Cardiovascular control during voluntary static exercise in humans with tetraplegia

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C6-C7). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.

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Carotid baroreceptor control of liver and spleen volume in cats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.260.1.h254 ◽

1991 ◽

Vol 260 (1) ◽

pp. H254-H259

Author(s):

R. Maass-Moreno ◽

C. F. Rothe

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Arterial Blood Pressure ◽

Total Peripheral Resistance ◽

Venous Pressure ◽

Peripheral Resistance ◽

Normal Brain ◽

Spleen Volume ◽

Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

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Chronic regulation of arterial blood pressure by ANP: role of endogenous vasoactive endothelial factors

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.275.5.h1826 ◽

1998 ◽

Vol 275 (5) ◽

pp. H1826-H1833 ◽

Cited By ~ 6

Author(s):

L. G. Melo ◽

A. T. Veress ◽

U. Ackermann ◽

H. Sonnenberg

Keyword(s):

Blood Pressure ◽

Enzyme Activity ◽

Arterial Blood Pressure ◽

Natriuretic Peptide ◽

Peripheral Resistance ◽

Cardiovascular Effects ◽

Hypotensive Effect ◽

Synthetic Activity ◽

Arterial Blood

Atrial natriuretic peptide (ANP) exerts a chronic hypotensive effect due to a decrease in total peripheral resistance (TPR). This study examines if chronic ANP-dependent vasodilation is attributable to differences in the cardiovascular regulatory activity of vascular endothelium (VE), based on evidence that ANP affects synthesis/release and target cardiovascular effects of endothelin-1 (ET-1), C-type natriuretic peptide (CNP), and nitric oxide (NO). To determine if the synthetic activity of resistance vasculature VE is chronically altered by plasma ANP activity, we measured ET-1, CNP, and endothelial constitutive NO synthase (ecNOS) concentration and total NOS enzyme activity in homogenates of kidney, heart, lung, hindquarter skeletal muscle, and brain from hypotensive transgenic mice with elevated plasma ANP, hypertensive knockout mice (−/−) characterized by the absence of ANP, and the corresponding normotensive wild-type (NT, +/+) mice. Tissue distribution and abundance patterns of ET-1, CNP, ecNOS, and NOS enzyme activity were comparable between the different genotypes and did not differ significantly between mutant and control mice. Antagonism of ETA/B receptors in −/− and +/+ mice in vivo with SB-209670 reduced arterial blood pressure (ABP) significantly and comparably in both genotypes (−27 ± 4 and −25 ± 2% change for −/− and +/+ mice, respectively) independent of any significant changes in heart rate (HR) (−6 ± 8 and −4 ± 4% change for −/− and +/+ mice, respectively). Immunoneutralization of CNP-specific guanylate cyclase-linked receptors (GC-B) with monoclonal antibodies (3G12) increased ABP slightly, but not significantly, by similar relative amounts in both −/− (10 ± 6% change) and +/+ mice (8 ± 3% change), without changing HR significantly (4 ± 1% change for both +/+ and −/− mice). Inhibition of NOS activity (by N G-nitro-l-arginine methyl ester) significantly increased ABP, but the changes were comparable between −/− (53 ± 5% change) and +/+ mice (50 ± 6% change) and occurred in the absence of significant changes in HR (−1 ± 5 and 7 ± 5% change for −/− and +/+ mice, respectively). We conclude that the differences in ABP associated with chronic variations in endogenous ANP activity are not due to alterations in synthesis or responsiveness of the cardiovascular system to the effects of ET-1, CNP, or NO.

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Epidural Spinal Cord Stimulation of Lumbosacral Networks Modulates Arterial Blood Pressure in Individuals With Spinal Cord Injury-Induced Cardiovascular Deficits

Frontiers in Physiology ◽

10.3389/fphys.2018.00565 ◽

2018 ◽

Vol 9 ◽

Cited By ~ 23

Author(s):

Sevda C. Aslan ◽

Bonnie E. Legg Ditterline ◽

Michael C. Park ◽

Claudia A. Angeli ◽

Enrico Rejc ◽

...

Keyword(s):

Blood Pressure ◽

Spinal Cord ◽

Spinal Cord Injury ◽

Arterial Blood Pressure ◽

Spinal Cord Stimulation ◽

Arterial Blood ◽

Cord Injury ◽

Epidural Spinal Cord Stimulation ◽

Stimulation Of

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Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.6.2761 ◽

1994 ◽

Vol 77 (6) ◽

pp. 2761-2766 ◽

Cited By ~ 36

Author(s):

S. W. Mittelstadt ◽

L. B. Bell ◽

K. P. O'Hagan ◽

P. S. Clifford

Keyword(s):

Blood Pressure ◽

Skeletal Muscle ◽

Blood Flow ◽

Arterial Blood Pressure ◽

Blood Pressure Response ◽

Pressor Response ◽

Vascular Conductance ◽

Arterial Blood ◽

Response To Exercise ◽

Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

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Effect of norepinephrine on plasma free fatty acids in dogs treated with reserpine

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.205.1.57 ◽

1963 ◽

Vol 205 (1) ◽

pp. 57-59 ◽

Cited By ~ 73

Author(s):

Francois M. Abboud ◽

Michael G. Wendling ◽

John W. Eckstein

Keyword(s):

Blood Pressure ◽

Fatty Acids ◽

Free Fatty Acids ◽

Arterial Blood Pressure ◽

Pressor Response ◽

Maximal Increase ◽

Arterial Blood ◽

Anesthetized Dogs ◽

Plasma Ffa

Some adrenergic blocking drugs reduce the mobilization of free fatty acids (FFA) in response to administration of catecholamines. The present experiments were done to see if potentiation of the pressor effect of norepinephrine by reserpine is accompanied by a greater increase in plasma FFA. Norepinephrine was infused intravenously into 16 anesthetized dogs. Eight of them had been treated with reserpine, 0.25 mg/kg daily, intraperitoneally for 2 days; the others were not treated. Arterial blood samples were drawn before, during, and after norepinephrine for determination of plasma FFA concentrations. Systemic arterial blood pressure was measured continuously. In the treated animals the maximal increase in arterial blood pressure as well as the progressive increments in FFA concentration were greater than in the untreated dogs. The experiments indicate that potentiation of the pressor response to norepinephrine after reserpine is accompanied by a greater FFA response.

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Cardiac Output by the Dye Dilution Technique Under Thiopental Sodium-Oxygen and Ether Anesthesia

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1956.186.1.101 ◽

1956 ◽

Vol 186 (1) ◽

pp. 101-104 ◽

Cited By ~ 2

Author(s):

Esther M. Greisheimer ◽

Dorothy W. Ellis ◽

George Stewart ◽

Lydia Makarenko ◽

Nadia Oleksyshyn ◽

...

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Arterial Blood Pressure ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Stroke Index ◽

Ether Anesthesia ◽

Dye Dilution ◽

Arterial Blood ◽

Thiopental Sodium

One hundred-twenty determinations of cardiac output by the dye dilution technic utilizing the cuvette oximeter were made on 20 dogs. Of these, 60 were done under thiopental sodium-oxygen analgesia and 60 were done after supplementing with ether. Arterial blood pressure was recorded by strain gauge. Electrocardiograms were taken periodically. Concentrations of thiopental and ether in arterial blood were determined. Cardiac output began to increase under thiopental analgesia and continued to increase when ether was administered. Arterial blood pressure and heart rate decreased slightly when ether was administered. Stroke index increased when ether was administered. Total peripheral resistance decreased markedly under thiopental analgesia, and continued to decrease when ether was administered. When compared with an earlier study in which cyclopropane was used as the supplementing agent, it was found that cyclopropane and ether exert opposite effects on cardiac output and peripheral resistance despite the fact that the effect on arterial blood pressure is similar under the two agents. Increase in cardiac output was found to be parallel with decrease in total peripheral resistance in this study. Amount of dye injected did not influence cardiac output. Under the conditions of this study, cardiac output was in no way dependent on the concentration of thiopental in the blood nor on the amount injected. Level of ether in the blood did not show much effect, if any, on cardiac output. It is probable that the changes observed in this study are comparable with those which obtain clinically when thiopental-oxygen analgesia is supplemented with ether. Systolic blood pressure is not an infallible guide to other cardiovascular functions since it may remain fairly steady while cardiac output and peripheral resistance undergo marked changes under anesthesia.

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LABORATORY DEMONSTRATION OF BAROREFLEX CONTROL OF HEART RATE IN CONSCIOUS RATS

AJP Advances in Physiology Education ◽

10.1152/advan.00040.2001 ◽

2002 ◽

Vol 26 (4) ◽

pp. 309-316 ◽

Cited By ~ 5

Author(s):

Theresa L. O’Donaughy ◽

Thomas C. Resta ◽

Benjimen R. Walker

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Peripheral Resistance ◽

Baroreflex Control ◽

Laboratory Exercise ◽

Conscious Animal ◽

Lecture Material ◽

Arterial Blood ◽

Lower Blood

We have developed a laboratory exercise that demonstrates arterial baroreflex control of heart rate (HR) in the conscious unrestrained rat, incorporating graduate level physiological topics as well as a hands-on exposure to conscious animal research. This demonstration utilizes rats chronically instrumented to measure cardiac output (CO), HR, and arterial blood pressure in response to agents that raise or lower blood pressure. The HR response to progressive increases or decreases in blood pressure is recorded, and a baroreflex curve is generated by plotting mean arterial blood pressure (MABP) vs. HR. Observation of altered CO allows for discussion of the relationship between MAP, CO, HR, stroke volume, and total peripheral resistance. Administration of arginine vasopressin demonstrates the ability of this hormone to alter the sensitivity of the baroreflex. Throughout the demonstration, students answer questions from a handout about general cardiovascular physiology, specific pathways of agonists, and the baroreflex system, encouraging group and individual critical analysis of the results. Interpretation of the data reemphasizes lecture material and allows students to observe the baroreflex response in a physiological setting.

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Chronic, complete cervical6–7 cord transection: distinct autonomic and cardiac deficits

Journal of Applied Physiology ◽

10.1152/japplphysiol.01104.2017 ◽

2018 ◽

Vol 124 (6) ◽

pp. 1471-1482 ◽

Cited By ~ 3

Author(s):

Heidi L. Lujan ◽

Anne Tonson ◽

Robert W. Wiseman ◽

Stephen E. DiCarlo

Keyword(s):

Blood Pressure ◽

Spinal Cord ◽

Arterial Blood Pressure ◽

Histological Examination ◽

Hormonal Responses ◽

Sympathetic Preganglionic Neurons ◽

Supraspinal Control ◽

Arterial Blood ◽

Cord Injury ◽

First Time

Spinal cord injury (SCI) resulting in tetraplegia is a devastating, life-changing insult causing paralysis and sensory impairment as well as distinct autonomic dysfunction that triggers compromised cardiovascular, bowel, bladder, and sexual activity. Life becomes a battle for independence as even routine bodily functions and the smallest activity of daily living become major challenges. Accordingly, there is a critical need for a chronic preclinical model of tetraplegia. This report addresses this critical need by comparing, for the first time, resting-, reflex-, and stress-induced cardiovascular, autonomic, and hormonal responses each week for 4 wk in 12 sham-operated intact rats and 12 rats with chronic, complete C6–7 spinal cord transection. Loss of supraspinal control to all sympathetic preganglionic neurons projecting to the heart and vasculature resulted in a profound bradycardia and hypotension, reduced cardiac sympathetic and parasympathetic tonus, reduced reflex- and stress-induced sympathetic responses, and reduced sympathetic support of blood pressure as well as enhanced reliance on angiotensin to maintain arterial blood pressure. Histological examination of the nucleus ambiguus and stellate ganglia supports the profound and distinct autonomic and cardiac deficits and reliance on angiotensin to maintain cardiovascular stability following chronic, complete cervical6–7 cord transection. NEW & NOTEWORTHY For the first time, resting-, reflex-, and stress-induced cardiovascular, autonomic, and hormonal responses were studied in rats with chronic, complete C6–7 cord transection. Loss of supraspinal control of all sympathetic preganglionic neurons reduced cardiac sympathetic and parasympathetic tonus, reflex and stress-induced sympathetic responses, and sympathetic support of blood pressure as well as enhanced reliance on angiotensin to maintain arterial blood pressure. Histological examination supports the distinct deficits associated with cervical cord injury.

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Peripheral Resistance Changes and Blood Pooling After Endotoxin in Eviscerated Dogs

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1958.195.3.631 ◽

1958 ◽

Vol 195 (3) ◽

pp. 631-634 ◽

Cited By ~ 26

Author(s):

Lerner B. Hinshaw ◽

Robert P. Gilbert ◽

Hiroshi Kuida ◽

Maurice B. Visscher

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

Mean Arterial Blood Pressure ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Endotoxin Shock ◽

E Coli ◽

Arterial Blood ◽

Later Phase

Studies were performed on eviscerated dogs maintained with a constant cardiac inflow with and without injections of lethal amounts of E. coli endotoxin. Continuous recordings of mean arterial blood pressure and total venous return permitted determination of changes in total peripheral resistance and extent of vascular pooling. A significant fall in mean arterial blood pressure occurs within 30 minutes after endotoxin in the eviscerated dog with constant cardiac inflow. There is therefore a decrease in total peripheral resistance. There is also a small but significant increase in vascular pooling exceeding that seen without endotoxin but much reduced from that observed in noneviscerated animals given endotoxin. It is concluded that a decrease in vascular tone occurs after endotoxin and that it probably plays a significant role in the later phase of endotoxin shock in the dog.

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