Effects of combined histamine H1 and H2 receptor blockade on hemodynamic responses to dynamic exercise in males with high-normal blood pressure

2020 ◽  
Vol 45 (7) ◽  
pp. 769-776
Author(s):  
Ashley Naylor ◽  
Brian Shariffi ◽  
Trevor L. Gillum ◽  
Boyer William ◽  
Sean Sullivan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Dynamic Exercise ◽  
Histamine Receptors ◽  
Normal Group ◽  
Receptor Blockade ◽  
Peripheral Vasoconstriction ◽  
Before And After ◽  
Group A ◽  
Postexercise Hypotension ◽  
Response To Exercise

While postexercise hypotension is associated with histamine H1 and H2 receptor-mediated postexercise vasodilation, effects of histaminergic vasodilation on blood pressure (BP) in response to dynamic exercise are not known. Thus, in 20 recreationally active male participants (10 normotensive and 10 with high-normal BP) we examined the effects of histamine H1 and H2 receptor blockade on cardiac output (CO), mean atrial pressure (MAP), aortic stiffness (AoStiff), and total vascular conductance (TVC) at rest and during progressive cycling exercise. Compared with the normotensive group, MAP, CO, and AoStiff were higher in the high-normal group before and after the blockade at rest, while TVC was similar. At the 40% workload, the blockade significantly increased MAP in both groups, while no difference was found in the TVC. CO was higher in the high-normal group than the normotensive group in both conditions. At the 60% workload, the blockade substantially increased MAP and decreased TVC in the normotensive group, while there were no changes in the high-normal group. A similar CO response pattern was observed at the 60% workload. These findings suggest that the mechanism eliciting an exaggerated BP response to exercise in the high-normal group may be partially due to the inability of histamine receptors. Novelty Males with high-normal BP had an exaggerated BP response to exercise. The overactive BP response is known due to an increase in peripheral vasoconstriction. Increase in peripheral vasoconstriction is partially due to inability of histamine receptors.

scholarly journals Postexercise hypotension is mediated by reductions in sympathetic nerve activity

1999 ◽  
Vol 276 (1) ◽  
pp. H27-H32 ◽  
Author(s):  
Jennifer M. Kulics ◽  
Heidi L. Collins ◽  
Stephen E. DiCarlo
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Dynamic Exercise ◽  
Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Before And After ◽  
Postexercise Hypotension ◽  
Carotid Arterial

Mean arterial pressure (MAP), the product of cardiac output (CO) and total peripheral resistance (TPR), is reduced below preexercise levels after a single bout of mild to moderate dynamic exercise. Thus acute, dynamic exercise may be used as a safe, therapeutic approach to reduce MAP. However, the mechanisms responsible for the postexercise hypotension (PEH) are unknown. We tested the hypothesis that PEH is associated with reductions in TPR and sympathetic nerve activity (SNA). Two experimental protocols were designed to test this hypothesis in male spontaneously hypertensive rats (SHR). In protocol 1( n = 9), CO and TPR were determined before, during, and after exercise. In protocol 2 ( n = 7), lumbar SNA (LSNA) was recorded before and after exercise. Rats in protocol 1 were chronically instrumented with left carotid arterial catheters and ascending aortic Doppler ultrasonic flow probes. Rats in protocol 2 were chronically instrumented with left carotid arterial catheters and electrodes around the lumbar sympathetic trunk. Dynamic treadmill exercise (9–12 m/min, 10% grade for 40 min) resulted in a postexercise reduction in MAP (from 143 ± 5 to 128 ± 4 mmHg, P < 0.05). Associated with the PEH was a reduction in TPR (from 28 ± 3 to 19 ± 2 mmHg/kHz; P < 0.05) and an elevation in CO (from 5.7 ± 0.4 to 7.2 ± 0.5 kHz; P < 0.05). The reductions in arterial pressure and TPR were associated with a decrease in LSNA (from 98 ± 3 to 49 ± 6%; P < 0.05). These results suggest that PEH is mediated by reductions in TPR and SNA.

Attenuated arterial baroreflex buffering of muscle metaboreflex in heart failure

2005 ◽  
Vol 289 (6) ◽  
pp. H2416-H2423 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Jaime Rodriguez ◽  
Tadeusz J. Scislo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Before And After ◽  
Chronically Instrumented Dogs

Previous studies have shown that heart failure (HF) or sinoaortic denervation (SAD) alters the strength and mechanisms of the muscle metaboreflex during dynamic exercise. However, it is still unknown to what extent SAD may modify the muscle metaboreflex in HF. Therefore, we quantified the contribution of cardiac output (CO) and peripheral vasoconstriction to metaboreflex-mediated increases in mean arterial blood pressure (MAP) in conscious, chronically instrumented dogs before and after induction of HF in both barointact and SAD conditions during mild and moderate exercise. The muscle metaboreflex was activated via partial reductions in hindlimb blood flow. After SAD, the metaboreflex pressor responses were significantly higher with respect to the barointact condition despite lower CO responses. The pressor response was significantly lower in HF after SAD but still higher than that of HF in the barointact condition. During control experiments in the barointact condition, total vascular conductance summed from all beds except the hindlimbs did not change with muscle metaboreflex activation, whereas in the SAD condition both before and after induction of HF significant vasoconstriction occurred. We conclude that SAD substantially increased the contribution of peripheral vasoconstriction to metaboreflex-induced increases in MAP, whereas in HF SAD did not markedly alter the patterns of the reflex responses, likely reflecting that in HF the ability of the arterial baroreflex to buffer metaboreflex responses is impaired.

Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

2005 ◽  
Vol 288 (3) ◽  
pp. H1374-H1380 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Jaime Rodriguez ◽  
Tadeusz J. Scislo ◽  
Donal S. O'Leary
Keyword(s):  
Pressor Response ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Major Mechanism ◽  
Pressor Responses ◽  
Before And After ◽  
Chronically Instrumented Dogs

Previous studies showed that the arterial baroreflex opposes the pressor response mediated by muscle metaboreflex activation during mild dynamic exercise. However, no studies have investigated the mechanisms contributing to metaboreflex-mediated pressor responses during dynamic exercise after arterial baroreceptor denervation. Therefore, we investigated the contribution of cardiac output (CO) and peripheral vasoconstriction in mediating the pressor response to graded reductions in hindlimb perfusion in conscious, chronically instrumented dogs before and after sinoaortic denervation (SAD) during mild and moderate exercise. In control experiments, the metaboreflex pressor responses were mediated via increases in CO. After SAD, the metaboreflex pressor responses were significantly greater and significantly smaller increases in CO occurred. During control experiments, nonischemic vascular conductance (NIVC) did not change with muscle metaboreflex activation, whereas after SAD NIVC significantly decreased with metaboreflex activation; thus SAD shifted the mechanisms of the muscle metaboreflex from mainly increases in CO to combined cardiac and peripheral vasoconstrictor responses. We conclude that the major mechanism by which the arterial baroreflex buffers the muscle metaboreflex is inhibition of metaboreflex-mediated peripheral vasoconstriction.

Comparison between Salbutamol and Salbutamol with Magnesium Sulphate by nebulization in Treatment of Acute Asthma in Asthmatic Patient

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Galal Adel El kady ◽  
Fady Adeb Abd Elmalek ◽  
Gerges Amine Shahaat
Keyword(s):  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Pulse Rate ◽  
Magnesium Sulphate ◽  
Acute Asthma ◽  
Asthma Exacerbations ◽  
Before And After ◽  
Group A ◽  
Significant Change ◽  
Group B

Abstract Background Asthma exacerbations are acute or subacute episodes of breathlessness, cough, wheezing, and chest tightness, or any combination of these symptoms. Exacerbations are associated with airways obstruction that should be documented and quantified by PEF or FEVI measurement. Early treatment of asthma exacerbations should be the best strategy for management. Objective To compare fast effectiveness between the nebulized salbutamol with normal Saline and salbutamol with magnesium sulphate by nebulizer in treatment of acute asthma. Patients and Methods: This two armed prospective randomized study included 60 patients admitted to Intensive Care Unit, Ain Shams University Hospital from July 2019 to July 2020. Patients were randomized into two equal groups: group A which included 30 patients on salbutamol nebulization and group B that included 30 patients on combination of salbutamol and magnesium sulphate. Results systolic blood pressure, diastolic Bl. P and FEVI were higher among salbutamol group (A) than combination group (B), meanwhile HR and 02% were significantly lower among group A than group B with statistically insignificant differences (p &gt; 0.05). Group A had significantly higher mean of RR (20±1.33) than group B (17.2 ±1.14) (p &lt; 0.001). Also, Group A had significantly higher mean of PEFR (217.5 ±74.72) than group B (125±78.05) (p = 0.014). There were significant differences between in group A in HR and 02% before and after TTT (p &lt; 0.05). With treatment, the pulse rate rose significantly (p = 0.010) but there was no significant change in the systolic or diastolic blood pressure. The 02% rose significantly (p&lt;O.001). There were significant differences between in group B in RR, HR, 02%, PEFR and FEVI before and after TTT (p &lt; 0.05). With treatment, the respiratory rate declined significantly (p &lt; 0.001), the pulse rate declined significantly (p = 0.013) in but there was no significant change in the systolic or diastolic blood pressure. The PEFR rose significantly (p = 0.001) and also the 02% rose significantly (p &lt; 0.001). Conclusion Nebulized MgS04, either alone or combined with salbutamol, has a clinically significant bronchodilator effect in acute asthma. This suggests that a combination of MgS04 and salbutamol may be the best choice for the management of acute exacerbations of asthma.

Hydration Does Not Change Postexercise Hypotension and Its Mechanisms

2020 ◽  
Vol 17 (5) ◽  
pp. 533-539 ◽  
Author(s):  
Fernando S. Lobo ◽  
Andreia C.C. Queiroz ◽  
Natan D. Silva Junior ◽  
Fabio L. Medina ◽  
Luiz A.R. Costa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hypotensive Effect ◽  
Cycle Ergometer ◽  
Autonomic Response ◽  
Previous Night ◽  
Water Ingestion ◽  
Before And After ◽  
Exercise Hemodynamics ◽  
Postexercise Hypotension ◽  
Response Exercise

Background: Drinking water is recommended before and after exercise to avoid dehydration. However, water ingestion may mitigate or prevent postexercise hypotension. This study investigated the effects of intentional hydration on postaerobic exercise hemodynamics and autonomic modulation. Methods: A total of 18 young men randomly underwent 4 experimental sessions as follows: (1) control with intentional hydration (1 L of water in the previous night, 500 mL 60 min before the intervention, and 1 mL for each 1 g of body mass lost immediately after the intervention); (2) control without intentional hydration (ad libitum water ingestion before the intervention); (3) exercise (cycle ergometer, 45 min, 50% of VO2peak) with intentional hydration; and (4) exercise without intentional hydration. Hemodynamic and autonomic parameters were measured before and after the interventions and were compared by 3-way analysis of variance. Results: Intentional hydration did not change any postexercise hemodynamic nor autonomic response. Exercise decreased systolic blood pressure and stroke volume (−4.1 [0.8] mm Hg and −4.9 [1.5] mL, P < .05), while increased cardiac sympathovagal balance (0.3 [0.3], P < .05) during the recovery. In addition, it abolished the increase in diastolic blood pressure and the decrease in heart rate observed in the control sessions. Conclusion: Intentional hydration does not modify the hypotensive effect promoted by previous aerobic exercise and did not alter its hemodynamic and autonomic mechanisms.

Cardiac receptors modulate the renal sympathetic response to dynamic exercise in rabbits

1994 ◽  
Vol 76 (2) ◽  
pp. 507-515 ◽  
Author(s):  
K. P. O'Hagan ◽  
L. B. Bell ◽  
S. W. Mittelstadt ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Peripheral Circulation ◽  
Afferent Input ◽  
Dynamic Exercise ◽  
Vagal Afferents ◽  
Sensory Receptors ◽  
Receptor Block ◽  
Response To Exercise ◽  
Cardiac Receptors ◽  
Renal Sympathetic

Activation of cardiac sensory receptors with vagal afferents can result in inhibition of sympathetic outflow to the peripheral circulation. This study investigated whether the regulation of renal sympathetic nerve activity (RSNA) during dynamic exercise was modulated by cardiac sensory receptors. RSNA, blood pressure, and heart rate were measured in seven New Zealand White rabbits during treadmill exercise while cardiac receptors were intact (saline), during cardiac neural block with 2% procaine (2% PCN), and during cardiac efferent receptor block with methscopolamine and atenolol (M + A). Drugs were infused into the pericardial space via a chronic catheter. Two exercise protocols were used: 7 m/min (5 min) and 12 m/min (2 min) at 0% grade. The increases in HR during exercise at 7 and 12 m/min were attenuated with 2% PCN or M + A. At 12 m/min, blood pressure was significantly lower with 2% PCN (76 +/- 4 mmHg) or M + A (76 +/- 3 mmHg) than with saline (86 +/- 2 mmHg). Abolition of cardiac afferent input with 2% PCN resulted in a potentiated RSNA response to exercise at 7 m/min (+134 +/- 37%) and 12 m/min (+234 +/- 45%) relative to saline (+62 +/- 24 and +101 +/- 28%) or M + A (+19 +/- 9 and +52 +/- 19%, P < 0.05). These results suggest that cardiac sensory receptors attenuate sympathetic drive to the kidney during dynamic exercise in conscious rabbits.

Substantial cardiac parasympathetic activity exists during heavy dynamic exercise in dogs

1997 ◽  
Vol 273 (5) ◽  
pp. H2135-H2140 ◽  
Author(s):  
Donal S. O’Leary ◽  
Noreen F. Rossi ◽  
Paul C. Churchill
Keyword(s):  
Steady State ◽  
Sympathetic Nerves ◽  
Cholinergic Receptor ◽  
Dynamic Exercise ◽  
Aortic Blood Flow ◽  
Receptor Blockade ◽  
Parasympathetic Nerves ◽  
Wide Range ◽  
Before And After ◽  
Β Receptor

We investigated the extent of functional parasympathetic and sympathetic activity to the heart at rest and during mild to heavy dynamic exercise in conscious dogs. The animals were chronically instrumented to monitor mean arterial pressure (MAP), heart rate (HR), and terminal aortic blood flow (TAQ) and trained to run on a motor-driven treadmill. MAP, HR, and TAQ were monitored at rest and during steady-state dynamic exercise ranging from mild [3.2 kilometers per hour (kph), 0% grade] to heavy exercise (8 kph, 15% grade). Experiments were performed before and after blocking the effects of either the parasympathetic nerves (atropine 0.2 mg/kg iv) or sympathetic nerves (atenolol 2.0 mg/kg iv) to the heart. In addition, blood samples were taken at rest and at steady state during exercise, and plasma levels of vasopressin and renin activity were assessed. At rest and during all levels of exercise, muscarinic cholinergic receptor blockade caused a marked increase in HR over control (saline treated) levels with little effect on MAP or TAQ. β-Adrenergic receptor blockade had no significant effect on HR at rest and during mild exercise. At moderate to heavy workloads, β-receptor blockade significantly reduced MAP, HR, and TAQ and increased plasma vasopressin levels. We conclude that, even during heavy dynamic exercise, significant functional parasympathetic tone to the heart exists. Thus, over a wide range of exercise workloads, HR is under the tonic control of both sympathetic and parasympathetic nerves.

Cardiovascular responses to hemorrhage and naloxone in conscious barodenervated rabbits

1986 ◽  
Vol 251 (5) ◽  
pp. R909-R915 ◽  
Author(s):  
J. C. Schadt ◽  
R. R. Gaddis
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Loss ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Plasma Norepinephrine ◽  
Receptor Blockade ◽  
Pressor Effect ◽  
Arterial Blood ◽  
Before And After

The hemodynamic and plasma catecholamine response to hypotensive hemorrhage and subsequent opioid receptor blockade with naloxone were evaluated before and after complete sinoaortic denervation (SAD). This study was done to test the general hypothesis that opioid-mediated failure of the baroreflex accounts for the hypotension of hemorrhage. The specific hypothesis we tested was that SAD would abolish the pressor effect of opioid receptor blockade with naloxone. The studies were done in conscious chronically prepared rabbits. Hemorrhage of 12 ml/kg did not change mean arterial blood pressure in intact animals due to a compensatory increase in heart rate and vascular resistance. When blood loss exceeded 12 ml/kg, pressure decreased abruptly due to a decrease in vascular resistance. Plasma norepinephrine (NE) and epinephrine (E) were higher after hemorrhage than before. Plasma E levels increased almost 70 times. After SAD, mean blood pressure began to decrease at the beginning of hemorrhage, the heart rate increase was abolished, and vascular resistance decreased throughout the blood loss. Plasma NE was no different after hemorrhage than before. Plasma E increased, but the increase was only fivefold. Naloxone increased mean arterial blood pressure, vascular resistance, cardiac index, and plasma NE before and after SAD. The increases in blood pressure and plasma norepinephrine were significantly greater after SAD. Therefore the pressor effect of naloxone in this model is not due to increased baroreflex sensitivity. Rather, intact baroreflexes buffer naloxone's effects.

scholarly journals Local adenosine receptor blockade accentuates the sympathetic responses to fatiguing exercise

2010 ◽  
Vol 298 (6) ◽  
pp. H2130-H2137 ◽  
Author(s):  
Jian Cui ◽  
Urs A. Leuenberger ◽  
Cheryl Blaha ◽  
Jonathan Yoder ◽  
Zhaohui Gao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Adenosine Receptor ◽  
Muscle Sympathetic Nerve Activity ◽  
Receptor Blockade ◽  
Isometric Handgrip ◽  
Before And After ◽  
Fatiguing Exercise ◽  
Blood Pressure Responses ◽  
Bier Block ◽  
Passive Stretch

The role adenosine plays in evoking the exercise pressor reflex in humans remains controversial. We hypothesized that localized forearm adenosine receptor blockade would attenuate muscle sympathetic nerve activity (MSNA) responses to fatiguing handgrip exercise in humans. Blood pressure (Finometer), heart rate, and MSNA from the peroneal nerve were assessed in 11 healthy young volunteers during fatiguing isometric handgrip, postexercise circulatory occlusion (PECO), and passive muscle stretch during PECO. The protocol was performed before and after adenosine receptor blockade by local infusion of 40 mg aminophylline in saline via forearm Bier block (regional intravenous anesthesia). In the second experiment, the same amount of saline was infused via the Bier block. After aminophylline, the MSNA and blood pressure responses to fatiguing handgrip, PECO, and passive stretch (all P < 0.05) were significantly greater than during the control condition. Saline Bier block had no similar effects on the MSNA and blood pressure responses. These data suggest that adenosine receptor antagonism in the exercising muscles may accentuate sympathetic activation during fatiguing exercise.

scholarly journals The Effects of a Multiflavonoid Supplement on Vascular and Hemodynamic Parameters following Acute Exercise

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Rebecca M. Kappus ◽  
Chelsea D. Curry ◽  
Steve McAnulty ◽  
Janice Welsh ◽  
David Morris ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Acute Exercise ◽  
Augmentation Index ◽  
Antioxidant Supplementation ◽  
Cardiovascular Hemodynamics ◽  
Reducing Ability ◽  
Before And After ◽  
Postexercise Hypotension ◽  
Young Subjects

Antioxidants can decrease oxidative stress and combined with acute exercise they may lead to further decreases in blood pressure. The purpose of this study was to investigate the effects of 2 weeks of antioxidant supplementation on vascular distensibility and cardiovascular hemodynamics during postexercise hypotension.Methods. Twenty young subjects were randomized to placebo () or antioxidant supplementation () for two weeks. Antioxidant status, vascular distensibility, and hemodynamics were obtained before, immediately, and 30 minutes after an acute bout of aerobic exercise both before and after supplementation.Results. Two weeks of antioxidant supplementation resulted in a greater systolic blood pressure (SBP) decrease during postexercise hypotension (PEH) and significant decreases in augmentation index versus placebo (12.5% versus 3.5%, resp.). Also ferric-reducing ability of plasma (FRAP) increased significantly (interactionP= 0.024) after supplementation.Conclusion. Supplementation showed an additive effect on PEH associated with increased FRAP values and decreases in systolic blood pressure and augmentation index.

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