Cardiovascular change and hypothalamic norepinephrine release in response to environmental stress

1993 ◽  
Vol 264 (4) ◽  
pp. R784-R789 ◽  
Author(s):  
T. Nakata ◽  
W. Berard ◽  
E. Kogosov ◽  
N. Alexander
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Environmental Stress ◽  
Dependent Manner ◽  
Norepinephrine Release ◽  
Major Objective ◽  
Pressor Responses ◽  
Cardiovascular Change ◽  
Baseline Values ◽  
Freely Moving

The major objective of this study was to compare the magnitude and duration of cardiovascular (CV) responses to acute environmental stresses with the associated patterns of noradrenergic activity in the paraventricular nucleus (PVN) and posterior nucleus (PH) of the hypothalamus. Simultaneous microdialysis samples of extracellular norepinephrine (NE) were collected at 5-min intervals from PVN and PH and the CV responses were recorded before, during, and for 15 min after acute shaker (cage oscillation) stress or inhalation of ether vapor in freely moving rats. Five minutes of shaker stress, 60 and 150 cycles/min, elicited pressor responses coupled with increases in dialysate NE from both PVN and PH in a frequency-dependent manner. Tachycardia occurred at 150 but not 60 cycles/min. Ten minutes after 60 cycles/min and 15 min after 150 cycles/min, NE efflux in PH was still increased, whereas in PVN it returned to control as had arterial pressure and heart rate. Ether vapor elicited a transient CV response but a continuing efflux of NE in PH and PVN. Urethan anesthesia raised baseline values of dialysate NE in PH and PVN but significantly attenuated cardiovascular and dialysate NE responses to shaker stress. We conclude that acute environmental stress simultaneously elicits CV responses and the efflux of NE from PVN and PH but, during or after stress, CV values may return to control levels while NE efflux remains elevated in PVN and/or PH.

Neurocirculatory consequences of abrupt change in sleep state in humans

1996 ◽  
Vol 80 (5) ◽  
pp. 1627-1636 ◽  
Author(s):  
B. J. Morgan ◽  
D. C. Crabtree ◽  
D. S. Puleo ◽  
M. S. Badr ◽  
F. Toiber ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Intrathoracic Pressure ◽  
Nrem Sleep ◽  
Auditory Stimuli ◽  
Sleep State ◽  
Healthy Humans ◽  
Pressor Responses

The arterial pressure elevations that accompany sleep apneas may be caused by chemoreflex stimulation, negative intrathoracic pressure, and/or arousal. To assess the neurocirculatory effects of arousal alone, we applied graded auditory stimuli during non-rapid-eye-movement (NREM) sleep in eight healthy humans. We measured muscle sympathetic nerve activity (intraneural microelectrodes), electroencephalogram (EEG; C4/A1 and O1/A2), arterial pressure (photoelectric plethysmography), heart rate (electrocardiogram), and stroke volume (impedance cardiography). Auditory stimuli caused abrupt increases in systolic and diastolic pressures (21 +/- 2 and 15 +/- 1 mmHg) and heart rate (11 +/- 2 beats/min). Cardiac output decreased (-10%). Stimuli that produced EEG evidence of arousal evoked one to two large bursts of sympathetic activity (316 +/- 46% of baseline amplitude). Stimuli that did not alter EEG frequency produced smaller but consistent pressor responses even though no sympathetic activation was observed. We conclude that arousal from NREM sleep evokes a pressor response caused by increased peripheral vascular resistance. Increased sympathetic outflow to skeletal muscle may contribute to, but is not required for, this vasoconstriction. The neurocirculatory effects of arousal may augment those caused by asphyxia during episodes of sleep-disordered breathing.

Balanced anesthesia with remifentanil and desflurane: Clinical considerations for dose adjustment in adults

2018 ◽  
Vol 4 (5) ◽  
pp. 305 ◽  
Author(s):  
Ralph Nöst, MD ◽  
Antje Thiel-Ritter, MD ◽  
Stefan Scholz, MD ◽  
Gunter Hempelmann, MD ◽  
Matthias Müller, MD
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Time Course ◽  
Study Groups ◽  
Skin Incision ◽  
Dependent Manner ◽  
Balanced Anesthesia ◽  
Desflurane Concentration ◽  
To Receive

Background: The intraoperative combination of volatile anesthetics with opioids is a well-accepted technique because of its hemodynamic stability and side effects. This study in adults was designed to determine the pharmacodynamic interactions between different dosages of remifentanil and desflurane in response to skin incision.Methods: A total of 60 patients were enrolled in this study. Patients were prospectively randomized to receive 0, 0.1, 0.15, or 0.25 μg/kg/min remifentanil. Anesthesia was induced with remifentanil, propofol, and succinylcholine. Thereafter, a group-specific desflurane concentration was administered using Dixon’s up-and-down technique. After a “wash out” and equilibration period, patients were observed for defense movements up to 1 minute after skin incision. Mean arterial pressure and heart rate were recorded before induction of anesthesia (baseline), at surgical incision, as well as 2 and 4 minutes thereafter. Time until extubation was assessed after stopping desflurane and remifentanil at the end of the surgery.Results: Remifentanil at 0.1, 0.15, or 0.25 μg/kg/min reduced desflurane requirements by 74, 83, and 90 percent, respectively. The time course of mean arterial pressure did not differ between the study groups. However, compared with the group without remifentanil, heart rate was significantly lower in patients receiving 0.15 or 0.25 μg/kg/min remifentanil. No difference between the groups was observed with regard to extubation time.Conclusion: Remifentanil reduces in a dose-dependent manner the desflurane requirements for skin incision without increasing recovery time. An infusion rate higher than 0.1 μg/kg/min results in a significantly decreased heart rate.

Neurons of C1 area mediate cardiovascular responses initiated from ventral medullary surface

1986 ◽  
Vol 250 (5) ◽  
pp. R932-R945 ◽  
Author(s):  
E. E. Benarroch ◽  
A. R. Granata ◽  
D. A. Ruggiero ◽  
D. H. Park ◽  
D. J. Reis
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Ventral Surface ◽  
Aminobutyric Acid ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Pressor Responses ◽  
Ventral Medullary Surface

We sought to establish whether neurons of the C1 area of the rostral ventrolateral medulla (RVL) mediate changes in arterial pressure and heart rate evoked by topical application of drugs to the ventral medullary surface of the rat. Animals were anesthetized, paralyzed, and ventilated. The ventral surface was mapped with L-glutamate, and a restricted zone was identified from which L-glutamate, as well as kainic acid, bicuculline, strychnine, carbachol, or physostigmine, increased arterial pressure and heart rate. The hypertensive effects of carbachol and physostigmine were blocked by previous local application of atropine but not hexamethonium. Application of gamma-aminobutyric acid (GABA) or glycine to this area produced hypotension and bradycardia. Located caudal to the trapezoid bodies and lateral to the pyramids, this area corresponded to points with lowest threshold for pressor responses evoked by electrical stimulation and overlapped the distribution of epinephrine-synthesizing cells of the RVL. Processes arising from these neurons were identified reaching and contacting the ventral surface. Unilateral lesions involving the C1 area or phenylethanolamine-N-methyltransferase-labeled descending axons derived from this area imparied by greater than 70% the response to ipsilateral application of L-glutamate, GABA, or glycine to the ventral surface. We suggest that neurons within the C1 area of RVL adjacent to or including epinephrine cells may mediate cardiovascular changes elicited from a restricted chemosensitive zone of the ventral medullary surface of the rat.

Effects of a novel orally effective V1-receptor antagonist, OPC-21268, on AVP-induced sympathoinhibition

1993 ◽  
Vol 264 (6) ◽  
pp. R1089-R1094
Author(s):  
H. Masaki ◽  
T. Imaizumi ◽  
S. Harada ◽  
M. Momohara ◽  
Y. Hirooka ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiovascular Diseases ◽  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Arginine Vasopressin ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Baseline Values ◽  
Renal Sympathetic

Arginine vasopressin (AVP) plays as important role in control of circulation and may be involved in pathophysiology of cardiovascular diseases. Recently a novel oral V1-receptor antagonist, OPC-21268, has been produced for possible human therapeutic use (Y. Yamamure et al. Science Wash. DC 252: 572-574, 1991). OPC-21268 is a nonpeptide antagonist and inhibits AVP-induced vasoconstriction in rats and humans. In this study, we examined the influence of OPC-21268 on the sympathoinhibitory and bradycardic effects of AVP in conscious rabbits. Before OPC-21268, AVP at doses of 1, 3, 10, and 30 mU/kg decreased renal sympathetic nerve activity (RSNA) by 24 +/- 5, 40 +/- 5, 65 +/- 6 and 86 +/- 5%, respectively, and decreased heart rate from 243 +/- 10 beats/min at control to 232 +/- 11, 221 +/- 10, 197 +/- 9, and 166 +/- 6 beats/min, respectively (n = 12). Oral OPC-21268 at 30 mg/kg (n = 12) and 90 mg/kg (n = 5) did not alter the baseline values of arterial pressure, heart rate, and RSNA. After oral OPC-21268 the decreases in RSNA and heart rate evoked with AVP at graded doses were partially but significantly attenuated (P < 0.01). The attenuation of the AVP-induced decreases in RSNA and heart rate was similar between the two doses of OPC-21268. In another group of rabbits (n = 6), intravenous OPC-21268 at 30 mg/kg almost completely abolished AVP-induced decreases in heart rate and RSNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of cardiac output in the pressor responses to graded muscle ischemia in man

1978 ◽  
Vol 45 (4) ◽  
pp. 574-580 ◽  
Author(s):  
F. Bonde-Petersen ◽  
L. B. Rowell ◽  
R. G. Murray ◽  
G. G. Blomqvist ◽  
R. White ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Conductance ◽  
Total Occlusion ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Leg Exercise

Ten men repeatedly performed leg exercise (100–150 W) for 7 min with 30-min recovery periods interspersed. Both legs were made ischemic by total occlusion (OCCL), first for 3 min immediately after exercise and second for 30 s before exercise ended and 3 min into recovery. In addition legs were occluded for 3 min at rest (seated). OCCL at rest increased mean arterial pressure (MAP) by 9 Torr but did not affect cardiac output (CO) or heart rate (HR). OCCL at the end of exercise significantly raised MAP and HR above control values during 3-min recovery but CO was unaffected. OCCL 30 s before the end of exercise further increased MAP and HR significantly during recovery; MAP, CO, and HR were significantly increased above control values (CO by 2.1 1-min-1) during the 3rd min of recovery. We conclude that a strong reflex from ischemic legs maintains normal or elevated CO during leg OCCL. Thus CO was too high relative to total vascular conductance so that MAP was elevated.

Anesthetic Potency of Remifentanil in Dogs

1996 ◽  
Vol 84 (4) ◽  
pp. 865-872. ◽  
Author(s):  
Luis G. Michelsen ◽  
Markku Salmenpera ◽  
Jr. Hug ◽  
Fania Szlam ◽  
Dirk VanderMeer
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Minimum Alveolar Concentration ◽  
Dependent Manner ◽  
Blood Concentrations ◽  
Remifentanil Infusion ◽  
Constant Rate ◽  
Dose Dependent ◽  
Anesthetic Potency

Background Remifentanil is an opioid that is rapidly inactivated by esterases in blood and tissues. This study examined the anesthetic potency and efficacy of remifentanil in terms of its reduction of enflurane minimum alveolar concentration (MAC) in dogs. Methods Twenty-five dogs were anesthetized with enflurane. One group received incremental infusion rates of remifentanil from 0.055 to 5.5 micrograms x kg(-1). A second group received constant rate infusions of remifentanil of 1.0 micrograms x kg(-1) x min(-1) for 6-8 h. Enflurane MAC was measured before, hourly during remifentanil infusion, and at the end of the experiment after naloxone administration. A third group received alternating infusions of 0.5 and 1.0 micrograms x kg(-1) x min(-1) with MAC determinations made 30 min after each change in the infusion rate. Heart rate, mean arterial pressure, and remifentanil blood concentrations were measured during MAC determinations. Results Enflurane MAC was reduced up to a maximum of 63 +/- 10.4% (mean +/- SD) in a dose-dependent manner by remifentanil infusion. The dose producing a 50% reduction in the enflurane MAC was calculated as 0.72 micrograms x kg(-1)x min(-1) and the corresponding blood concentration was calculated as 9.2 ng/ml. Enflurane MAC reduction remained stable during continuous, constant rate infusions for periods of 6-8 h without any signs of tolerance. Recovery of enflurane MAC to baseline occurred in 30 min (earliest measurement) after stopping the remifentanil infusion. Conclusions Remifentanil is equally efficacious and about half as potent as fentanyl, judging from the blood concentrations causing equivalent reductions in enflurane MAC in the dog. The characteristics of MAC reduction are similar to those of other opioids, including the ceiling effect. Recovery from remifentanil anesthesia is much more rapid than for any other opioid studied to date, especially after continuous infusions maintained for 6 or more h.

Activation of GABAA but not GABAB receptors in the NTSblocked bradycardia of chemoreflex in awake rats

1999 ◽  
Vol 276 (6) ◽  
pp. H1902-H1910 ◽  
Author(s):  
João Carlos Callera ◽  
Leni G. H. Bonagamba ◽  
Anne Nosjean ◽  
Raul Laguzzi ◽  
Benedito H. Machado
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Nucleus Tractus Solitarius ◽  
Pressor Response ◽  
Potassium Cyanide ◽  
Gabab Receptors ◽  
Basal Heart Rate ◽  
Pressor Responses ◽  
Awake Rats

In the present study we analyzed effects of bilateral microinjections of muscimol (a GABAA agonist) and baclofen (a GABAB agonist) into the nucleus tractus solitarius (NTS) on bradycardic and pressor responses to chemoreflex activation (potassium cyanide, 40 μg/rat iv) in awake rats. Bilateral microinjections of muscimol (25 and 50 pmol/50 nl) into the NTS increased baseline mean arterial pressure (MAP): 119 ± 8 vs. 107 ± 2 mmHg ( n = 6) and 121 ± 8 vs. 103 ± 3 mmHg ( n= 6), respectively. Muscimol at 25 pmol/50 nl reduced the bradycardic response to chemoreflex activation 5 min after microinjection; with 50 pmol/50 nl the bradycardic response to chemoreflex activation was reduced 5, 15, 30, and 60 min after microinjection. Neither muscimol dose produced an effect on the pressor response of the chemoreflex. Effects of muscimol (50 pmol/50 nl) on basal MAP and on the bradycardic response of the chemoreflex were prevented by prior microinjection of bicuculline (a GABAA antagonist, 40 pmol/50 nl) into the NTS. Bilateral microinjections of baclofen (12.5 and 25 pmol/50 nl) into the NTS produced an increase in baseline MAP [137 ± 9 vs. 108 ± 4 ( n= 7) and 145 ± 5 vs. 105 ± 2 mmHg ( n = 7), respectively], no changes in basal heart rate, and no effects on the bradycardic response; 25 pmol/50 nl only attenuated the pressor response to chemoreflex activation. The data show that activation of GABAA receptors in the NTS produces a significant reduction in the bradycardic response, whereas activation of GABAB receptors produces a significant reduction in the pressor response of the chemoreflex. We conclude that 1) GABAA but not GABAB plays an inhibitory role in neurons of the lateral commissural NTS involved in the parasympathetic component of the chemoreflex and 2) attenuation of the pressor response of the chemoreflex by activation of GABAB receptors may be due to inhibition of sympathoexcitatory neurons in the NTS or may be secondary to the large increase in baseline MAP produced by baclofen.

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog

1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Plasma Angiotensin

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.

Activation of 5-HT1A receptors in the medullary raphe reduces cardiovascular changes elicited by acute psychological and inflammatory stresses in rabbits

2005 ◽  
Vol 289 (2) ◽  
pp. R596-R604 ◽  
Author(s):  
Eugene Nalivaiko ◽  
Youichirou Ootsuka ◽  
William W. Blessing
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Beta Blockers ◽  
Drug Effects ◽  
Dependent Manner ◽  
Cardiovascular Changes ◽  
Air Jet ◽  
Medullary Raphe ◽  
Stressful Stimulation ◽  
The Brain

The present strategy for the prevention of excessive sympathetic neural traffic to the heart relies on the use of beta-blockers, drugs that act at the heart end of the brain-heart axis. In the present study, we attempted to suppress cardiac sympathetic nerve activity by affecting the relevant cardiomotoneurons in the brain using the selective serotonin-1A (5-HT1A) receptor agonist 8-hydroxy-2-(di- n-propylamino)tetralin (8-OH-DPAT). In conscious, unrestrained rabbits, instrumented for recordings of heart rate, arterial pressure, or cardiac output, we provoked increases in cardiac sympathetic activity by psychological (loud sound, pinprick, and air jet) or inflammatory (0.5 μg/kg iv lipopolysaccharide) stresses. Pinprick and air-jet stresses elicited transient increases in heart rate (+50 ± 7 and +38 ± 4 beats/min, respectively) and in mean arterial pressure (+16 ± 2 and +15 ± 3 mmHg, respectively). Lipopolysaccharide injection caused sustained increases in heart rate (from 210 ± 3 to 268 ± 10 beats/min) and in arterial pressure (from 74 ± 3 to 92 ± 4 mmHg). Systemically administered 8-OH-DPAT (0.004–0.1 mg/kg) substantially attenuated these responses in a dose-dependent manner. Drug effects were prevented by a selective 5-HT1A receptor antagonist, WAY-100635 (0.1 mg/kg iv). Similarly to systemic administration, microinjection of 8-OH-DPAT (500 nl of 10 mM solution) into the medullary raphe-parapyramidal region caused antitachycardic effects during stressful stimulation and during lipopolysaccharide-elicited tachycardia. This is the first demonstration that activation of 5-HT1A receptors in the medullary raphe-parapyramidal area causes suppression of neurally mediated cardiovascular changes during acute psychological and immune stresses.

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