Effect of indomethacin on the pressor responses to sustained isometric contraction in humans

1993 ◽  
Vol 75 (1) ◽  
pp. 273-278 ◽  
Author(s):  
K. P. Davy ◽  
W. G. Herbert ◽  
J. H. Williams
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Plasma Norepinephrine ◽  
Isometric Handgrip ◽  
Double Blind ◽  
Muscle Ischemia ◽  
Stimulation Of

The purpose of this study was to test the hypothesis that prostaglandins participate in metaboreceptor stimulation of the pressor response to sustained isometric handgrip contraction in humans. To accomplish this, mean arterial pressure, heart rate (n = 10), and plasma norepinephrine levels (n = 8) were measured in healthy male subjects during sustained isometric handgrip at 40% of maximal voluntary contraction force to exhaustion and during a period of postcontraction muscle ischemia. The subjects were given a double-blind and counterbalanced administration of placebo or a single 100-mg dose of indomethacin. A period of 1 wk was allowed for systemic clearance of the drug. Mean arterial pressure increased 25 +/- 5 vs. 22 +/- 4 mmHg during the final minute of isometric handgrip contraction and 26 +/- 2 vs. 21 +/- 5 during the last minute of postcontraction muscle ischemia in the placebo vs. the indomethacin trial (P > 0.05), respectively. Heart rate was increased 21 +/- 4 vs. 17 +/- 3 beats/min during the final minute of isometric handgrip contraction in the placebo vs. the indomethacin trial (P > 0.05), respectively, and returned to control values during postcontraction muscle ischemia. Plasma norepinephrine levels increased 343 +/- 89 vs. 289 +/- 89 pg/ml after isometric handgrip contraction and 675 +/- 132 vs. 632 +/- 132 pg/ml after postcontraction muscle ischemia (P > 0.05) in the placebo vs. the indomethacin trial, respectively. These results suggest that prostaglandin inhibition does not significantly modulate muscle contraction-induced stimulation of mean arterial pressure, heart rate, or plasma norepinephrine levels.

Isometric handgrip training reduces arterial pressure at rest without changes in sympathetic nerve activity

2000 ◽  
Vol 279 (1) ◽  
pp. H245-H249 ◽  
Author(s):  
Chester A. Ray ◽  
Dario I. Carrasco
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Muscle Ischemia

The purpose of this study was to determine whether isometric handgrip (IHG) training reduces arterial pressure and whether reductions in muscle sympathetic nerve activity (MSNA) mediate this drop in arterial pressure. Normotensive subjects were assigned to training ( n = 9), sham training ( n = 7), or control ( n = 8) groups. The training protocol consisted of four 3-min bouts of IHG exercise at 30% of maximal voluntary contraction (MVC) separated by 5-min rest periods. Training was performed four times per week for 5 wk. Subjects' resting arterial pressure and heart rate were measured three times on 3 consecutive days before and after training, with resting MSNA (peroneal nerve) recorded on the third day. Additionally, subjects performed IHG exercise at 30% of MVC to fatigue followed by muscle ischemia. In the trained group, resting diastolic (67 ± 1 to 62 ± 1 mmHg) and mean arterial pressure (86 ± 1 to 82 ± 1 mmHg) significantly decreased, whereas systolic arterial pressure (116 ± 3 to 113 ± 2 mmHg), heart rate (67 ± 4 to 66 ± 4 beats/min), and MSNA (14 ± 2 to 15 ± 2 bursts/min) did not significantly change following training. MSNA and cardiovascular responses to exercise and postexercise muscle ischemia were unchanged by training. There were no significant changes in any variables for the sham training and control groups. The results indicate that IHG training is an effective nonpharmacological intervention in lowering arterial pressure.

scholarly journals Human carotid baroreflex during isometric lower arm contraction and ischemia

1998 ◽  
Vol 275 (3) ◽  
pp. H940-H945 ◽  
Author(s):  
Jonas Spaak ◽  
Patrik Sundblad ◽  
Dag Linnarsson
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Response Curve ◽  
Pressor Response ◽  
Response Curves ◽  
Muscle Ischemia ◽  
Carotid Baroreflex ◽  
Neck Chamber ◽  
Human Carotid

Our aim was to determine the roles of somatomotor activation and muscle ischemia for the tachycardia and hypertension of isometric arm contraction. Carotid-cardiac and carotid-mean arterial pressure (MAP) baroreflex response curves were determined in 10 men during rest, during isometric arm contraction at 30% of maximum, and during postcontraction ischemia. Carotid distending pressure (CDP) was changed by applying pressure and suction in a neck chamber. Pressures ranged from +40 to −80 mmHg and were applied repeatedly for 15 s during the three conditions. Maximum slopes and ranges of the response curves did not differ among conditions. The heart rate (HR) curve was shifted to a 14 ± 1.8 (mean ± SE) beats/min higher HR and a 9 ± 5.7 mmHg higher CDP during contraction and to a 14 ± 5.9 mmHg higher CDP during postcontraction ischemia with no change of HR compared with rest. The MAP curve was shifted to a 20 ± 2.8 mmHg higher MAP and to a 18 ± 5.4 mmHg higher CDP during contraction, and the same shifts were recorded during postcontraction ischemia. We conclude that neither somatomotor activation nor muscle ischemia changes the sensitivity of arterial baroreflexes. The upward shift of the MAP response curve, with no shift of the HR response curve during postexercise ischemia, supports the notion of parallel pathways for MAP and HR regulation in which HR responses are entirely caused by somatomotor activation and the pressor response is mainly caused by muscle ischemia.

Direct and reflexive effects of nitric oxide synthase inhibition on blood pressure

2008 ◽  
Vol 294 (1) ◽  
pp. H190-H197 ◽  
Author(s):  
Jill M. Wecht ◽  
Joseph P. Weir ◽  
David S. Goldstein ◽  
Annmarie Krothe-Petroff ◽  
Ann M. Spungen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Nitric Oxide Synthase ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Control Group ◽  
Plasma Norepinephrine ◽  
Oxide Synthase

Direct effects of vasoactive substances on blood pressure can be examined in individuals with tetraplegia due to disruption of descending spinal pathways to sympathetic preganglionic neurons, as cervical lesions interfere with baroreceptor reflex buffering of sympathetic outflow. In this study, we assessed effects of the nitric oxide synthase inhibitor nitro-l-arginine methyl ester (l-NAME) on mean arterial pressure, heart rate, and plasma norepinephrine concentrations in individuals with tetraplegia vs. effects shown in a neurologically intact control group. Seven individuals with tetraplegia and seven age-matched controls received, on separate visits and in the following order, placebo (30 ml normal saline) and 0.5, 1, 2, and 4 mg/kg l-NAME intravenously over 60 min. Supine hemodynamic data were collected, and blood was sampled at the end of each infusion and at 120, 180, and 240 min thereafter. l-NAME increased mean arterial pressure, and the relative increase was greater in the tetraplegia group than in the control group. Heart rate was reduced after l-NAME administration in both groups. l-NAME decreased plasma norepinephrine in the control group but not in the group with tetraplegia. These findings suggest that reflexive sympathoinhibition normally buffers the pressor response to nitric oxide synthase inhibition, an effect that is not evident in individuals with tetraplegia as a result of decentralized sympathetic vasomotor control.

scholarly journals Developmental Changes in Hemodynamic Responses and Cardiovagal Modulation during Isometric Handgrip Exercise

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Bo Fernhall ◽  
Jill A. Kanaley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Isometric Contraction ◽  
Pressor Response ◽  
Reflex Response ◽  
Group Differences ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Pressor Reflex

The purpose of this study was to examine differences in pressor response and cardiovagal modulation during isometric handgrip exercise (IHG) between children and adults. Beat-to-beat heart rate (HR) and blood pressure were measured in 23 prepubertal children and 23 adults at baseline and during IHG. Cardiovagal modulation was quantified by analysis of HR variability. Mean arterial pressure responses to IHG were greater in adults compared to children (P<.05) whereas there were no group differences in HR responses (P>.05). Children had a greater reduction in cardiovagal modulation in response to IHG compared to adults (P<.05). Changes in mean arterial pressure during IHG were correlated with baseline cardiovagal modulation and force produced during isometric contraction (P<.05). In conclusion, differences in pressor reflex response between children and adults cannot be solely explained by differences in autonomic modulation and appear to be associated with factors contributing to the force produced during isometric contraction.

Carotid arterial hemodynamics in response to LBNP in normal subjects: methodological aspects

1995 ◽  
Vol 79 (5) ◽  
pp. 1546-1555 ◽  
Author(s):  
B. Pannier ◽  
M. A. Slama ◽  
G. M. London ◽  
M. E. Safar ◽  
J. L. Cuche
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressure Wave ◽  
Plasma Norepinephrine ◽  
Tensile Forces ◽  
Cyclic Changes ◽  
Carotid Arterial ◽  
Tangential Tension

Pulsatile changes in blood pressure and arterial diameter were studied noninvasively with applanation tonometry and echo-tracking techniques at the sites of the common carotid artery (CCA) and the carotid arterial bulb (CAB) in 12 healthy volunteers. Determinations were performed before and during application of -10 and -40 mmHg lower body negative pressure (LBNP) to investigate noninvasively the tensile forces acting on the CAB. Together with significantly decreased mean arterial pressure, increased heart rate, forearm vascular resistance, and plasma norepinephrine, the -40 mmHg LBNP stimulus produced the following significant changes in CCA and CAB hemodynamics: 1) for the same decrease in mean arterial pressure, a greater decrease in carotid than in brachial pulse pressure was observed (P < 0.01) due to a significant change in pressure wave transmission and in the timing of the carotid backward pressure wave; and 2) a highly significant decrease in pulsatile changes in diameter and tangential tension occurred, with a greater decrease in systolic than in diastolic tangential tension. Subsequently, cyclic tangential tension decreased more substantially than mean tangential tension. The cyclic changes in tension were quite significant after -40 mmHg LBNP but were already observed for mild -10 mmHg LBNP in which mean systemic blood pressure and heart rate were not modified. During -10 and -40 mmHg LBNP, CCA and CAB compliance and distensibility were unchanged. This study provides evidence that the autonomic nervous system activation produced by the LBNP procedure is associated with significant changes in pressure-wave amplification and in cyclic tensile forces acting on the CAB. These changes, which may occur even for mild LBNP, should be taken into account when interpreting results of the LBNP procedure in humans.

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

2014 ◽  
Vol 306 (2) ◽  
pp. H251-H260 ◽  
Author(s):  
Kazuhito Watanabe ◽  
Masashi Ichinose ◽  
Rei Tahara ◽  
Takeshi Nishiyasu
Keyword(s):  
Individual Differences ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Coefficients Of Variation ◽  
Isometric Handgrip Exercise ◽  
Induced Changes

We tested the hypotheses that, in humans, changes in cardiac output (CO) and total peripheral vascular resistance (TPR) occurring in response to isometric handgrip exercise vary considerably among individuals and that those individual differences are related to differences in muscle metaboreflex and arterial baroreflex function. Thirty-nine healthy subjects performed a 1-min isometric handgrip exercise at 50% of maximal voluntary contraction. This was followed by a 4-min postexercise muscle ischemia (PEMI) period to selectively maintain activation of the muscle metaboreflex. All subjects showed increases in arterial pressure during exercise. Interindividual coefficients of variation (CVs) for the changes in CO and TPR between rest and exercise periods (CO: 95.1% and TPR: 87.8%) were more than twofold greater than CVs for changes in mean arterial pressure (39.7%). There was a negative correlation between CO and TPR responses during exercise ( r = −0.751, P < 0.01), but these CO and TPR responses correlated positively with the corresponding responses during PEMI ( r = 0.568 and 0.512, respectively, P < 0.01). The CO response during exercise did not correlate with PEMI-induced changes in an index of cardiac parasympathetic tone and cardiac baroreflex sensitivity. These findings demonstrate that the changes in CO and TPR that occur in response to isometric handgrip exercise vary considerably among individuals and that the two responses have an inverse relationship. They also suggest that individual differences in components of the pressor response are attributable in part to variations in muscle metaboreflex-mediated cardioaccelerator and vasoconstrictor responses.

Differential cardiovascular effects of central clonidine and B-HT 920 in conscious rats

1988 ◽  
Vol 66 (11) ◽  
pp. 1455-1460 ◽  
Author(s):  
Kathryn A. King ◽  
Catherine C. Y. Pang
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Plasma Concentrations ◽  
Cardiovascular Effects ◽  
Plasma Noradrenaline ◽  
Adrenoceptor Agonists ◽  
Noradrenaline And Adrenaline ◽  
Prior Administration

The effect of intracerebroventricular (i.c.v.) injection of the α2-adrenoceptor agonists clonidine and B-HT 920 on mean arterial pressure (MAP), heart rate (HR), and plasma concentrations of noradrenaline and adrenaline was examined in conscious unrestrained rats. The injection of 1.0 μg clonidine significantly decreased MAP and slightly decreased HR. Plasma noradrenaline and adrenaline levels were slightly but not significantly decreased after the injection of 1 μg clonidine. In contrast, the injection of 0.1–10.0 μg B-HT 920 increased MAP and decreased HR. Plasma noradrenaline and adrenaline levels were slightly increased after the injection of the 1- and 10-μg doses. The i.c. v. injection of the α2-antagonist rauwolscine slightly but not significantly increased MAP and plasma noradrenaline and adrenaline levels. The responses to i.c. v. injection of clonidine and B-HT 920 were not changed by prior administration of rauwolscine. Neither the pressor response to B-HT 920 nor the depressor response to clonidine was abolished by rauwolscine, suggesting that neither response was mediated by α2-adrenoceptors.

Cardiorespiratory response patterns to afferent stimulation of muscle nerves in the rabbit

1996 ◽  
Vol 81 (1) ◽  
pp. 266-273 ◽  
Author(s):  
G. Raimondi ◽  
J. M. Legramante ◽  
F. Iellamo ◽  
S. Cassarino ◽  
G. Peruzzi
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Venous Pressure ◽  
Response Patterns ◽  
Central Venous ◽  
Frequency Stimulation ◽  
End Tidal ◽  
Stimulation Of

The aim of this study was to test the hypothesis that stimulation of thin fiber muscle afferents is capable of matching the cardiovascular and ventilatory responses. In 46 anesthetized rabbits, the central end of the gastrocnemius nerves was electrically stimulated at 3 [low-frequency stimulation (LFS)] and 100 Hz [high-frequency stimulation (HFS)]. Intensities up to 200 times motor threshold were used. LFS induced a decrease in both mean arterial pressure (-19.9 +/- 2.9%) and systemic vascular resistance (-23.9 +/- 3.2%) an increase in cardiac output (CO) (6.4 +/- 1.7%), stroke volume (7.3 +/- 3.0%) and pulmonary ventilation (VE) (26.7 +/- 2.3%); heart rate and central venous pressure were not changed significantly. HFS induced an increase in mean arterial pressure (11.1 +/- 4.9%), CO (15.8 +/- 5.4%), stroke volume (13.4 +/- 5.4%), and VE but no significant changes in heart rate, systemic vascular resistance and central venous pressure. In both response patterns, arterial and end-tidal CO2 did not change significantly. The patterns of cardiorespiratory responses to both LFS and HFS were characterized by an increase in Co and VE without concomitant decreases in arterial and end-tidal PCO2 (isocapnic hyperpnea).

Effects of lignocaine on pressor response to laryngoscopy and endotracheal intubation during general anaesthesia in rigid suspension laryngoscopy

2014 ◽  
Vol 129 (1) ◽  
pp. 79-85 ◽  
Author(s):  
I S Kocamanoglu ◽  
S Cengel Kurnaz ◽  
A Tur
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
General Anaesthesia ◽  
Endotracheal Intubation ◽  
Pressor Response ◽  
Physiological Saline ◽  
American Society ◽  
Rate Ratios ◽  
Suspension Laryngoscopy

AbstractObjective:This study aimed to compare the effects of topical and systemic lignocaine on the circulatory response to direct laryngoscopy performed under general anaesthesia.Methods:Ninety-nine patients over 20 years of age, with a physical status of I–II (classified according to the American Society of Anesthesiologists), were randomly allocated to 3 groups. One group received 5 ml of 0.9 per cent physiological saline intravenously, one group received 1.5 mg/kg lignocaine intravenously, and another group received seven puffs of 10 per cent lignocaine aerosol applied topically to the airway. Mean arterial pressures, heart rates and peripheral oxygen saturations were recorded, and changes in mean arterial pressure and heart rate ratios were calculated.Results:Changes in the ratios of mean arterial pressure and heart rate were greater in the saline physiological group than the other groups at 1 minute after intubation. Changes in the ratios of mean arterial pressure (at the same time point) were greater in the topical lignocaine group than in the intravenous lignocaine group, but this finding was not statistically significant.Conclusion:Lignocaine limited the haemodynamic responses to laryngoscopy and endotracheal intubation during general anaesthesia in rigid suspension laryngoscopy.

Stimulation of parabrachial neurons elicits a sympathetically mediated pressor response in cats

1988 ◽  
Vol 255 (6) ◽  
pp. H1349-H1358 ◽  
Author(s):  
J. S. Hade ◽  
S. W. Mifflin ◽  
T. S. Donta ◽  
R. B. Felder
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Electrical Stimulus ◽  
Respiratory Drive ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Low Intensity ◽  
Stimulation Of

We examined the role of the parabrachial neuronal mass in mediating the pressor response to electrical stimulation of parabrachial nucleus (PBN). In anesthetized cats, 100 mM L-glutamate (L-glu) was microinjected into PBN at sites from which low-intensity (25 microA) electrical stimulation evoked a pressor response. Arterial pressure, heart rate, and, in some animals, renal or phrenic nerve activity were monitored. Microinjection of L-glu caused an increase in arterial pressure that was comparable with that elicited by low-intensity electrical stimulation. Electrical stimulation, and to a lesser extent L-glu microinjection, caused an increase in renal sympathetic nerve activity but no significant change in heart rate. No consistent change in central respiratory drive accompanied the pressor response. These responses were preserved after baroreceptor denervation but were blocked by intravenous administration of the alpha-adrenergic receptor antagonist phentolamine. Microinjection into PBN of 2 mM kainic acid, which selectively depolarizes neurons but spares axons, reversibly blocked the arterial pressure and renal nerve responses to the 25-microA electrical stimulus. We conclude that the pressor response elicited by electrical stimulation of PBN in the anesthetized cat is mediated by cellular elements in PBN, not by fibers of passage. Because phentolamine completely blocked the pressor response, we suggest that it is subserved peripherally by sympathetic alpha-adrenergic rather than humoral (e.g., angiotensin, vasopressin) vasoconstrictor mechanisms. Finally, our data indirectly suggest that PBN stimulation may differentially engage efferent components of the sympathetic nervous system to elicit the pressor response.

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