Cardiovascular responses to a laboratory stressor in women: Assessing the role of body awareness

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.

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Ouabain- and central sodium-induced hypertension depend on the ventral anteroventral third ventricle region

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.276.1.h63 ◽

1999 ◽

Vol 276 (1) ◽

pp. H63-H70 ◽

Cited By ~ 8

Author(s):

Shereeni J. Veerasingham ◽

Frans H. H. Leenen

Keyword(s):

Hypertonic Saline ◽

Wistar Rats ◽

Third Ventricle ◽

Cardiovascular Responses ◽

Ibotenic Acid ◽

Air Jet ◽

Artificial Cerebrospinal Fluid ◽

Induced Hypertension ◽

Chronic Infusion

To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Sham-operated or lesioned Wistar rats were administered ouabain (50 μg/day) or placebo for 3 wk from subcutaneously implanted controlled release pellets or artificial cerebrospinal fluid (CSF) or CSF containing 0.8 mol/l NaCl (5 μl/h) infused intracerebroventricularly for 2 wk. At the end of the experiment, mean arterial pressure (MAP) and heart rate at rest and in response to ganglionic blockade by intravenous hexamethonium (30 mg/kg) were assessed. In rats infused with hypertonic saline, responses to air jet stress were also assessed. Baseline MAP in sham-operated rats receiving intracerebroventricular hypertonic saline or subcutaneous ouabain was significantly higher than in control rats (115 ± 1 vs. 97 ± 3 and 121 ± 3 vs. 103 ± 3 mmHg, respectively). vAV3V lesions abolished the increase in MAP elicited by chronic infusion of hypertonic saline or administration of ouabain. Sham-operated rats treated with hypertonic saline or ouabain exhibited significantly enhanced decreases in MAP to hexamethonium, but lesioned rats did not. Rats infused with hypertonic saline demonstrated enhanced responses to air jet stress that were similar in sham-operated and lesioned rats. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. Cardiovascular responses to air jet stress appear not to be mediated by the vAV3V.

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Role of lateral hypothalamus on fluid, electrolyte, and cardiovascular responses to activation of the MSA

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.266.2.r496 ◽

1994 ◽

Vol 266 (2) ◽

pp. R496-R502 ◽

Cited By ~ 1

Author(s):

A. S. Haibara ◽

W. A. Saad ◽

J. V. Menani ◽

L. A. Camargo ◽

A. Renzi

Keyword(s):

Water Intake ◽

Lateral Hypothalamus ◽

Cardiovascular Responses ◽

Electrolytic Lesion ◽

Opioid Agonist ◽

Inhibitory Mechanisms ◽

Pressor Responses ◽

Medial Septal Area ◽

Opiate Agonist

In this study we investigated the influence of electrolytic lesion or of opioid agonist injections into the lateral hypothalamus (LH) on the dipsogenic, natriuretic, kaliuretic, antidiuretic, pressor, and bradycardiac effects of cholinergic stimulation of the medial septal area (MSA) in rats. Sham- and LH-lesioned male Holtzman rats received a stainless steel cannula implanted into the LH. Other groups of rats had cannulas implanted simultaneously into the MSA and LH. Carbachol (2 nmol) injection into the MSA induced water intake, pressor, and bradycardic responses. LH lesion reduced all of these effects (1-3 and 15-18 days). Previous injection of synthetic opiate agonist, FK-33824 (100 ng), into the LH reduced the water intake, natriuresis, kaliuresis, and pressor responses induced by carbachol injected into the MSA. These data show that both electrolytic lesion or injection of an opiate agonist in the LH reduces the fluid-electrolyte and cardiovascular responses to cholinergic activation of the MSA. The involvement of LH with central excitatory and inhibitory mechanisms related to fluid-electrolytic and cardiovascular control is suggested.

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Role of pre–extubation fentanyl in mastectomy: a randomized, controlled, double–blind study

Anaesthesia, Pain & Intensive Care ◽

10.35975/apic.v25i2.1462 ◽

2021 ◽

Vol 25 (2) ◽

Author(s):

Ahmed Salman ◽

Norma Osama Zayed ◽

Ahmed Mansour ◽

Ramy Howaidi ◽

Ahmed Gamaleldin Foly ◽

...

Keyword(s):

Short Form ◽

Cardiovascular Responses ◽

Blind Study ◽

Double Blind Study ◽

Double Blind ◽

Randomized Controlled ◽

Arterial Blood ◽

Extubation Time ◽

Significant Difference

Background: Both tracheal intubation and extubation are associated with dangerous consequences such as tachycardia, hypertension, myocardial ischemia and arrhythmias. The aim was to evaluate pre–extubation two different doses of fentanyl on hemodynamic stabilization and delayed recovery in mastectomy. Methodology: The randomized controlled double–blind study was conducted on 126 patients aged 16–60 years, with controlled hypertension, receiving chemotherapy before surgery and underwent mastectomy for breast cancer. Patients were randomly allocated into 3 equal groups. Before extubation, patients received 10 ml saline in group (C), 1 µg/kg fentanyl in Group–F1: and 2 µg/kg fentanyl in Group–F2. Mean arterial blood pressure (MAP) and heart rate (HR) were recorded at T1 (after maintenance of anesthesia), T2 (after giving the test drug), T3 (immediately after extubation), T4 (5 min. after extubation) and T5 (15 min after extubation). Results: MAP was significantly lower in fentanyl groups compared to Group–C at T2 and T3 without significant deference between fentanyl groups. HR was significantly lower in fentanyl groups compared to Group–C and in Group–F2 compared to Group–F1 at T3, T4 and T5. Time of extubation was significantly prolonged in Group–F2 compared to Group–F1 and Group–C without a significant difference between Group–F1 and Group–C. Conclusions: Pre–extubation fentanyl 1 µg/kg blunted cardiovascular responses to extubation without respiratory depression or prolonged recovery. Pre–extubation fentanyl 2 µg/kg provide more control in HR but with delay in the extubation time compared to 1 µg/kg of fentanyl. Key words: Pre–Extubation, Fentanyl, Mastectomy, Hemodynamics, Recovery Preregistration: The study was registered in the Ethical Committee of Faculty of Medicine, Cairo University, Cairo, Egypt (approval number: 281) Citation: Salman A, Zayed NO, Mansour A, Howaidi R, Foly AG, ElSharkawy MS, Abdelgalil AS. Role of pre–extubation fentanyl in mastectomy: a randomized, controlled, double–blind study. Anaesth. pain intensive care 2021;25(2):143-149. DOI: 10.35975/apic.v25i2.1462. Abbreviations: CST=Craniosacral therapy; SMT=Sensorimotor training; NCLBP=Nonspecific chronic low back pain; VAS=Visual analogue scale; ODI=Oswestry disability index, BDI-II=Beck depression inventory-II, and SF-36=Short Form-36; CSF=cerebral spinal fluid; CSS=craniosacral system; PRM=primary respiratory movements Received: 27 June 2020, Reviewed: 24 July 2020, Accepted: 27 July 2020

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Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.00842.2013 ◽

2014 ◽

Vol 116 (11) ◽

pp. 1371-1381 ◽

Cited By ~ 3

Author(s):

James P. Mendoza ◽

Rachael J. Passafaro ◽

Santhosh M. Baby ◽

Alex P. Young ◽

James N. Bates ◽

...

Keyword(s):

Nitric Oxide ◽

Heart Rate ◽

Cardiovascular Responses ◽

Vital Role ◽

Initial Increase ◽

Ventilatory Responses ◽

Arterial Blood ◽

Anesthetized Rats ◽

Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

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The Role of Visual Complexity in Affective Reactions to Webpages: Subjective, Eye Movement, and Cardiovascular Responses

IEEE Transactions on Affective Computing ◽

10.1109/t-affc.2011.18 ◽

2011 ◽

Vol 2 (4) ◽

pp. 230-236 ◽

Cited By ~ 13

Author(s):

Alexandre Tuch ◽

Sylvia Kreibig ◽

Sandra Roth ◽

Javier Bargas-Avila ◽

Klaus Opwis ◽

...

Keyword(s):

Eye Movement ◽

Visual Complexity ◽

Cardiovascular Responses ◽

Affective Reactions

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Abstract 424: Activation of the S1P3 Receptors is Responsible for S1P-mediated RhoA Activation and Cardioprotection

Circulation Research ◽

10.1161/res.117.suppl_1.424 ◽

2015 ◽

Vol 117 (suppl_1) ◽

Author(s):

Bryan S Yung ◽

Sunny Y Xiang ◽

Nicole Purcell ◽

Hugh Rosen ◽

Jerold Chun ◽

...

Keyword(s):

Infarct Size ◽

Ischemia Reperfusion ◽

Cardiovascular Responses ◽

Neonatal Rat ◽

Receptor Subtype ◽

Receptor Subtypes ◽

S1p Receptors ◽

Rhoa Activation ◽

Therapeutic Benefits

Sphingosine-1-phoshpate (S1P) is a bioactive lysophospholipid, generated and released at sites of tissue injury. S1P signals through a variety of G-protein coupled receptor subtypes and there are three major sub-types, S1P 1 , S1P 2 , and S1P 3 , to mediate cardiovascular responses. S1P 2 and S1P 3 receptors couple to Gα i , Gα 12 , Gα 13 and Gα q and we first examined the contribution of S1P 2 and S1P 3 to cardiac hypertrophy using S1P 2 and S1P 3 knockout (KO) mice and found that there is no difference in hypertrophy induced by pressure-overload. We previously showed that S1P provides cardioprotection against oxidative stress such as ischemia/reperfusion in which RhoA activation and its downstream effector PKD1 play an important role. It has not, however, been determined which S1P receptor subtype is responsible for S1P mediated cardioprotection. We knocked down the three major S1P receptors using siRNA in neonatal rat ventricular myocytes (NRVMs) and assessed RhoA and PKD1 activation induced by S1P. Knockdown of S1P 3 abolished RhoA activation and largely attenuated phosphorylation of PKD1 while knockdown of S1P 1 and S1P 2 did not. Using siRNA or pertussis toxin to inhibit different G-proteins, we further established that S1P regulates RhoA activation through Gα 13 , but not Gα 12 , Gα q , or Gα i . To investigate the role of S1P 3 receptors in the adult heart, hearts were isolated from wild-type or S1P 3 KO adult mice, perfused in the Langendorff mode and subjected to ex vivo ischemia/reperfusion. As previously reported, S1P perfusion significantly reduced infarct size induced by ischemia/reperfusion in WT hearts (by 50%), but this protection was abolished in the S1P 3 KO mouse heart. To further confirm the role of S1P 3 in cardioprotection we perfused WT mouse hearts with an S1P 3 -specific agonist CYM-51736. We observed that CYM-51736 attenuated the infarct size to a similar degree as that observed with S1P. Our findings reveal that activation of the S1P 3 receptor coupling to Gα 13 and subsequent RhoA activation is responsible for cardioprotection against ischemia/reperfusion. Accordingly specific drug targeting of S1P 3 receptors could provide therapeutic benefits in ischemic heart disease without the undesirable effects of global activation of other cardiac S1P receptors.

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Effect of pharmacological blockade on cardiovascular responses to voluntary and forced diving in muskrats.

Journal of Experimental Biology ◽

10.1242/jeb.198.11.2307 ◽

1995 ◽

Vol 198 (11) ◽

pp. 2307-2315 ◽

Cited By ~ 5

Author(s):

P E Signore ◽

D R Jones

Keyword(s):

Heart Rate ◽

Neural Control ◽

Peripheral Resistance ◽

Cardiovascular Responses ◽

Adrenergic Blocker ◽

Adrenergic Blockers ◽

Pharmacological Blockade ◽

Parasympathetic Influences ◽

Neural Effect

Neural control of free and forced diving bradycardia and peripheral resistance was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine, the alpha-adrenergic blocker phentolamine and the beta-adrenergic blockers nadolol and propranolol. Saline injection was used as a control. Heart rate in control animals increased before voluntary dives and dropped markedly as soon as the animals submerged. Heart rate started increasing towards the end of voluntary dives and reached pre-dive values within the first 5 s of recovery. Pre-dive and post-dive tachycardia were reduced in beta-blocked animals, emphasizing the role of the sympathetic system during the preparatory and recovery periods of voluntary dives. Diving bradycardia and the acceleration in heart rate before surfacing were abolished by atropine and unaffected by nadolol, demonstrating the importance of vagal efferent activity during diving. The results after blockade with nadolol suggest that there is an accentuated antagonism between the two branches of the autonomic nervous system during diving, so that parasympathetic influences on the heart predominate. Propranolol-treated muskrats had a higher diving heart rate than saline- and nadolol-treated animals, which may be due to a sedative effect caused by propranolol crossing the blood-brain barrier, a blockade of central catecholaminergic pathways or a peripheral neural effect, due to the anaesthetic properties of propranolol. Phentolamine did not affect diving bradycardia, indicating that diving bradycardia occurs independently of peripheral vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

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The Effects of Branchial Denervation and Pseudobranch Ablation on Cardioventilatory Control in an Air-Breathing Fish

Journal of Experimental Biology ◽

10.1242/jeb.161.1.347 ◽

1991 ◽

Vol 161 (1) ◽

pp. 347-365 ◽

Cited By ~ 6

Author(s):

DAVID J. McKENZIE ◽

MARK L. BURLESON ◽

DAVID J. RANDALL

Keyword(s):

Cardiovascular Responses ◽

Sodium Cyanide ◽

Air Breathing ◽

Ventilatory Responses ◽

Reflex Bradycardia ◽

Afferent Information ◽

Gill Ventilation ◽

Air Ventilation ◽

Amia Calva

Present address and address for reprint requests: Istituto di Scienze Farmacologiche, via Balzaretti 9, Università di Milano, Milano 20133, Italy. The role of sensory afferent information from the gills of Amia calva in cardiovascular and ventilatory control was investigated by bilateral branchial denervation and pseudobranch ablation. Aquatic hypoxia or 1 mg of sodium cyanide (NaCN) in the water flowing over the gills stimulated bradycardia, and gill and air ventilation in sham-operated fish. Sodium cyanide, noradrenaline (NA) and adrenaline (A) infusion into the dorsal aorta increased gill ventilation, and NA and A infusion also stimulated tachycardia and an increase in blood pressure. Following denervation and pseudobranch ablation, O2 consumption (V·OO2), airbreathing frequency (fAB) and arterial O2 tension (PaOO2) declined, and circulating NA levels increased, as compared with sham-operated fish. Cardiovascular and air-breathing responses to hypoxia were abolished and gill ventilatory responses attenuated. All ventilatory and cardiovascular responses to NaCN were abolished and gill ventilatory responses to NA and A were attenuated in animals following denervation and pseudobranch ablation. These results demonstrate that O2-sensitive chemoreceptors in the gills and pseudobranch control reflex bradycardia and air-breathing responses in Amia, but that gill ventilatory responses to hypoxia, NA and A are partially mediated by extrabranchial mechanisms. Plasma NA levels increased during hypoxia in shamoperated and denervated animals, indicating that circulating NA may have mediated gill ventilatory responses in denervated animals.

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