Ejection Fraction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Mibg Scintigraphy ◽  
Nerve Activity ◽  
Reduced Ejection Fraction ◽  
Significant Difference ◽  
Renal Sympathetic

Abstract Background Sympathetic nerve activity is related to cardio-renal syndrome, which plays a crucial role in deterioration in heart failure with reduced ejection fraction (HFrEF). Previous studies reported that renal denervation was effective in HFrEF patients. Recently, we have demonstrated that renal 123-iodine metaiodobenzylguanidine (MIBG) scintigraphy is useful for assessment of renal sympathetic function in hypertension. However, it is unclear whether renal MIBG would reflect disease severity in HFrEF patients. Methods Twenty-four HFrEF patients and eleven control without heart failure were included in this study. HFrEF patients were performed MIBG and MSNA and hemodynamics inspection using Swan-Ganz's catheter (SGC). HFrEF was defined as echocardiography with EF of 50% or less. MSNA was recorded from the right peroneal nerve to evaluate direct sympathetic nerve activity to the peripheral vascular bed. MSNA was expressed as the number per minute (burst frequency = BF) and the number per 100 heartbeats (burst incidence = BI). Renal MIBG scintigraphy was simultaneously performed with cardiac MIBG scintigraphy. The 20 minutes (early) and 180 minutes (delayed) kidney-to-mediastinum ratio (K/M), early and delayed heart-to-mediastinum ratio (H/M), and washout rate (WR) were measured. Results In the HFrEF group, the EF was significantly lower than control group (EF 34.8±9.51% vs. 63.0±7.43, p<0.01), and MSNA parameters were significantly increased (burst incidence (BI), 57.7±18.7 vs. 37.0±11.3, p<0.01; BF 42.7±14.4 vs. 24.1±8.50, p<0.01). WR of cardiac MIBG was not related to MSNA parameters but negatively related to cardiac output (r=−0.46, p<0.05) and stroke volume (r=−0.61, p<0.01) and delayed H/M negatively correlated with mean pulmonary capillary wedge pressure (r=−0.57, P<0.05). WR of both left and right renal MIBG showed a strong correlation with MSNA (BI; left, r=0.69, p<0.01, right 0.60, p<0.01, BF; left, r=0.64, p<0.01, right, r=0.58, p<0.01) and no significant correlation between renal MIBG and hemodynamics parameters. HFrEF patients were divided into stage B and stage C based on American College of Cardiology/American Heart Association (ACC/AHA) classification (stage B, n=13; stage C, n=11). There was no significant difference between the two groups in cardiac MIBG parameters. Renal WRs in stage C was increased than stage B (Lt renal WR,51.6±10.6 vs. 40.6±6.53, p<0.05; Rt renal WR, 43.9±9.97 vs. 35.1±11.3, p<0.05). Conclusions Cardiac WR negatively correlated with cardiac output and renal WR correlated with MSNA. Renal WRs had a significant difference in the heart failure stage of ACC/AHA classification, but cardiac MIBG parameters did not. These results indicate that renal MIBG might be useful to assess renal sympathetic nerve activity in patients with HFrEF and suggesting that renal SNA might be promising therapeutic target in HFrEF.

Splanchnic sympathetic nerve activity and circulating catecholamines in the hyperthermic rat

1991 ◽  
Vol 70 (4) ◽  
pp. 1821-1826 ◽  
Author(s):  
C. V. Gisolfi ◽  
R. D. Matthes ◽  
K. C. Kregel ◽  
R. Oppliger
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Heat Exposure ◽  
Splanchnic Nerve ◽  
Plasma Catecholamine ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Sprague Dawley Rats ◽  
Greater Splanchnic Nerve ◽  
Alpha Chloralose

The mechanisms responsible for the initial rise in splanchnic vascular resistance with environmental heating are controversial, and those responsible for the subsequent fall in splanchnic resistance in the severely hyperthermic animal are unknown. Thus we examined the effect of environmental heating on plasma catecholamine concentration, splanchnic sympathetic nerve activity (SNA), and select blood chemistries. In one study, 25 male Sprague-Dawley rats (270-300 g) were assigned to one of five groups on the basis of their core temperature (Tc, 37, 39, 41, 43, or 44 degrees C) at death. Heart rate (HR), mean arterial pressure (MAP), and Tc were monitored during heat stress under alpha-chloralose anesthesia (12.5 mg.ml-1.h-1). At each predetermined Tc, an aortic blood sample was drawn and analyzed for mean plasma concentration of norepinephrine (NE), epinephrine (E), Na+, K+, and lactate. From 41 to 43 degrees C, NE and E rose significantly, and the animals became hyperkalemic and lactacidemic. In a separate study, we quantitated SNA from the greater splanchnic nerve during heat exposure of artificially respired animals anesthetized with pentobarbital sodium (50 mg/kg). MAP, splanchnic SNA, and Tc were recorded. Tc was elevated from 37.0 +/- 0.12 to 41.3 +/- 0.18 degrees C in 70 min by increase of ambient temperature to 38 degrees C in an environmental chamber. Splanchnic SNA was 54 +/- 8 spikes/s at a Tc of 37 degrees C and increased significantly as Tc exceeded 39 degrees C (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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