Effect of endorphins on heart rate and blood pressure in adult dogs

1986 ◽  
Vol 250 (5) ◽  
pp. H796-H805 ◽  
Author(s):  
G. G. Haddad ◽  
H. J. Jeng ◽  
T. L. Lai
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Opioid Receptor ◽  
Time Course ◽  
Marked Change ◽  
Cardiovascular Function ◽  
Base Line ◽  
Mu Opioid ◽  
Arterial Blood ◽  
Mu Agonists

To investigate the role of opioids in regulating cardiovascular function, we administered delta-opioid receptor agonists D-Ala-D-Leu enkephalin (DADLE) and D-Ala-Met enkephalinamide (DAME), and mu-opioid receptor agonist, a morphiceptin analogue (MA), intracisternally in 13 unanesthetized, chronically instrumented adult dogs in 2 doses (25 and 125 micrograms/kg). After an initial transient drop, the R-R interval increased (peak approximately 25–60 min) postadministration of opioids. The time course and the magnitude of the change in R-R interval depended on the agonist: delta-agonists induced a more prolonged and marked change in R-R interval than mu-agonists at both doses. Mean arterial blood pressure (MAP) increased initially but dropped toward or even below base line 30 min after opioids administration. Atropine, given intravenously or intra-arterially at peak action of agonist in relatively low doses (0.02 mg/kg), induced an AV block followed by a marked decrease in R-R interval. There was also an increase in MAP after atropine. Naloxone, given intracisternally, reversed both delta- and mu-opioid effects but did not induce changes in the R-R interval without prior administration of opioids. We conclude that in unanesthetized adult dogs 1) both mu- and delta-receptor opioid agonists prolong the R-R interval, and this depends on the type of receptor stimulated; 2) opioids induce slowing in heart rate, possibly by increasing parasympathetic activity to the heart; 3) enkephalin and morphiceptin analogues induce a biphasic response in MAP; and 4) endorphins do not modulate cardiovascular function tonically; we speculate that they can alter the R-R interval and MAP in the presence of stimuli.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

Sympathetic Neural Activation Evoked by μ-Receptor Blockade in Patients Addicted to Opioids Is Abolished by Intravenous Clonidine

2002 ◽  
Vol 96 (2) ◽  
pp. 346-351 ◽  
Author(s):  
Peter Kienbaum ◽  
Thorsten Heuter ◽  
Martin C. Michel ◽  
Norbert Scherbaum ◽  
Markus Gastpar ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Opioid Receptor ◽  
Sympathetic Activity ◽  
Plasma Concentrations ◽  
Mu Opioid Receptor ◽  
Receptor Blockade ◽  
Mu Opioid ◽  
Arterial Blood ◽  
Adrenoceptor Agonist ◽  
Alpha2 Adrenoceptor

Background Mu-opioid receptor blockade by naloxone administered for acute detoxification in patients addicted to opioids markedly increases catecholamine plasma concentrations, muscle sympathetic activity (MSA), and is associated with cardiovascular stimulation despite general anesthesia. The current authors tested the hypothesis that the alpha2-adrenoceptor agonist clonidine (1) attenuates increased MSA during mu-opioid receptor blockade for detoxification, and (2) prevents cardiovascular activation when given before detoxification. Methods Fourteen mono-opioid addicted patients received naloxone during propofol anesthesia. Clonidine (10 microg x kg(-1) administered over 5 min + 5 microg x kg(-1) x h(-1) intravenous) was infused either before (n = 6) or after (n = 6) naloxone administration. Two patients without immediate clonidine administration occurring after naloxone administration served as time controls. Muscle sympathetic activity (n = 8) in the peroneal nerve, catecholamine plasma concentrations (n = 14), arterial blood pressure, and heart rate were assessed in awake patients, during propofol anesthesia before and after mu-opioid receptor blockade, and after clonidine administration. Results Mu-receptor blockade markedly increased MSA from a low activity (burst frequency: from 2 burst/min +/- 1 to 24 +/- 8, means +/- SD). Similarly, norepinephrine (41 pg/ml +/- 37 to 321 +/- 134) and epinephrine plasma concentration (13 pg/ml +/- 6 to 627 +/- 146) significantly increased, and were associated with, increased arterial blood pressure and heart rate. Clonidine immediately abolished both increased MSA (P < 0.001) and catecholamine plasma concentrations (P < 0.001). When clonidine was given before mu-opioid receptor blockade, catecholamine plasma concentrations and hemodynamic variables did not change. Conclusions Administration of the alpha2-adrenoceptor agonist clonidine decreases both increased MSA and catecholamine plasma concentrations observed after mu-opioid receptor blockade for detoxification. Furthermore, clonidine pretreatment prevents the increase in catecholamine plasma concentration that otherwise occurs during mu-opioid receptor blockade.

scholarly journals High fructose corn syrup supplementation progressively increased serum adenosine and inosine: Inosine raising blood pressure and heart rate in rats

2021 ◽  
Vol 31 ◽  
pp. 1-9
Author(s):  
Rafael Villalobos-Molina
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Wistar Rats ◽  
Cardiovascular Function ◽  
High Fructose Corn Syrup ◽  
Long Term Effects ◽  
Corn Syrup ◽  
Arterial Blood ◽  
High Fructose

High fructose corn syrup (HFCS) over-consumption underlies the obesity worldwide epidemics. Hepatic fructose metabolism includes fructolysis, lipogenesis, and purines degradation to uric acid. The aim of this study was to evaluate HFCS long-term effects on serum and hepatic adenosine (Ado) and inosine (Ino), as well as in vivo Ino effects on cardiovascular function. Fed male Wistar rats were subjected to 30% HFCS-enriched drinking water for five months (n = 15); every month, nucleosides were determined in serum and in isolated liver perfusate. Three months-old male naive Wistar rats were pithed and cannulated to record blood pressure and heart rate after Ino administration (n = 3). Rats consuming HFCS increased both Ado and Ino progressively in serum and livers’ perfusate; Ino increased cardiovascular function. The progressive Ado and Ino hepatic release by fructose-enriched diet suggests their contribution to raise glycemia through their gluconeogenic activation, and a higher serum Ino concentration might be related to increase in arterial blood pressure.

Epicardial serotonin receptors in circulatory control in conscious Sprague-Dawley rats

1990 ◽  
Vol 258 (2) ◽  
pp. H466-H472 ◽  
Author(s):  
R. Veelken ◽  
L. L. Sawin ◽  
G. F. DiBona
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Time Course ◽  
Isotonic Saline ◽  
Vagal Afferents ◽  
Right Atrial ◽  
Neural Pathways ◽  
Mdl 72222 ◽  
Arterial Blood ◽  
Dose Dependent

To investigate cardiac chemoreceptors in rats a catheter was chronically implanted into the pericardial sac via the thymus. Intrapericardial (ipc) injection of 200 microliters isotonic saline vehicle did not alter arterial blood pressure, heart rate, right atrial pressure, or respiratory rate. Phenyl biguanide (PBG) and nicotine (NIC) were injected into the pericardial sac. In intact rats anesthetized with methohexital sodium, 90 micrograms PBG ipc decreased blood pressure (BP), heart rate (HR), and renal nerve activity (RNA), whereas 300 micrograms NIC ipc increased BP and decreased HR and RNA. Sinoaortic baroreceptor denervation (SAD) did not affect the responses to PBG and abolished only the HR response to NIC. When vagotomy was added to SAD, all responses to intrapericardial PBG were abolished, but the increase in BP and decrease in RNA resulting from intrapericardial NIC persisted. In SAD rats anesthetized with methohexital, PBG produced dose-dependent decreases in BP and RNA, whereas NIC produced dose-dependent increases in BP and decreases in RNA; the serotonin (5-HT3) antagonist MDL 72222 (80 micrograms ipc) abolished the responses to PBG but not to NIC. MDL 72222 inhibited BP and RNA responses to PBG to a similar extent in conscious and anesthetized SAD rats. Anesthesia attenuated the magnitude and time course of BP and RNA responses to PBG compared with the conscious state. In conclusion, 1) sympathoinhibitory responses to intrapericardial PBG and NIC are mediated by epicardial receptors with different afferent neural pathways, PBG by cardiac vagal afferents and NIC by nonvagal, possibly cardiac sympathetic afferents; 2) PBG exerts its effects via epicardial 5-HT3 receptors; 3) anesthesia attenuates the responses to PBG.

Aging, opioid-receptor agonists and antagonists, and the vestibulosympathetic reflex in humans

2004 ◽  
Vol 96 (5) ◽  
pp. 1761-1766 ◽  
Author(s):  
Chester A. Ray ◽  
Kevin D. Monahan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Opioid Receptor ◽  
Muscle Sympathetic Nerve Activity ◽  
Endogenous Opioids ◽  
Arterial Blood ◽  
Before And After ◽  
Vestibulosympathetic Reflex ◽  
Older Subjects

Animal studies indicate that opioids inhibit the firing rate of vestibular neurons, which are important in mediating the vestibulosympathetic reflex. Furthermore, this inhibition appears to be greater in more mature rats. In the present study, we tested the hypotheses that opioids inhibit the vestibulosympathetic reflex in humans and that endogenous opioids contribute to the age-related impairment of the vestibulosympathetic reflex. These hypotheses were tested by measuring muscle sympathetic nerve activity (MSNA), arterial blood pressure, and heart rate responses to otolith organ engagement during head-down rotation (HDR) in young (24 ± 2 yr old) and older (63 ± 2 yr) subjects before and after administration of either an opioid-receptor antagonist (16 mg naloxone in 9 young and 8 older subjects) or an opioid-receptor agonist (60 mg codeine in 7 young and 7 older subjects). Naloxone did not augment the reflex increase in MSNA during HDR in young (Δ7 ± 2 vs. Δ4 ± 2 bursts/min and Δ81 ± 23 vs. Δ60 ± 24% change in burst frequency and total MSNA before and after naloxone, respectively) or older subjects (Δ2 ± 2 vs. Δ1 ± 2 burst/min and Δ8 ± 7 vs. Δ8 ± 9% before and after naloxone). Similarly, codeine did not attenuate the increase in MSNA during HDR in young (Δ8 ± 1 vs. Δ7 ± 2 bursts/min and Δ53 ± 4 vs. Δ64 ± 16% before and after codeine) or older subjects (Δ6 ± 4 vs. Δ3 ± 3 bursts/min and Δ38 ± 21 vs. Δ33 ± 20%). Mean arterial blood pressure and heart rate responses to HDR were not altered by either naloxone or codeine. These data do not provide experimental support for the concept that opioids modulate the vestibulosympathetic reflex in humans. Moreover, endogenous opioids do not appear to contribute the age-associated impairment of the vestibulosympathetic reflex.

Cardiovascular Function After Spinal Cord Injury

2013 ◽  
Vol 28 (3) ◽  
pp. 219-229 ◽  
Author(s):  
Henrike J. C. (Rianne) Ravensbergen ◽  
Sonja de Groot ◽  
Marcel W. M. Post ◽  
Hans J. Slootman ◽  
Lucas H. V. van der Woude ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Spinal Cord Injury ◽  
Autonomic Dysfunction ◽  
Time Course ◽  
Cardiovascular Function ◽  
Normative Values ◽  
Cord Injury ◽  
Cardiovascular Variables

Background. Autonomic dysfunction after spinal cord injury (SCI) is an under-researched area when compared with motor and sensory dysfunction. Cardiovascular autonomic dysfunction is a particular concern, leading to impaired control of blood pressure and heart rate. Objectives. (1) To determine the prevalence of hypotension in individuals with SCI during and after rehabilitation; (2) To investigate changes in cardiovascular variables during and after rehabilitation; (3) To evaluate the influence of personal and lesion characteristics on cardiovascular variables. Methods. Cardiovascular variables (resting systolic [SAP] and diastolic [DAP] arterial pressures and resting [HRrest] and peak heart rates [HRpeak]) were measured on 5 test occasions: start of inpatient rehabilitation, 3 months later, at discharge, and at 1 and 5 years after discharge. The time course and effects of personal and lesion characteristics on cardiovascular variables were studied using multilevel regression analyses. Results. The prevalence of hypotension was unchanged during rehabilitation and for 5 years after discharge. Odds for hypotension were highest in those with cervical and high thoracic lesions, younger individuals, and men. DAP increased during the 5 years after discharge. HRrest decreased during and after rehabilitation. SAP, DAP, HRrest, and HRpeak were lowest in those with cervical and high thoracic lesions. SAP and DAP increased with age; HRpeak decreased with age. Conclusions. These longitudinal data provide normative values for blood pressure and heart rate changes with time after injury according to lesion and personal characteristics. These results can be used to guide clinical practice and place changes in cardiovascular function caused by interventions in perspective.

Sustained Arterial Blood Pressure Elevation Associated with Pneumothoraces: Early Detection via Continuous Monitoring

PEDIATRICS ◽  
1981 ◽  
Vol 68 (6) ◽  
pp. 775-777
Author(s):  
Ronald N. Goldberg
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Continuous Monitoring ◽  
Clinical Signs ◽  
Vital Signs ◽  
Blood Gases ◽  
Base Line ◽  
Blood Pressure Elevation ◽  
Arterial Blood

The diagnosis of pneumothorax in the neonate is often heralded by such signs as deterioration of arterial blood gases, arterial hypotension, and cardiac arrest. An awareness of more subtle clinical signs of accumulating extra-alveolar gas may lead to earlier intervention and a decrease in morbidity. Fourteen episodes of pneumothorax developed in seven of 69 neonates who received ventilatory assistance (mean birth weight 1,828 ± 295 gm), of whom six were ventilated for hyaline membrane disease and one for pneumonia. Instantaneous heart rate and arterial blood pressure (ABP) were monitored continuously in all patients. Changes in vital signs were noted at a mean of 48 minutes (range 12 to 116 minutes) prior to thoracentesis. There was an increase in systolic ABP (7 to 26 mm Hg) associated with 70% of the episodes, and an increase in heart rate and pulse pressure associated with 57% of the episodes. By 20 minutes after thoracentesis there was a rapid decrease in ABP values toward levels not significantly different from base line. A sustained increase in ABP may be an early sign of accumulating extra-alveolar gas. Continuous monitoring and graphic representation of vital signs in the ventilated neonate may suggest the diagnosis of pneumothorax before clinical decompensation occurs.

Acute hypoxemia stimulates atrial natriuretic factor secretion in vivo

1988 ◽  
Vol 255 (2) ◽  
pp. H295-H300 ◽  
Author(s):  
A. J. Baertschi ◽  
J. M. Adams ◽  
M. P. Sullivan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Atrial Natriuretic Factor ◽  
Minute Ventilation ◽  
Base Line ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Arterial Po2

The hypothesis was tested that acute hypoxemia may be a physiological stimulus for atrial natriuretic factor (ANF) secretion in anesthetized, spontaneously breathing rabbits. Base-line plasma ANF (range from 29.8 to 219 pg/ml; mean +/- SE = 87.0 +/- 14.1 pg/ml; n = 16 rabbits) was negatively correlated with base-line arterial PO2 (r = -0.759; P less than 0.01) but not with PCO2, pH, mean arterial blood pressure, central venous pressure (CVP), minute ventilation, heart rate, or type of anesthetics used. Acute hypoxemia (arterial PO2 22.3-44.3 mmHg) lasting 10 min increased plasma ANF levels over base line by 69.2 +/- 47.7 (SE) pg/ml at 6 min and 87.5 +/- 46.8 (SE) pg/ml at 9 min (P less than 0.01; n = 9). The increase in arterial pH and minute ventilation and the decrease of arterial PCO2 paralleled the changes in plasma ANF. Mean arterial blood pressure, CVP, and heart rate did not change significantly. ANF responses to hypoxemia (range from 4.4 to 423 pg/ml) correlated with base-line CVP (r = 0.761; P less than 0.01) and base-line ANF (r = 0.523; P less than 0.05) but with no other measured variable. Although the mediators of hypoxemia-induced release of ANF need to be explored further, this study raises the possibility that ANF might be involved in the adaptation to hypoxemia.

Compression Stocking Length Effects on Arterial Blood Pressure and Heart Rate Following Head-Up Tilt in Healthy Volunteers

2014 ◽  
Vol 63 (6) ◽  
pp. 435-438 ◽  
Author(s):  
Kunihiko Tanaka ◽  
Shiori Tokumiya ◽  
Yumiko Ishihara ◽  
Yumiko Kohira ◽  
Tetsuro Katafuchi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Volunteers ◽  
Arterial Blood Pressure ◽  
Compression Stocking ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Length Effects
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