scholarly journals Occlusion of the upper airway does not augment the cardiovascular response to arousal from sleep in humans

2005 ◽  
Vol 98 (4) ◽  
pp. 1349-1355 ◽  
Author(s):  
Denise M. O'Driscoll ◽  
Konstantinos Kostikas ◽  
Anita K. Simonds ◽  
Mary J. Morrell
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Upper Airway ◽  
Healthy Men ◽  
Obstructive Apnea ◽  
Airway Occlusion ◽  
Arterial Blood ◽  
Stage 2 Sleep ◽  
Stimulation Of

The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (>10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean ± SE: age, 25 ± 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s ( P < 0.001) and a significant decrease in R-R interval at 3 s ( P < 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 ± 3 to 104 ± 3 mmHg; O, 86 ± 3 to 105 ± 3 mmHg; P = 0.99. R-R interval: C, 1.12 ± 0.03 to 0.89 ± 0.04 s; O, 1.11 ± 0.02 to 0.87 ± 0.02 s, P = 0.99). Ventilation significantly increased during arousals under both conditions at the second breath ( P < 0.001); this increase was not different between the two conditions (C: 4.40 ± 0.29 to 6.76 ± 0.61 l/min, O: 4.35 ± 0.34 to 7.65 ± 0.73 l/min; P = 0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young men.

Cardiovascular response to arousal from sleep under controlled conditions of central and peripheral chemoreceptor stimulation in humans

2004 ◽  
Vol 96 (3) ◽  
pp. 865-870 ◽  
Author(s):  
Denise M. O'Driscoll ◽  
Guy E. Meadows ◽  
Douglas R. Corfield ◽  
Anita K. Simonds ◽  
Mary J. Morrell
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Peripheral Chemoreceptor ◽  
Healthy Men ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia

The cardiovascular response to an arousal occurring at the termination of an obstructive apnea is almost double that to a spontaneous arousal. We investigated the hypothesis that central plus peripheral chemoreceptor stimulation, induced by hypercapnic hypoxia (HH), augments the cardiovascular response to arousal from sleep. Auditory-induced arousals during normoxia and HH (>10-s duration) were analyzed in 13 healthy men [age 24 ± 1 (SE) yr]. Subjects breathed on a respiratory circuit that held arterial blood gases constant, despite the increased ventilation associated with arousal. Arousals were associated with a significant increase in mean arterial blood pressure at 5 s ( P < 0.001) and with a significant decrease in the R-R interval at 3 s ( P < 0.001); however, the magnitude of the changes was not significantly different during normoxia compared with HH (mean arterial blood pressure: normoxia, 91 ± 4 to 106 ± 4 mmHg; HH, 91 ± 4 to 109 ± 5 mmHg; P = 0.32; R-R interval: normoxia, 1.12 ± 0.04 to 1.02 ± 0.05 s; HH, 1.09 ± 0.05 to 0.92 ± 0.04 s; P = 0.78). Mean ventilation increased significantly at the second breath postarousal for both conditions ( P < 0.001), but the increase was not significantly different between the two conditions (normoxia, 5.35 ± 0.40 to 9.57 ± 1.69 l/min; HH, 8.57 ± 0.63 to 11.98 ± 0.70 l/min; P = 0.71). We conclude that combined central and peripheral chemoreceptor stimulation with the use of HH does not interact with the autonomic outflow associated with arousal from sleep to augment the cardiovascular response.

Bradykinin in reflex cardiovascular responses to static muscular contraction

1986 ◽  
Vol 61 (1) ◽  
pp. 271-279 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Time Derivative ◽  
Cardiovascular Responses ◽  
Carboxypeptidase B ◽  
Arterial Blood ◽  
Static Contraction ◽  
Stimulation Of

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3–4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000–30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500–750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Abstract 446: Rostral Ventrolateral Lateral Medulla Mediates the Sympathetic and Cardiovascular Response to Increased Cerebrospinal Fluid Sodium Concentration

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Sean D Stocker
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Lateral Ventricle ◽  
Cardiovascular Response ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Nerve Recordings

Compelling evidence indicates increased cererbrospinal fluid (CSF) sodium elevates sympathetic nerve activity (SNA) and arterial blood pressure (ABP) in salt-sensitive hypertension. RVLM neurons project to the spinal cord and regulate SNA and ABP under a number of physiological challenges and pathophysiological states. Therefore, we hypothesized that RVLM neurons mediate the sympathoexcitatory response to increased CSF sodium. Inactin-anesthetized, male Sprague-Dawley rats (n=5/group) were prepared for sympathetic nerve recordings and a lateral ventricle brain cannula. Infusion of 1M NaCl (5 μL/10 min) to increase CSF sodium concentrations by 5mM produced a significant (P’s<0.05, n=6) increase in lumbar SNA (Δ: 115±3%), adrenal SNA (Δ: 122±3%), and mean arterial blood pressure (Δ: 8±1 mmHg). The infusion did not affect splanchnic SNA (Δ: 102±4%) but decreased renal SNA (Δ: 91±2%). Inhibition of the RVLM with bilateral injection of the GABA agonist muscimol (2.5mM per 50 nL per side) significantly (P’s<0.05; n=5) attenuated the increased lumbar SNA (Δ:101±2%), adrenal SNA (Δ:105±2%), and mean arterial blood pressure (Δ: 1±1mmHg, P’s<0.05; n=6). Blockade of ionotropic glutamate receptors in the RVLM with bilateral injection of kynurenic acid (30mM per 50 nL per side) also significantly (P’s<0.05; n=5) attenuated the increase in lumbar SNA (Δ: 101±3%), adrenal SNA (Δ: 110±3%) and mean ABP (Δ: 1±2 mmHg) to lateral ventricle infusion of 1M NaCl (5uL/10 min). In a final set of experiments, in vivo single-unit recordings demonstrate that ventricular infusion of 1M NaCl (5uL per 10 min) increased discharge in 60% (6/10) of spinally-projecting, barosensitive RVLM neurons (2.1±0.4 to 5.8±0.2 Hz, P<0.05). Infusion of artificial CSF did not affect any variable. These findings suggest increased CSF sodium activates a glutamatergic pathway to RVLM neurons to elevate SNA and ABP.

scholarly journals Role of oral gabapentin in attenuating cardiovascular response to laryngoscopy and tracheal intubation.

2020 ◽  
Vol 27 (07) ◽  
pp. 1470-1475
Author(s):  
Mohsin Riaz Askri ◽  
Shumyala Maqbool ◽  
Kausar Abbas Shah ◽  
Shahbaz Ahmad
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Tracheal Intubation ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Arterial Blood ◽  
Group I ◽  
Group Ii

Objectives: To determine the role of 800 mg oral gabapentin in attenuating cardiovascular response to laryngoscopy and tracheal intubation. Study Design: Double Blind Randomized Control Trial. Setting: Independent University Hospital/Independent Medical College, Faisalabad, Pakistan. Period: Six months from January1st 2019 to June 30th 2019. Material & Methods: This study included 60 patients which were divided into two equal groups. 800 mg oral gabapentin was given to group I while capsule placebo was administrated to group II patients in pre-operative area one hour prior to surgery. Heart rate, systolic, diastolic and mean arterial blood pressure were taken after induction of anesthesia at base line and then 1,2,3,4,5,10 and 15 minutes after endotracheal intubation. SPSS version 11 was used to analyze the data. Heart rate systolic, diastolic and mean arterial blood pressure were dependent variables while placebo and gabapentin were independent variables. Results: Out of total 60 patients there were 36 (60 %) males and 24 (40 %) females. In group I mean age was 37.1 while in group II it was 36.3. As compare to group II there was decreased cardiovascular response in group I. There was a significant decrease in systolic blood pressure at 1,2 and 10 minutes; diastolic blood pressure at 3 minutes; heart rate at 10 and 15 minutes and mean arterial blood pressure at 3 minutes after induction in group I. Conclusion: Cardiovascular response to laryngoscopy and intubation is significantly reduced with oral gabapentin.

Changes in cardiac output and vascular resistance during behavioral stress in the rat

1986 ◽  
Vol 251 (1) ◽  
pp. R82-R90 ◽  
Author(s):  
J. W. Hubbard ◽  
R. H. Cox ◽  
B. J. Sanders ◽  
J. E. Lawler
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Plasma Norepinephrine ◽  
Wky Rats ◽  
Arterial Blood ◽  
Behavioral Stress

Normotensive Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHR) were exposed to aversive classical conditioning procedures and chronically instrumented with arterial catheters and electromagnetic flow probes around the ascending aorta. After postoperative recovery, hemodynamic measurements and blood samples were obtained from conscious animals at rest and during aversive conditioning. The cardiovascular response to the behavioral stress consisted of a significant increase in mean arterial blood pressure, total peripheral resistance index, cardiac index, heart rate, and aortic dP/dt for both strains. However, the elevated vascular resistance seen in the BHR resulted in a significantly greater increase in mean arterial blood pressure (21 mmHg) compared with the WKY rats (14 mmHg). In addition, the BHR showed a significantly (P less than 0.05) greater plasma norepinephrine concentration (760 +/- 99 pg/ml) in response to the stress than did the WKY rats (559 +/- 53 pg/ml). These data suggest that an increase in cardiac output, elevated vascular resistance, and increased sympathetic drive may contribute to the development of stress-induced hypertension in this animal model.

scholarly journals On the Pathology of the dropsy produced by obstruction of the superior and inferior venœ and the portal vein.— Preliminary communication

1907 ◽  
Vol 79 (532) ◽  
pp. 267-283 ◽  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Mean Arterial Blood Pressure ◽  
Normal Limit ◽  
The Body ◽  
Diastolic Filling ◽  
Arterial Blood ◽  
Preliminary Communication ◽  
The Mean

In August, 1903, I published a paper in the ‘Journal of Pathology’(1) in which I demonstrated a method experimentally producing uncompensated hear disease in an animal, which was compatible with life. This method consisted in diminishing the size of the pericardial sac by stitches, so that the diastolic filling of the heart was impeded. The main symptoms of this condition were dropsy and diminution in the amount of urine excreted. As the immediate result of this interference with the action of the heart, there occurred a rise of pressure throughout the whole systemic venous system extending as far back as the capillaries, and a fall of the mean arterial blood-pressure. Further, I found that the pressure in all the veins fell to the normal limit again within the space of about one hour, and that subsequently when dropsy was being produced, the vanous pressure in all parts of the body was normal, and the arterial pressure had almost recovered itself.

Central indomethacin enhances volume-dependent vasopressin release

1984 ◽  
Vol 247 (6) ◽  
pp. R1017-R1021
Author(s):  
D. P. Brooks ◽  
L. Share ◽  
J. T. Crofton ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E2 ◽  
Mean Arterial Blood Pressure ◽  
Inhibitory Effect ◽  
Volume Depletion ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Ventriculocisternal Perfusion ◽  
Severe Hemorrhage ◽  
Vasopressin Secretion

The effect of centrally administered indomethacin on hemorrhage-induced vasopressin release was studied in the morphine-sedated, urethan/chloralose-anesthetized dog. Ventriculocisternal perfusion of indomethacin 1) significantly reduced the amount of prostaglandin E2 in the effluent from the cisterna magna, 2) significantly enhanced the vasopressin response to volume depletion, and led to a greater fall in mean arterial blood pressure during severe hemorrhage. The results suggest that central prostaglandins may have an inhibitory effect on vasopressin secretion during volume depletion.

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