S  (+)-Ketamine Increases Muscle Sympathetic Activity and Maintains the Neural Response to Hypotensive Challenges in Humans

2001 ◽  
Vol 94 (2) ◽  
pp. 252-258 ◽  
Author(s):  
Peter Kienbaum ◽  
Thorsten Heuter ◽  
Goran Pavlakovic ◽  
Martin C. Michel ◽  
Jürgen Peters
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Concentration ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Arterial Blood Pressure ◽  
Sympathetic Activity ◽  
Sympathetic Outflow ◽  
Arterial Blood ◽  
Ketamine Anesthesia

Background S(+)-Ketamine is reported to exert twofold greater analgesic and hypnotic effects but a shorter recovery time in comparison with racemic ketamine, indicating possible differential effects of stereoisomers. However, cardiovascular regulation during S(+)-ketamine anesthesia has not been studied. Muscle sympathetic activity (MSA) may be an indicator of the underlying alterations of sympathetic outflow. Whether S(+)-ketamine decreases MSA in a similar manner as the racemate is not known. Thus, the authors tested the hypothesis that S(+)-ketamine changes MSA and the muscle sympathetic response to a hypotensive challenge. Methods Muscle sympathetic activity was recorded by microneurography in the peroneal nerve of six healthy participants before and during anesthesia with S(+)-ketamine (670 microg/kg intravenously followed by 15 microg x kg(-1) x min(-1)). Catecholamine and ketamine plasma concentrations, heart rate, and arterial blood pressure were also determined. MSA responses to a hypotensive challenge were assessed by injection of sodium nitroprusside (2-10 microg/kg) before and during S(+)-ketamine anesthesia. In the final step, increased arterial pressure observed during anesthesia with S(+)-ketamine was adjusted to preanesthetic values by sodium nitroprusside infusion (1-6 microg x kg(-1) x min(-1)). Results Anesthesia with S(+)-ketamine (ketamine plasma concentration 713 +/- 295 microg/l) significantly increased MSA burst frequency (mean +/- SD; 18 +/- 6 to 35 +/- 11 bursts/min) and burst incidence (32 +/- 10 to 48 +/- 15 bursts/100 heartbeats) and was associated with a doubling of norepinephrine plasma concentration (from 159 +/- 52 to 373 +/- 136 pg/ml) parallel to the increase in MSA. Heart rate and arterial blood pressure also significantly increased. When increased arterial pressure during S(+)-ketamine was decreased to awake values with sodium nitroprusside, MSA increased further (to 53 +/- 24 bursts/min and 60 +/- 20 bursts/100 heartbeats, respectively). The MSA increase in response to the hypotensive challenge was fully maintained during anesthesia with S(+)-ketamine. Conclusions S(+)-Ketamine increases efferent sympathetic outflow to muscle. Despite increased MSA and arterial pressure during S(+)-ketamine anesthesia, the increase in MSA in response to arterial hypotension is maintained.

Racemic Ketamine Decreases Muscle Sympathetic Activity but Maintains the Neural Response to Hypotensive Challenges in Humans

2000 ◽  
Vol 92 (1) ◽  
pp. 94-94 ◽  
Author(s):  
Peter Kienbaum ◽  
Thorsten Heuter ◽  
Martin C. Michel ◽  
Jürgen Peters
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sodium Nitroprusside ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Plasma Concentrations ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Ketamine Anesthesia ◽  
Racemic Ketamine

Background Cardiovascular stimulation and increased catecholamine plasma concentrations during ketamine anesthesia have been attributed to increased central sympathetic activity as well as catecholamine reuptake inhibition in various experimental models. However, direct recordings of efferent sympathetic nerve activity have not been performed in humans. The authors tested the hypothesis that racemic ketamine increases efferent muscle sympathetic activity (MSA) and maintains the muscle sympathetic response to hypotensive challenges. Methods Muscle sympathetic activity was recorded by microneurography in the peroneal nerve of six healthy subjects before and during anesthesia with racemic ketamine (2 mg/kg intravenously plus 30 microg x kg(-1) x min(-1)). Catecholamine plasma concentrations, heart rate, and blood pressure were also determined. Muscle sympathetic neural responses to a hypotensive challenge were assessed by injection of sodium nitroprusside (2-10 microg/kg) before and during ketamine anesthesia. In the final step, increased arterial pressure observed during ketamine anesthesia was adjusted to preanesthetic baseline by sodium nitroprusside infusion (1-6 microg x kg(-1) x min(-1)). Results Ketamine significantly decreased MSA burst frequency (mean +/- SD, 18 +/- 9 bursts/min to 9 +/- 8 bursts/min) and burst incidence (26 +/- 11 bursts/100 heart beats to 9 +/- 6 bursts/100 heart beats). However, when increased mean arterial pressure (85 +/- 8 mmHg to 121 +/- 20 mmHg) was normalized to the awake baseline by sodium nitroprusside, MSA recovered (25 +/- 18 bursts/min; 23 +/- 14 bursts/100 heart beats). During ketamine anesthesia, both epinephrine (15 +/- 10 pg/ml to 256 +/- 193 pg/ml) and norepinephrine (250 +/- 105 pg/ml to 570 +/- 270 pg/ml) plasma concentrations significantly increased, as did heart rate (67 +/- 13 beats/min to 113 +/- 15 beats/min). Hypotensive challenges similarly increased MSA both in the awake state and during ketamine anesthesia. Conclusions During increased arterial blood pressure associated with ketamine, sympathetic discharge to muscle blood vessels decreases at the same time that plasma concentrations of norepinephrine increase. When this increase in arterial blood pressure is reversed, MSA during ketamine is not changed from preketamine baseline recordings. Finally, hypotensive challenges still evoke an unchanged sympathetic reflex response. Thus, our results do not support the assumption that ketamine anesthesia increases sympathetic nerve activity in a generalized fashion.

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.

Baroreceptor reflex control of heart rate in rats studied by induced and autogenic changes in arterial pressure

2005 ◽  
Vol 288 (5) ◽  
pp. H2422-H2430 ◽  
Author(s):  
Julia A. Moffitt ◽  
Angela J. Grippo ◽  
Alan Kim Johnson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Surgical Stress ◽  
Pressure Fluctuations ◽  
Pulse Interval ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Sequence Method

The function of the arterial baroreflex has traditionally been assessed by measurement of reflex changes in heart rate (HR) or sympathetic nerve activity resulting from experimenter-induced manipulation of arterial blood pressure (the Oxford method, also termed the pharmacological method). However, logistical and flexibility limitations of this technique have promoted the development of new methods for assessing baroreflex function such as the evaluation of changes in spontaneous arterial pressure and HR. Although this new spontaneous method has been validated in dogs and humans, it has not been rigorously tested in rats. In the present study, the method of correlating spontaneous changes in systolic blood pressure and HR was evaluated in resting, normotensive Sprague-Dawley rats. This technique was found to be neither reliable nor valid under the conditions employed in the present protocol. We also tested a variation of the spontaneous method that evaluates particular sequences of data during which arterial pressure and pulse interval are changing in the same direction for at least three consecutive heartbeats (the sequence method). The sequence method did not provide extra reliability or validity over the spontaneous method. We conclude that due to the restricted range of variability obtained by measuring spontaneous blood pressure fluctuations, the spontaneous and sequence techniques do not provide data that are comparable to the traditional method of assessing HR changes triggered by arterial blood pressure increases and decreases induced by vasoactive drugs. However, it is possible that surgical stress obscured the relationship between blood pressure and HR, and therefore additional studies are needed to determine whether the spontaneous and sequence methods can be applied to rats during different behavioral states.

Cardiac- and noncardiac-related coherence between sympathetic drives to muscles of different human limbs

1999 ◽  
Vol 276 (6) ◽  
pp. R1608-R1616 ◽  
Author(s):  
Bernat Kocsis ◽  
Tomas Karlsson ◽  
B. Gunnar Wallin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Activity ◽  
Partial Coherence ◽  
Coherence Analysis ◽  
Sympathetic Outflow ◽  
Related Factors ◽  
Arterial Blood ◽  
The Common ◽  
Resting Muscle

Partial coherence analysis was used to evaluate the extent to which coherence between resting muscle sympathetic activity (MSA) in different pairs of limbs in humans is explained by the common baroreceptor input and by other noncardiac-related factors. Multiunit MSA in two or three nerves, arterial blood pressure, and electrocardiogram were recorded simultaneously. Correlated MSA consisted of a sharp periodic component at the heart rate and a wideband component of relatively low power distributed between 0 and 2–2.5 Hz. Quantitative analysis revealed stronger coupling between MSAs in close limbs than in distant limbs (peak coherence leg-leg, 0.94 ± 0.03; arm-leg, 0.76 ± 0.11). Furthermore, the wideband component, unaffected by partialization with circulatory signals, was significantly stronger between leg-leg (0.67 ± 0.10) than between arm-leg pairs (0.29 ± 0.10), i.e., noncardiac-related components explained 71% of leg-leg and 38% of arm-leg coherences at the frequency of the heart. Our results indicate that nonuniform relationship exists between resting sympathetic outflow to muscles in close and distant extremities which is, however, partially masked by the effect of the common rhythmic baroreceptor input.

Regulation of arterial blood pressure in the common green iguana

1975 ◽  
Vol 228 (2) ◽  
pp. 386-391 ◽  
Author(s):  
LA Hohnke
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Carotid Arterial

Arterial blood pressure (ABP) responses to graded hemorrhage and passive head-up tilt were studied in restrained, anesthetized, and unanesthetized iguanas. The ABP fell slowly in response to hemorrhage up to a critical deficit of 35 plus or minus 19% of the estimated blood volume; the rate of ABP fall then increased nearly 40-fold to continued hemorrhage. Increased heart rate and decreased femoral arterial blood flow accompanied progressive hemorrhage. Propranolol (2-3 mug/kg) did not appreciably alter arterial pressure-hemorrhage curves but hemorrhage-induced increases in heart rate were diminished nearly 50%. Atropine had little effect on either the blood pressure or heart rate changes induced by hemorrhage. During passive tilts of 0-90 degrees carotid arterial pressure fell 33% before returning to control levels (2 min). Heart rate increased and femoral arterial blood flow and central venous pressure fell in response to head-up tilts. It is concluded that hemorrhage and passive head-up tilting can induce reflex cardiovascular changes that assist ABP regulation in iguanas.

Responses of ACTH, epinephrine, norepinephrine, and cardiovascular system to hemorrhage

1986 ◽  
Vol 251 (3) ◽  
pp. H612-H618 ◽  
Author(s):  
D. N. Darlington ◽  
J. Shinsako ◽  
M. F. Dallman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Random Order ◽  
Plasma Acth ◽  
Arterial Blood ◽  
The Relationship ◽  
Subsequent Rise

Hemorrhages of various magnitudes were performed on conscious rats, and arterial pressure, heart rate, and plasma levels of adrenocorticotropin hormone (ACTH), epinephrine, and norepinephrine were measured. Eight rats were prepared with chronic femoral arterial cannulas and received a 10, 15, or 20 ml/kg X 3 min hemorrhage in random order on day 4, 7, or 10 after surgery. Mean arterial blood pressure, heart rate, and plasma ACTH, epinephrine, and norepinephrine concentrations were determined before and 20 min after hemorrhage. Arterial blood pressure decreased significantly immediately after each hemorrhage and slowly recovered over the next 20 min. Heart rate did not change during the 10 ml/kg X 3 min hemorrhage but decreased significantly after 15 and 20 ml/kg X 3 min hemorrhages. Plasma ACTH and epinephrine levels increased significantly 20 min after the 15 and 20 ml/kg X 3 min hemorrhages but not after 10 ml/kg X 3 min hemorrhage. Norepinephrine increased significantly 20 min after the 20 ml/kg X 3 min hemorrhage but not after the 10 or 15 ml/kg X 3 min hemorrhage. There was no significant effect of time and repeated hemorrhages on resting levels of plasma ACTH, epinephrine, norepinephrine, osmolality, or proteins. Since hemorrhage leads to a fall in arterial pressure and a subsequent rise in plasma ACTH, the relationship between plasma ACTH and mean arterial blood pressure during hemorrhage was examined in both conscious and acutely prepared pentobarbital sodium-anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

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