Effects of aortic nerve on hemodynamic response to obstructive apnea in sedated pigs

2000 ◽  
Vol 89 (4) ◽  
pp. 1455-1461 ◽  
Author(s):  
Ling Chen ◽  
Steven M. Scharf
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Airway Pressure ◽  
Pressor Response ◽  
Blood Gas ◽  
Aortic Nerve ◽  
Cervical Vagotomy

In this study we test the hypothesis that aortic nerve traffic is responsible for the pressor response to periodic apneas. In nine intubated, sedated chronically instrumented pigs, periodic obstructive apneas were caused by occlusion of the endotracheal tube for 30 s, followed by spontaneous breathing for 30 s. This was done under control (C) conditions, after section of the aortic nerve (ANS), and after bilateral cervical vagotomy (Vagot). Blood-gas tensions and airway pressure changed similarly under all conditions: Po 2 decreased to 50–60 Torr, Pco 2 increased to ∼55 Torr, and airway pressure decreased by 40–50 mmHg during apnea. With C, mean arterial pressure (MAP) increased from 111 ± 4 mmHg at baseline to 120 ± 5 mmHg at late apnea ( P < 0.01). After ANS and Vagot, there was no change in MAP with apneas compared with baseline. Relative to baseline, cardiac output and stroke volume decreased with C but not with ANS or Vagot during apneas. Increased MAP was due to increased systemic vascular resistance. Heart rate behaved similarly with C and ANS, being greater at early interapnea than late apnea. With Vagot, heart rate increased throughout the apnea-interapnea cycle relative to baseline. We conclude that, in sedated pigs, aortic nerve traffic mediates the increase in MAP and systemic vascular resistance observed during periodic apneas. Increase in MAP is responsible for decreased cardiac output and stroke volume. Additional vagal reflexes, most likely parasympathetic efferents, are responsible for interacting with sympathetic excitatory influences in modulating heart rate.

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.

Peripheral circulatory control of preload-afterload mismatch with angiotensin in dogs

1987 ◽  
Vol 253 (1) ◽  
pp. H126-H132
Author(s):  
R. W. Lee ◽  
L. D. Lancaster ◽  
D. Buckley ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Peripheral Circulation ◽  
Aortic Pressure ◽  
Venous Compliance ◽  
Mean Aortic Pressure

To determine whether changes in the venous circulation were responsible for preload-afterload mismatch with angiotensin, we examined the changes in the heart and the peripheral circulation in six splenectomized dogs after ganglion blockade during an angiotensin infusion to increase mean aortic pressure 25 and then 50%. The peripheral circulation was evaluated by measuring mean circulatory filling pressure (MCFP), arterial compliance, and venous compliance. A 25% increase in mean aortic pressure increased MCFP from 6.2 +/- 0.3 to 7.6 +/- 0.3 mmHg (P less than 0.001) but did not change cardiac output, heart rate, or stroke volume. Systemic vascular resistance increased (P less than 0.01) from 0.50 +/- 0.02 to 0.59 +/- 0.03 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.03 to 0.06 +/- 0.03 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.6 +/- 0.1 ml X mmHg-1 X kg-1, respectively. A 50% elevation in mean aortic pressure increased MCFP from 7.1 +/- 0.4 to 9.5 +/- 0.9 mmHg (P less than 0.001) but did not change heart rate. At this level of aortic pressure, cardiac output and stroke volume decreased (P less than 0.01) 12 and 19%, respectively, whereas systemic vascular resistance increased (P less than 0.001) from 0.48 +/- 0.03 to 0.83 +/- 0.05 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.01 to 0.05 +/- 0.01 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.4 +/- 0.1 ml X mmHg-1 X kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Hemodynamic Changes Associated with Spinal Anesthesia for Cesarean Delivery in Severe Preeclampsia

2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Spinal Anesthesia ◽  
Cesarean Delivery ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Severe Preeclampsia

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.

Cardiac output changes during neonatal growth

1978 ◽  
Vol 234 (5) ◽  
pp. H520-H524 ◽  
Author(s):  
J. R. Woods ◽  
A. Dandavino ◽  
C. R. Brinkman ◽  
B. Nuwayhid ◽  
N. S. Assali
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Beta Blockade ◽  
Receptor Stimulation ◽  
Progressive Decline ◽  
Neonatal Growth

Changes in resting cardiac output (CO), stroke volume (SV), and systemic vascular resistance (SVR) during neonatal growth were studied in chronically instrumented lambs from the 1st to 5th wk of age; adult nonpregnant sheep values measured simultaneously were used as standard reference. Neonatal responses to autonomic agonists and antagonists were also investigated. Total CO increased linearly with neonatal growth, but decreased strikingly when expressed per weight unit; at 5 wk of age, CO/kg was still significantly higher than the adult value. SV also increased with neonatal growth but did not change when related to body weight; at 5 wk of age, SV/kg values were still higher than those of adult sheep. SVR changed reciprocally to CO. The decrease in CO/kg during neonatal growth paralleled the progressive decline in heart rate (HR). Beta receptor stimulation increased neonatal CO markedly and the increment was the same from the first through the fifth neonatal week. Beta blockade had insignificant effects, but cholinergic blockade produced moderate CO increases.

Hemodynamic Changes During Discontinuation of Mechanical Ventilation in Medical Intensive Care Unit Patients

2006 ◽  
Vol 15 (6) ◽  
pp. 580-593 ◽  
Author(s):  
Susan K. Frazier ◽  
Kathleen S. Stone ◽  
Debra Moser ◽  
Rebecca Schlanger ◽  
Carolyn Carle ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mechanical Ventilation ◽  
Cardiac Output ◽  
Continuous Positive Airway Pressure ◽  
Stroke Volume ◽  
Cardiac Dysfunction ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Plasma Catecholamine ◽  
Medical Intensive Care

• Background Cardiac dysfunction can prevent successful discontinuation of mechanical ventilation. Critically ill patients may have undetected cardiac disease, and cardiac dysfunction can be produced or exacerbated by underlying pathophysiology. • Objective To describe and compare hemodynamic function and cardiac rhythm during baseline mechanical ventilation with function and rhythm during a trial of continuous positive airway pressure in medical intensive care patients. • Methods A convenience sample of 43 patients (53% men; mean age 51.1 years) who required mechanical ventilation were recruited for this pilot study. Cardiac output, stroke volume, arterial blood pressure, heart rate, cardiac rhythm, and plasma catecholamine levels were measured during mechanical ventilation and during a trial of continuous positive airway pressure. • Results One third of the patients had difficulty discontinuing mechanical ventilation. Successful patients had significantly increased cardiac output and stroke volume without changes in heart rate or arterial pressure during the trial of continuous positive airway pressure. Unsuccessful patients had no significant changes in cardiac output, stroke volume, or heart rate but had a significant increase in mean arterial pressure. The 2 groups of patients also had different patterns in ectopy. Concurrently, catecholamine concentrations decreased in the successful patients and significantly increased in the unsuccessful patients during the trial. • Conclusions Patterns of cardiac function and plasma catecholamine levels differed between patients who did or did not achieve spontaneous ventilation with a trial of continuous positive airway pressure. Cardiac function must be systematically considered before and during the return to spontaneous ventilation to optimize the likelihood of success.

scholarly journals CK (Creatine Kinase) Is Associated With Cardiovascular Hemodynamics

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 373-380 ◽  
Author(s):  
Lizzy M. Brewster ◽  
Yentl C. Haan ◽  
Aeilko H. Zwinderman ◽  
Bert Jan van den Born ◽  
Gert A. van Montfrans
Keyword(s):  
Blood Pressure ◽  
Creatine Kinase ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
African Ancestry ◽  
Cardiac Contractility ◽  
Urban Setting ◽  
Cardiovascular Hemodynamics

The ATP-regenerating enzyme CK (creatine kinase) is strongly associated with blood pressure, which lowers upon experimental CK inhibition. The enzyme is thought to affect cardiovascular hemodynamics through enhanced systemic vascular resistance, stroke volume, and cardiac contractility, but data on these parameters are lacking. We hereby report hemodynamics by CK levels in the multiethnic, cross-sectional HELIUS study (Healthy Life in an Urban Setting). Physical examination included sitting brachial blood pressure and noninvasively assessed supine systemic vascular resistance, stroke volume, cardiac output, and cardiac contractility, which we associated with resting plasma CK. Data from 14 937 men and women (mean age, 43.3; SD, 12.9) indicated that per log CK increase, blood pressure increased with 20.2 (18.9–21.4) mm Hg systolic/13.0 (12.2–13.7) diastolic, an odds ratio for hypertension of 6.1 (5.1–7.2). Outcomes were similar by sex, body mass index, and ancestry, although higher blood pressures in men, with overweight/obesity, and West-African ancestry were partially explained by higher CK, with an adjusted increase in systolic/diastolic pressure of 10.5 (10.0–10.9)/6.4 (6.0–6.7) mm Hg per log CK increase. Systemic vascular resistance, stroke volume, cardiac output, and cardiac contractility (n=7876), increased by respectively 20%, 39%, 14%, and 23% SD per log CK increase. This study indicates that the association of CK with blood pressure likely results from an increase in systemic vascular resistance and stroke volume. These data expand the knowledge on the nature of hypertension associated with CK and may inform further experiments on CK inhibition as a means to lower blood pressure.

Dynamics of Circulatory Adjustments to Head-Up Tilt and Tilt-Back in Healthy and Sympathetically Denervated Subjects

1998 ◽  
Vol 94 (4) ◽  
pp. 347-352 ◽  
Author(s):  
W. Wieling ◽  
J. J. Van Lieshout ◽  
A. D. J. Ten Harkel
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Healthy Subjects ◽  
Mean Blood Pressure ◽  
Head Up Tilt ◽  
Change In Mean

1. The initial circulatory adjustments induced by head-up tilt and tilt-back were investigated in six healthy subjects (aged 30–58 years) and six patients with orthostatic hypotension due to pure autonomic failure (aged 33–65 years). 2. Continuous responses of finger arterial pressure and heart rate were recorded by Finapres. A pulse contour algorithm applied to the arterial pressure waveform was used to compute stroke volume responses. 3. In the healthy subjects, head-up tilt induced gradual circulatory adjustments. After 1 min upright stroke volume and cardiac output had decreased by 39 ± 9% and 26 ± 10% respectively. Little change in mean blood pressure at heart level (+1 ± 7 mmHg) indicated that systemic vascular resistance had increased by 39 ± 24%. The gradual responses to head-up tilt contrasted with the pronounced and rapid circulatory responses upon tilt-back. After 2–3 s a rapid increase in stroke volume (from 62 ± 8% to 106 ± 10%) and cardiac output (from 81 ± 11% to 118 ± 20%) was observed with an overshoot of mean arterial pressure above supine control values of 16 ± 3 mmHg at 7 s. In the patients a progressive fall in blood pressure on head-up tilt was observed. After 1 min upright mean blood pressure had decreased by 59 ± 8 mmHg. No change in systemic vascular resistance and a larger decrease in stroke volume (60 ± 7%) and cardiac output (53 ± 8%) were found. On tilt-back a gradual recovery of blood pressure was observed. 4. In healthy humans upon head-up tilt neural compensatory mechanisms are very effective in maintaining arterial pressure at heart level. The gradual circulatory adjustments to head-up tilt in healthy subjects contrast with the pronounced and abrupt circulatory changes on tilt-back. In patients with a lack of neural circulatory reflex adjustments, gradual blood pressure decreases to head-up tilt and gradual increases to tilt-back are observed.

Hemodynamic effects of angiotensin, norepinephrine, and bradykinin continuously measured in unanesthetized dogs

1961 ◽  
Vol 201 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Irvine H. Page ◽  
Frederick Olmsted
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Partial Recovery ◽  
Slight Rise ◽  
Abrupt Rise

Cardiac output, arterial pressure, heart rate and the derived functions, peripheral resistance and stroke volume, were registered continuously from intact, unanesthetized, unrestrained dogs. Isoleucyl5- or valyl5-angiotensin octapeptide caused output, heart rate and stroke volume to fall sharply when peripheral resistance rose. When infused for an hour, systolic and diastolic pressure remained elevated with unchanged infusion rate. Heart rate decreased in most animals, stroke volume and cardiac output fell, while peripheral resistance rose. Pentobarbital anesthesia increased somewhat the pressor response and decreased the bradycardia. Norepinephrine elicited, first, an abrupt rise in pressure and peripheral resistance, slight rise in heart rate and stroke volume. Arterial pressure then tended to stabilize, followed by a slow decrease associated with continued depression of cardiac output. Bradykinin caused fall in pressure, partial recovery, then further fall. Heart rate slowed, then rose. Cardiac output rose sharply during the initial fall in arterial pressure and remained elevated during the hypotensive response. Stroke volume was reduced during the initial fall but was reduced less during the rest of the response. Peripheral resistance was decreased sharply.

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.

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