scholarly journals Hemodynamic response pattern predicts susceptibility to stress-induced elevation in arterial pressure in the rat

2001 ◽  
Vol 281 (1) ◽  
pp. R31-R37 ◽  
Author(s):  
Jay R. Muller ◽  
Khoi M. Le ◽  
William R. Haines ◽  
Qi Gan ◽  
Mark M. Knuepfer
Keyword(s):  
Cardiac Output ◽  
Conditioned Stimulus ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Acute Stress ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Response Patterns ◽  
Air Jet ◽  
Poststress Period

Cocaine or air jet stress evokes pressor responses due to either a large increase in systemic vascular resistance (vascular responders) or small increases in both cardiac output and vascular resistance (mixed responders) in conscious rats. Repeated cocaine administration results in elevated arterial pressure in vascular responders but not in mixed responders. The present study examined the hypothesis that the pattern of cardiovascular responses to an unconditioned stimulus (UCS; air jet) is related to responses to a conditioned stimulus (CS; tone followed by brief foot shock) in individual rats. Our data demonstrate that presentation of the UCS produced variable cardiac output responses that correlated with responses to the CS ( n = 60). We also determined whether individual cardiovascular response patterns to acute stress correlated with predisposition to a sustained stress-induced elevation in arterial pressure. Rats were exposed to three different stressors presented one per day successively for 4 wk and during a poststress period of 3 wk while arterial pressure was recorded periodically. Mean arterial pressure was elevated in all rats during chronic stress but, during the poststress period, remained at significantly higher levels in vascular responders but not mixed responders. Therefore, we conclude that acute behavioral stress to a conditioned stimulus elicits variable hemodynamic responses that predict the predisposition to a sustained stress-induced elevation in arterial pressure.

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Hemodynamic response patterns to acute behavioral stressors resemble those to cocaine

2001 ◽  
Vol 281 (6) ◽  
pp. R1778-R1786 ◽  
Author(s):  
Mark M. Knuepfer ◽  
Robert M. Purcell ◽  
Qi Gan ◽  
Khoi M. Le
Keyword(s):  
Cardiac Output ◽  
Cold Stress ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cold Water ◽  
Hemodynamic Response ◽  
Suitable Model ◽  
Response Patterns ◽  
Water Exposure ◽  
Air Jet

Hemodynamic responses to cocaine vary greatly between animals, and the variability is related to the incidence of cocaine-induced cardiomyopathies and hypertension. The variability in cardiac output and systemic vascular resistance responses to cocaine in individuals is correlated with the responses to acute startle (air jet). This experiment was designed to determine whether responses to cocaine and to air jet are related to those evoked by a conditioned stimulus (tone preceding foot shock) and to an unconditioned stimulus (cold water). We verified the relationship in hemodynamic response patterns between cocaine and cold stress using selective receptor antagonists. Rats were instrumented with a pulsed Doppler flow probe on the ascending aorta for determination of cardiac output and with an arterial cannula for recording arterial pressure and heart rate. After recovery, some rats were tested multiple times with four different stimuli: air jet (6 trials), 15-s tone preceding 1-s foot shock (12 trials), cold water exposure (1 cm deep for 1 min, 4–12 trials), and cocaine (5 mg/kg iv, 4–6 trials) while hemodynamic parameters were recorded. Each stimulus was capable of eliciting a pressor response that was associated with variable changes in cardiac output. The cardiac output response to cocaine was correlated with the initial responses to each stressor in individual rats. Responses evoked by cold stress were most similar to those elicited by cocaine. Furthermore, nicardipine (25 μg/kg iv) or atropine methylbromide (0.5 mg/kg iv) pretreatment prevented the cardiac output differences to acute cold stress, as noted after cocaine administration. On the other hand, propranolol (1 mg/kg iv) exacerbated both the decrease in cardiac output and the stress-induced increase in systemic vascular resistance as previously reported with cocaine. Therefore, the initial response to cold water exposure is a reliable method of evoking characteristic hemodynamic response patterns that, as seen with cocaine, may provide a suitable model for identifying the causes for predilection to stress-induced cardiovascular disease.

scholarly journals Analysis of cardiovascular responses to the H2S donors Na2S and NaHS in the rat

2015 ◽  
Vol 309 (4) ◽  
pp. H605-H614 ◽  
Author(s):  
Daniel Yoo ◽  
Ryan C. Jupiter ◽  
Edward A. Pankey ◽  
Vishwaradh G. Reddy ◽  
Justin A. Edward ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Potassium Channels ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Tissue ◽  
Sinus Node ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure

Hydrogen sulfide (H2S) is an endogenous gaseous molecule formed from L-cysteine in vascular tissue. In the present study, cardiovascular responses to the H2S donors Na2S and NaHS were investigated in the anesthetized rat. The intravenous injections of Na2S and NaHS 0.03–0.5 mg/kg produced dose-related decreases in systemic arterial pressure and heart rate, and at higher doses decreases in cardiac output, pulmonary arterial pressure, and systemic vascular resistance. H2S infusion studies show that decreases in systemic arterial pressure, heart rate, cardiac output, and systemic vascular resistance are well-maintained, and responses to Na2S are reversible. Decreases in heart rate were not blocked by atropine, suggesting that the bradycardia was independent of parasympathetic activation and was mediated by an effect on the sinus node. The decreases in systemic arterial pressure were not attenuated by hexamethonium, glybenclamide, Nw-nitro-l-arginine methyl ester hydrochloride, sodium meclofenamate, ODQ, miconazole, 5-hydroxydecanoate, or tetraethylammonium, suggesting that ATP-sensitive potassium channels, nitric oxide, arachidonic acid metabolites, cyclic GMP, p450 epoxygenase metabolites, or large conductance calcium-activated potassium channels are not involved in mediating hypotensive responses to the H2S donors in the rat and that responses are not centrally mediated. The present data indicate that decreases in systemic arterial pressure in response to the H2S donors can be mediated by decreases in vascular resistance and cardiac output and that the donors have an effect on the sinus node independent of the parasympathetic system. The present data indicate that the mechanism of the peripherally mediated hypotensive response to the H2S donors is uncertain in the intact rat.

scholarly journals Hemodynamic effects of acute stressors in the conscious rabbit

1998 ◽  
Vol 274 (3) ◽  
pp. R814-R821 ◽  
Author(s):  
James C. Schadt ◽  
Eileen M. Hasser
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Cardiovascular Response ◽  
Venous Pressure ◽  
Sensory Stimulation ◽  
Cardiovascular Responses ◽  
Baroreflex Control ◽  
Conscious Rabbit ◽  
Air Jet ◽  
Arterial Blood

Chronically instrumented, conscious rabbits were used to test the hypothesis that sensory stimulation with an air jet or oscillation produces differential hemodynamic changes that may be appropriate for an active or a passive behavioral response, respectively. Both stressors increased arterial pressure, central venous pressure, and hindquarters blood flow and produced visceral vasoconstriction. Neither stimulus altered hindquarters conductance. Although air jet increased heart rate and cardiac output, oscillation did not. The two stressors affected arterial baroreflex control of heart rate differently. Oscillation reset arterial pressure to a higher level with no change in heart rate maximum or minimum, whereas air jet reset both heart rate and arterial pressure to higher levels. Neither stressor affected baroreflex sensitivity. We conclude that the conscious rabbit shows at least two distinct cardiovascular responses when exposed to acute stressors. Air jet produces a cardiovascular response including tachycardia, which resembles the defense reaction and appears appropriate for active defense or flight. The response to oscillation, on the other hand, appears better suited for a passive response such as “freezing” behavior. During exposure to either stressor, the baroreflex is altered to allow simultaneous increases in heart rate and arterial blood pressure, but the sensitivity is maintained, allowing normal moment to moment control of heart rate.

scholarly journals Activation of angiotensin-converting enzyme 2/angiotensin-(1–7)/Mas axis attenuates the cardiac reactivity to acute emotional stress

2013 ◽  
Vol 305 (7) ◽  
pp. H1057-H1067 ◽  
Author(s):  
Augusto Martins Lima ◽  
Carlos Henrique Xavier ◽  
Anderson José Ferreira ◽  
Mohan K. Raizada ◽  
Gerd Wallukat ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Intravenous Injection ◽  
Emotional Stress ◽  
Acute Stress ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Air Jet ◽  
Acute Emotional Stress

Recent data indicate the brain angiotensin-converting enzyme/ANG II/AT1 receptor axis enhances emotional stress responses. In this study, we investigated whether its counterregulatory axis, the angiotensin-converting enzyme 2 (ACE2)/ANG-(1–7)/Mas axis, attenuate the cardiovascular responses to acute emotional stress. In conscious male Wistar rats, the tachycardia induced by acute stress (air jet 10 l/min) was attenuated by intravenous injection of ANG-(1–7) [Δ heart rate (HR): saline 136 ± 22 vs. ANG-(1–7) 61 ± 25 beats/min; P < 0.05]. Peripheral injection of the ACE2 activator compound, XNT, abolished the tachycardia induced by acute stress. We found a similar effect after intracerebroventricular injections of either ANG-(1–7) or XNT. Under urethane anesthesia, the tachycardia evoked by the beta-adrenergic agonist was markedly reduced by ANG-(1–7) [ΔHR: saline 100 ± 16 vs. ANG-(1–7) 18 ± 15 beats/min; P < 0.05]. The increase in renal sympathetic nerve activity (RSNA) evoked by isoproterenol was also abolished after the treatment with ANG-(1–7) [ΔRSNA: saline 39% vs. ANG-(1–7) −23%; P < 0.05]. The tachycardia evoked by disinhibition of dorsomedial hypothalamus neurons, a key nucleus for the cardiovascular response to emotional stress, was reduced by ∼45% after intravenous injection of ANG-(1–7). In cardiomyocyte, the incubation with ANG-(1–7) (1 μM) markedly attenuated the increases in beating rate induced by isoproterenol. Our data show that activation of the ACE2/ANG-(1–7)/Mas axis attenuates stress-induced tachycardia. This effect might be either via the central nervous system reducing anxiety level and/or interfering with the positive chronotropy mediated by activation of cardiac β adrenergic receptors. Therefore, ANG-(1–7) might contribute to reduce the sympathetic load to the heart during situations of emotional stress, reducing the cardiovascular risk.

scholarly journals Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

1999 ◽  
Vol 86 (6) ◽  
pp. 1890-1896 ◽  
Author(s):  
D. Slamowitz ◽  
L. Chen ◽  
S. M. Scharf
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Mechanical Effects

There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; +19 ± 25%, P < 0.05), systemic vascular resistance (SVR; +33 ± 16%, P < 0.0005), and heart rate (HR; +5 ± 6%, P < 0.05) and decreased cardiac output (CO) and stroke volume (SV; −16 ± 10% P < 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater (∼14%, P < 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes.

Arginine vasopressin mediates cardiovascular responses to hypoxemia in fetal sheep

1989 ◽  
Vol 256 (5) ◽  
pp. R1011-R1018 ◽  
Author(s):  
R. Perez ◽  
M. Espinoza ◽  
R. Riquelme ◽  
J. T. Parer ◽  
A. J. Llanos
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Arginine Vasopressin ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Potent Vasoconstrictor

Acute hypoxemia results in hypertension, bradycardia, and cardiac output redistribution in fetal sheep. The blood flow redistribution is produced by differential changes in vascular resistance of various fetal organs. alpha-Adrenergic activity is one of the few vasoconstrictor mechanisms thus far identified in the hypoxemic fetal sheep. Arginine vasopressin (AVP) is a potent vasoconstrictor in adults. Since AVP administration to the normoxic fetus mimics some of the fetal cardiovascular responses to hypoxemia and fetal plasma AVP levels increase with hypoxemia, we examined the hypothesis that AVP modifies the fetal cardiovascular response to hypoxemia by changing the vascular resistance of some fetal vascular beds. To test this we determined fetal systemic arterial pressure and fetal cardiac output and its distribution during hypoxemia with and without the V1 AVP antagonist d(CH2)5-Tyr(Me)AVP. Fourteen fetal sheep (0.79-0.90 of gestation) were chronically catheterized. Five days after surgery fetal hypoxemia was induced by introducing a mixture of 95% N2-5% CO2 (10-20 l/min) into a maternal tracheal catheter. The hypoxemia was maintained for 40 min. Fetal heart rate, systemic arterial blood pressure, and combined ventricular output and its distribution (radiolabeled microspheres) were measured before hypoxemia, at 20 min of hypoxemia alone, and at 20 min of hypoxemia plus either AVP antagonist (n = 5) or NaCl 0.9% (n = 5, controls). Fetal hypertension and bradycardia were partially reversed after the AVP antagonist administration during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular and Valsalva responses during parabolic flight

1998 ◽  
Vol 85 (5) ◽  
pp. 1957-1965 ◽  
Author(s):  
Todd T. Schlegel ◽  
Edgar W. Benavides ◽  
Donald C. Barker ◽  
Troy E. Brown ◽  
Deborah L. Harm ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Human Subjects ◽  
Parabolic Flight ◽  
Cardiovascular Responses ◽  
Systematic Evaluation ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Flight Measurements

We investigated the integrated cardiovascular responses of 15 human subjects to the acute gravitational changes (micro- and hypergravity portions) of parabolic flight. Measurements were made with subjects quietly seated and while subjects performed controlled Valsalva maneuvers. During quiet, seated, parabolic flight, mean arterial pressure increased during the transition into microgravity but decreased as microgravity was sustained. The decrease in mean arterial pressure was accompanied by immediate reflexive increases in heart rate but by absent (or later-than-expected) reflexive increases in total vascular resistance. Mean arterial pressure responses in Valsalva phases IIl, III, and IV were accentuated in hypergravity relative to microgravity ( P < 0.01, P < 0.01, and P < 0.05, respectively), but accentuations differed qualitatively and quantitatively from those induced by a supine-to-seated postural change in 1 G. This study is the first systematic evaluation of temporal and Valsalva-related changes in cardiovascular parameters during parabolic flight. Results suggest that arterial baroreflex control of vascular resistance may be modified by alterations of cardiopulmonary, vestibular, and/or other receptor activity.

scholarly journals INDIVIDUAL DIFFERENCES IN EMOTION REGULATION AND CARDIOVASCULAR RESPONDING TO STRESS

2021 ◽  
Author(s):  
Siobhán M Griffin ◽  
Siobhán Howard
Keyword(s):  
Blood Pressure ◽  
Emotion Regulation ◽  
Individual Differences ◽  
Acute Stress ◽  
Negative Emotion ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Emotional Valence ◽  
Emotion Words

Instructed use of reappraisal to regulate stress in the laboratory is typically associated with a more adaptive cardiovascular response to stress, indexed by either: (i) lower cardiovascular reactivity (CVR; e.g., lower blood pressure); or (ii) a challenge-oriented response profile (i.e., greater cardiac output paired with lower total peripheral resistance). In contrast, instructed use of suppression is associated with exaggerated CVR (e.g., greater heart rate, blood pressure). Despite this, few studies have examined if the habitual use of these strategies are related to cardiovascular responding during stress. The current study examined the relationship between cardiovascular responses to acute stress and individual differences in emotion regulation style: trait reappraisal, suppression, and emotion regulation difficulties. Forty-eight participants (25 women, 23 men) completed a standardised laboratory stress paradigm incorporating a 20-minute acclimatization period, a 10-minute baseline, and two 5-minute speech tasks separated by a 10-minute inter-task rest period. The emotional valence of the speech task was examined as a potential moderating factor; participants spoke about a block of negative-emotion words and a block of neutral-emotion words. Cardiovascular parameters were measured using the Finometer Pro. Greater habitual use of suppression was associated with exaggerated blood pressure responding to both tasks. However, only in response to the negative-emotion task was greater use of reappraisal associated with a challenge-oriented cardiovascular response. The findings suggest that individual differences in emotion regulation translate to differing patterns of CVR to stress, but the emotional valence of the stressor may play a role.

Subregions of rostral ventral medulla control arterial pressure and regional hemodynamics

1989 ◽  
Vol 257 (3) ◽  
pp. R635-R640 ◽  
Author(s):  
B. F. Cox ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Tidal Volume ◽  
Vascular Resistance ◽  
Neural Control ◽  
Cardiovascular Response ◽  
Cardiovascular Effects ◽  
Ventrolateral Medulla ◽  
Ventral Medulla ◽  
Ventromedial Medulla ◽  
Regional Hemodynamics

The cardiovascular effects of inactivating rostral ventromedial medulla (RVMM) under conditions of normal (2.5 ml) and reduced (1.5 ml) tidal volume were studied in urethan-anesthetized rats. Bilateral microinjection of lidocaine (200 nl, 4%) reduced mean arterial pressure (MAP), renal, mesenteric, and particularly hindquarter vascular resistance. These effects were not significantly altered by reducing tidal volume. Electrical stimulation of RVMM increased MAP and regional vascular resistances, again with the hindquarter change most prominent. The integrated cardiovascular response to stimulating rostral ventrolateral medulla (RVLM) appears to require integrity of RVMM; however, the converse is not true. Overall, these studies indicate that 1) the potential for RVMM to maintain neurogenic control of arterial pressure is as great as RVLM; 2) RVMM is capable of playing a proportionally greater role in the controlling hindquarter vascular resistance; 3) the integrity of RVMM appears to be important for responses elicited from RVLM; and 4) unlike RVLM, neural control of arterial pressure is sustained by RVMM under conditions of reduced tidal volume. We conclude that RVLM and RVMM are functionally and anatomically distinct subregions of rostral ventral medulla with equivalent capacity to maintain vasomotor tone.

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