Reflex sympathetic activation in humans is accompanied by inhibition of gastric HCO3- secretion

1988 ◽  
Vol 255 (6) ◽  
pp. G752-G758 ◽  
Author(s):  
H. Sjovall ◽  
H. Forssell ◽  
J. Haggendal ◽  
L. Olbe
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
Sympathetic Activity ◽  
Plasma Catecholamine ◽  
Series Of Experiments ◽  
Plasma Catecholamine Concentrations ◽  
Peripheral Sympathetic Activity ◽  
Forearm Vascular Resistance

The study was performed to determine whether the sympathetic nervous system contributes to the reflex control of gastric HCO3- secretion in humans. Gastric HCO3- secretion was registered by a computerized technique based on measurements of pH and PCO2 in gastric effluent. To minimize formation of CO2 in the stomach, subjects were pretreated with the H2-receptor blocker ranitidine. Compensations were made for HCO3- of nongastric origin. As indicators of cardiovascular sympathetic activity, we measured heart rate, forearm vascular resistance, and plasma catecholamine concentrations. In one series of experiments, peripheral sympathetic activity was enhanced by the application of a negative pressure around the lower part of the body (lower body negative pressure, LBNP), at a rate sufficient to induce a slight decrease in systemic arterial pressure. In another series of experiments, peripheral sympathetic activity was inhibited by elevation of the legs, a procedure that simulates volume loading by redistributing blood volume toward the central circulation. LBNP at -20 mmHg decreased systolic pressure and pulse pressure and significantly increased heart rate, forearm vascular resistance, and plasma catecholamine levels. All these effects were observed in the first 15-min period of LBNP and were well maintained throughout the 45-min observation period. LBNP also inhibited basal gastric HCO3- secretion rate in seven of eight individuals, but this response was slower in onset with a latency of at least 15 min. Elevation of the legs increased pulse pressure and decreased forearm vascular resistance. Catecholamines were not measured in these experiments. Gastric HCO3- secretion tended to increase, but the magnitude of the response was highly variable.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Differential Effects of Low- and High-Intensity Lower Body Negative Pressure on Noradrenaline and Adrenaline Kinetics in Humans

1996 ◽  
Vol 90 (5) ◽  
pp. 337-343 ◽  
Author(s):  
Marie-Cecile Jacobs ◽  
David S. Goldstein ◽  
Jacques J. Willemsen ◽  
Paul Smits ◽  
Theo Thien ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
High Intensity ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Total Body ◽  
Noradrenaline And Adrenaline ◽  
Forearm Vascular Resistance

1. Lower body negative pressure provides a means to examine neurocirculatory reflexive responses to decreases in venous return to the heart. We assessed whether the pattern of catecholaminergic responses to lower body negative pressure depends on the intensity of the stimulus (−15 versus −40 mmHg). 2. In 14 healthy subjects, responses of forearm blood flow and noradrenaline spillover and of total body noradrenaline and adrenaline spillover were assessed during infusion of [3H]noradrenaline and [3H]adrenaline during −15 and −40 mmHg of lower body negxative pressure. 3. During lower body negative pressure at −15 mmHg, heart rate and pulse pressure did not change, but forearm vascular resistance increased by 25–50%. Forearm noradrenaline spillover increased by about 50%, from 0.63 ± 0.16 to 0.94 ± 0.23 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover did not change, and total body adrenaline spillover increased significantly by about 30%. Clearances of noradrenaline and adrenaline were unchanged. 4. During lower body negative pressure at −40 mmHg, heart rate increased and pulse pressure decreased. Forearm vascular resistance increased by about 100%, and forearm noradrenaline spillover increased by 80%, from 0.73 ± 0.19 to 1.32 ± 0.36 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover increased by 30%, and total body adrenaline spillover increased by about 50%. Clearances of both noradrenaline and adrenaline decreased. 5. The results are consistent with the view that selective deactivation of cardiopulmonary baroreceptors during low-intensity lower body negative pressure increases sympathoneural traffic to forearm skeletal muscle and increases adrenomedullary secretion without a concomitant generalized increase in sympathoneural outflows. Concurrent deactivation of cardiopulmonary and arterial baroreceptors during high-intensity lower body negative pressure evokes a more generalized increase in sympathoneural activity, accompanied by further increased adrenomedullary secretion and decreased plasma clearances of noradrenaline and adrenaline. The findings support differential increases in skeletal sympathoneural and adrenomedullary outflows during orthostasis, with more generalized sympathoneural responses to systemic hypotension.

Mesenteric Blood Flow as Influenced by Progressive Hypercapnia

1956 ◽  
Vol 184 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Eugene W. Brickner ◽  
E. Grant Dowds ◽  
Bruce Willitts ◽  
Ewald E. Selkurt
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Oxygen Content ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Mesenteric Blood Flow ◽  
Initial Tendency ◽  
Elevated Heart Rate

The influence of hypercapnia on mesenteric blood flow was studied in dogs subjected to progressive increments in CO2 content of inspired air produced by rebreathing from a large spirometer. Oxygen content was maintained above 21 volumes %. Although some animals showed an initial tendency for mesenteric blood flow to decrease and arterial pressure to increase in the range 0–5 volumes % of CO2, the usual hemodynamic change in the range 5–16 volumes % was an increase in mesenteric blood flow resulting from decrease in intestinal vascular resistance, accompanied by a decline in arterial pressure. Portal venous pressure was progressively elevated. Heart rate slowed in association with an increase in pulse pressure. The observations suggest that in higher ranges of hypercapnia, CO2 has a direct dilating action on the mesenteric vasculature.

scholarly journals Cardiovascular Responses to the Induction of Mild Hypothermia in the Presence of Epidural Anesthesia

2001 ◽  
Vol 94 (4) ◽  
pp. 678-682 ◽  
Author(s):  
Masahiro Yoshida ◽  
Keizo Shibata ◽  
Hironori Itoh ◽  
Ken Yamamoto
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Ejection Fraction ◽  
General Anesthesia ◽  
Epidural Anesthesia ◽  
Mild Hypothermia ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Plasma Catecholamine ◽  
Plasma Catecholamine Concentrations

Background The combining of epidural anesthesia with general anesthesia impairs central and peripheral thermoregulatory control and therefore is often accompanied by unintended intraoperative hypothermia. However, little is known about the cardiovascular response to hypothermia during combined epidural and general anesthesia. The authors assessed the effects of hypothermia during such combined anesthesia. Methods The authors randomly assigned 30 mongrel dogs anesthetized with isoflurane (1.0%) to three groups of 10: control, receiving general anesthesia alone; thoracic injection, additionally receiving thoracic epidural anesthesia; and lumbar injection, additionally receiving thoracolumbar epidural anesthesia. Core temperature was lowered from 38.5 degrees C to approximately 34 degrees C (mild hypothermia) using a femoral arteriovenous shunt in an external cool water bath. During hypothermia, the authors measured heart rate, cardiac output, and plasma catecholamine concentrations in each group. Ejection fraction was also measured using echocardiography. Results Compared with measurements during baseline conditions (general anesthesia alone with no epidural injection and no hypothermia) in the control, thoracic, and lumbar injection groups, the injections followed by hypothermia produced 17, 32, and 41% decreases in heart rate; 22, 32, and 47% reductions in cardiac output; 66, 85, and 92% decreases in the epinephrine concentrations; and 27, 44, and 85% decreases in the norepinephrine concentrations. In contrast, ejection fraction did not change in any group. Conclusion Mild hypothermia during combined epidural anesthesia and general anesthesia markedly reduced cardiac output in dogs, mainly by decreasing heart rate.

Cardiovascular reflex responses in Bangladeshi and European subjects

1991 ◽  
Vol 80 (1) ◽  
pp. 39-45 ◽  
Author(s):  
M. A. Rahman ◽  
I. Farquhar ◽  
T. Bennett
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Mean Blood Pressure ◽  
Valsalva Manoeuvre ◽  
Deep Breathing ◽  
Reflex Responses ◽  
Forearm Vascular Resistance

1. Cardiovascular responses to three different interventions, namely the Valsalva manoeuvre, deep breathing and a cold stimulus on the face, were studied in two ethnic groups (European and Bangladeshi) that have been shown to differ in the prevalence of hypertensive-vascular disease. The data obtained consisted of systolic blood pressure, diastolic blood pressure, mean blood pressure, heart rate measured by using a beat-by-beat non-invasive blood pressure monitor (the Finapres), forearm blood flow determined by venous occlusion plethysmography, and calculated forearm vascular resistance. 2. The resting haemodynamic status was similar in European and Bangladeshi subjects. However, Bangladeshi subjects showed a greater increase in heart rate, but only after 20 s into the Valsalva manoeuvre, and greater overshoots in mean blood pressure after the manoeuvre than the European subjects. Furthermore, after cold face stimulation the fall in forearm vascular resistance to baseline levels was delayed in Bangladeshi subjects relative to that in the European subjects. 3. There were no inter-group differences in the reflex bradycardia relative to mean blood pressure or in the cardiac baroreflex sensitivity estimated from systolic blood pressure and pulse interval after the Valsalva manoeuvre. In addition, values for the mean difference between maximum and minimum pulse intervals during deep breathing did not differ in Bangladeshi and European subjects. 4. These findings together suggest that, although cardiac vagal reflex responses appear similar in the two groups, sympatho-adrenal influences on the heart and vasculature may be greater in Bangladeshi subjects than in European subjects.

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
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Animal Models ◽  
Sympathetic Nervous System ◽  
Rectal Temperature ◽  
Plasma Catecholamines ◽  
Plasma Catecholamine ◽  
Sympathetic Nervous ◽  
Plasma Catecholamine Concentrations

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.

scholarly journals Hemodynamic response during lower body negative pressure: role of volume status.

1998 ◽  
Vol 9 (1) ◽  
pp. 105-113 ◽  
Author(s):  
G Ligtenberg ◽  
P J Blankestijn ◽  
H A Koomans
Keyword(s):  
Heart Rate ◽  
Cardiac Index ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Peripheral Resistance ◽  
Hemodynamic Response ◽  
Volume Status ◽  
Lower Body

Sudden dialysis-related hypotension is characterized by paradoxical vasodilation, suggestive of sympathoinhibition. A similar hypotensive reaction can be evoked by lower body negative pressure (LBNP), which thus allows the study of the numerous factors involved in dialysis hypotension separately. This article examines the influence of changes in volume status on the hemodynamic response to LBNP (45 mmHg up to the iliac crest, maximum 60 min) in 12 healthy subjects. LBNP caused a decrease in cardiac index and pulse pressure, and an increase in heart rate and total peripheral resistance, most of which developed within the first 3 min of LBNP. Six subjects developed sudden hypotension characterized by vasodilation after 9 +/- 4 min of LBNP. After saline expansion (25 ml/kg), which increased blood volume by approximately 8%, five subjects endured LBNP for the full 60 min. However, after 60 min of LBNP, the circulatory parameters suggested a similar critical situation as that observed before presyncope in their first experiment. The other six subjects endured the full 60 min of LBNP. After furosemide-induced volume reduction associated with 1.6 +/- 0.2 kg weight loss and approximately 7% blood volume reduction, five of them developed vasodilatory presyncope after 17 +/- 5 min of LBNP. Comparison of presyncopal and nonpresyncopal experiments within subjects, as well as between subjects, showed that the early (3 min) response to LBNP was different: Despite similar decreases in cardiac index, the values for systolic pressure, pulse pressure, peripheral resistance, and stroke volume were lower, and the heart rate was higher in the experiments ending in presyncope. It is concluded that the volume status is a determinant of the tolerance to LBNP, probably by affecting the vasoconstrictive response. By inference, this study suggests that the vasoconstrictive response to the hemodynamic stress of hemodialysis is also influenced by the volume status.

Haemodynamic and Neurohumoral Effects of Caffeine in Elderly Patients with Symptomatic Postprandial Hypotension: A Double-Blind, Randomized, Placebo-Controlled Study

1994 ◽  
Vol 87 (2) ◽  
pp. 259-267 ◽  
Author(s):  
Lewis A. Lipsitz ◽  
Rene W. M. M. Jansen ◽  
Carolyn M. Connelly ◽  
Margaret M. Kelley-Gagnon ◽  
Anthony J. Parker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Elderly Patients ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Controlled Study ◽  
Pathophysiological Mechanism ◽  
Double Blind ◽  
Postprandial Hypotension ◽  
Forearm Vascular Resistance

1. The aim of this study was to determine the effects of caffeine on haemodynamic and neurohumoral responses to meal ingestion in elderly patients with a history of symptomatic postprandial hypotension. 2. Postprandial hypotension is a common disorder of blood pressure regulation in the elderly, associated with falls and syncope. The pathophysiological mechanism is thought to be related to impaired vascular compensation for splanchnic blood pooling after a meal. Since caffeine inhibits vasodilatory adenosine receptors in the splanchnic circulation, we postulated that caffeine would reduce splanchnic blood pooling and prevent the development of postprandial hypotension. 3. We conducted a randomized, double-blind, placebo-controlled, cross-over study in nine elderly patients [age 76 ± 9 (SD) years] with histories of symptomatic postprandial hypotension. Standardized 1674 kJ liquid meals with 250 mg of caffeine or placebo were given on two occasions, at least 1 week apart. Blood pressure, heart rate, forearm vascular resistance (by venous occlusion plethysmography), and plasma caffeine and catecholamine levels were measured. Cardiac and splanchnic blood volume were determined by radionuclide scans. 4. By 30 min after both caffeine and placebo meal studies, supine mean arterial blood pressure fell significantly (P = 0.006) by 31 ± 7 and 19 ± 6 mmHg, respectively (mean ± SEM, between group difference was not significant). Heart rate, cardiac output and splanchnic blood volume increased significantly, but to a similar extent, after caffeine and placebo. Forearm vascular resistance was unchanged after both meals. 5. Oral caffeine given with a meal does not reduce splanchnic blood pooling nor prevent postprandial hypotension in symptomatic elderly patients.

Effects of Rapid Increases of Desflurane and Sevoflurane to Concentrations of 1.5 MAC on Systemic Vascular Resistance and Catecholamine Response during Cardiopulmonary Bypass 

1997 ◽  
Vol 87 (4) ◽  
pp. 801-807 ◽  
Author(s):  
Gabriele Rodig ◽  
Cornelius Keyl ◽  
Mirko Kaluza ◽  
Frieder Kees ◽  
Jonny Hobbhahn
Keyword(s):  
Cardiopulmonary Bypass ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Baseline Level ◽  
Time Course ◽  
Resistance Index ◽  
Coronary Bypass ◽  
Plasma Catecholamine ◽  
Catecholamine Response ◽  
Plasma Catecholamine Concentrations

Background Airway irritation was hypothesized to trigger the transient cardiovascular stimulation associated with desflurane. The authors administered desflurane during cardiopulmonary bypass (CPB), thus avoiding airway contact, and compared the effects of rapid increases of desflurane to 1.5 MAC on systemic vascular resistance index (SVRI) and catecholamine response to those of 1.5 MAC sevoflurane. Methods Forty-eight patients, undergoing elective coronary bypass surgery, were randomly allocated to receive either desflurane or sevoflurane during hypothermic (32-33 degrees C) nonpulsatile CPB at exhaust gas concentrations of 1.5 MAC for 15 min. SVRI was calculated at baseline, 1, 2, 3, 4, 5, 7, 9, 12, and 15 min after starting volatile anesthetics' delivery. Plasma catecholamine concentrations were determined in 12 desflurane-treated patients and 12 sevoflurane-treated patients at baseline, 5, and 15 min. Results The time-course of deltaSVRI, (changes in SVRI from baseline), from baseline to 5 min was significantly different between desflurane- and sevoflurane-treated patients, whereas there was no difference from 7 to 15 min. In the desflurane group, SVRI from 1 to 7 min remained unchanged to baseline level, thereafter declining to significantly lower values at 9, 12, and 15 min compared with values from 0 to 5 min, whereas sevoflurane produced an immediate and significant reduction in SVRI. With desflurane, catecholamine concentrations remained unchanged to baseline level at 5 and 15 min; with sevoflurane, they decreased with time. Conclusions The authors' results indicate that desflurane is associated with a different hemodynamic and catecholamine response compared with sevoflurane when administered into the oxygenator's gas supply line during CPB.

Does Spinal Anesthesia Result in a More Complete Sympathetic Block Than That from Epidural Anesthesia?

1995 ◽  
Vol 82 (4) ◽  
pp. 877-883. ◽  
Author(s):  
Rom A. Stevens ◽  
David Beardsley ◽  
J. Lee White ◽  
Tzu-Cheg Kao ◽  
Rod Gantt ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Cardiac Index ◽  
Arterial Pressure ◽  
Spinal Anesthesia ◽  
Epidural Anesthesia ◽  
Conduction Block ◽  
Plasma Catecholamine ◽  
Sympathetic Block ◽  
Plasma Catecholamine Concentrations

Background Spinal and epidural injection of local anesthetics are used to produce sympathetic block to diagnose and treat certain chronic pain syndromes. It is not clear whether either form of regional anesthesia produces a complete sympathetic block. Spinal anesthesia using tetracaine has been reported to produce a decrease in plasma catecholamine concentrations. This has not been demonstrated for epidural anesthesia in humans with level of anesthesia below C8. One possible explanation is that spinal anesthesia results in a more complete sympathetic block than epidural anesthesia. To examine this question, a cross-over study was performed in young, healthy volunteers. Methods Ten subjects underwent both spinal and epidural anesthesia with lidocaine (plain) on the same day with complete recovery between blocks. By random assignment, spinal anesthesia and epidural anesthesia were induced via lumbar injection. Before and 30 min after local anesthetic injection, a cold pressor test (CPT) was performed. Blood was obtained to determine epinephrine and norepinephrine plasma concentrations at four stages: (1) 20 min after placing peripheral catheters, (2) at the end of a 2-min CPT (before conduction block), (3) 30 min after injection of epidural or spinal lidocaine, and (4) at the end of a second CPT (during anesthesia). Mean arterial pressure, heart rate, noninvasive cardiac index, and analgesia to pin-prick were monitored. Results Neither spinal nor epidural anesthesia changed baseline resting values of catecholamines or any hemodynamic variable, except heart rate, which was slightly decreased during spinal anesthesia. Median level of analgesia was T4 during spinal and T3 during epidural anesthesia. CPT before conduction block reliably increased heart rate, mean arterial pressure, cardiac index, epinephrine, and norepinephrine. Conduction block attenuated the increase in response to CPT only in mean arterial pressure (spinal and epidural) and cardiac index (spinal only). Neither technique blocked the increase in heart rate, norepinephrine, or epinephrine to CPT. Conclusions Spinal anesthesia did not result in a more complete attenuation of the sympathetic response to a CPT than did epidural anesthesia. In response to the CPT, spinal anesthesia blocked the increase in cardiac index, and epidural anesthesia resulted in a decrease in total peripheral resistance compared to the pre-anesthesia state. The differences between the techniques are not significant and are of uncertain clinical implications.

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