Cardiopulmonary reflexes and blood pressure in exercising sinoaortic-denervated dogs

1984 ◽  
Vol 57 (5) ◽  
pp. 1417-1421 ◽  
Author(s):  
D. A. Daskalopoulos ◽  
J. T. Shepherd ◽  
S. C. Walgenbach
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vagal Afferents ◽  
Systemic Resistance ◽  
Vigorous Exercise ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Cardiopulmonary Receptors

To examine the role of cardiopulmonary receptors in arterial blood pressure regulation during and after exercise, conscious dogs with chronic sinoaortic denervation were subjected to 12 min of light exercise and 12 min of exercise that increased in severity every 3 min. Hemodynamic measurements were made before and after interruption of cardiopulmonary afferents by bilateral cervical vagotomy. During both exercise protocols, after an initial transient decrease, the arterial blood pressure remained close to resting values before and after vagotomy. On cessation of the graded exercise, the arterial blood pressure did not change before, but a rapid and sustained increase in pressure occurred after vagotomy. At the time of this increase the cardiac output and heart rate were returning rapidly to the resting level. The study demonstrates that in the chronic absence of arterial baroreflexes, vagal afferents prevent a rise in arterial blood pressure after vigorous exercise presumably by the action of cardiopulmonary receptors causing a rapid dilatation of systemic resistance vessels.

Cardiovascular effects of atrial extracts in anesthetized rats

1984 ◽  
Vol 62 (7) ◽  
pp. 819-826 ◽  
Author(s):  
Uwe Ackermann ◽  
Terumi G. Irizawa ◽  
Susan Milojevic ◽  
Harald Sonnenberg
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Hypotensive Effect ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
Direct Stimulation ◽  
Arterial Blood ◽  
Cardiopulmonary Receptors

Tissue extracts derived from atria or ventricles of Sprague–Dawley rats were injected into Inactin-anesthetized assay rats. Compared with ventricular extracts, atrial extracts produced a 20 mmHg (1 mmHg = 133.322 Pa) fall in mean arterial blood pressure. This fall resulted from failure to increase cardiac output in compensation for peripheral vasodilation. Two factors were responsible: depression of heart rate (by 25 beats/min) and failure to increase cardiac performance. The time patterns and magnitudes of changes in cardiovascular parameters after cardiac extracts were not changed by prior atropinization. However, assay rats that were vagotomized showed no cardiac slowing after atrial extract and showed a significantly smaller decrease in mean arterial blood pressure than did sham-vagotomized or intact rats. Another group of assay rats was vagotomized as well as carotid-sinus-denervated before extract injection. In these rats the degree of hypotension caused by atrial extract was significantly greater than that observed after vagotomy alone and was not significantly different from that observed in rats with intact innervation. The results suggest that the hypotension that is caused by atrial extract, but not by ventricular extracts, results in part from the reflex effects of direct stimulation of chemosensitive cardiopulmonary receptors with vagal afferents and partly from the reflex effects of baroreceptor unloading. Ventricular extract had no hypotensive effect in any group of assay rats.

Cardiopulmonary reflexes and arterial pressure during rest and exercise in dogs

1983 ◽  
Vol 244 (3) ◽  
pp. H362-H369 ◽  
Author(s):  
S. C. Walgenbach ◽  
D. E. Donald
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Aortic Arch ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
General Level ◽  
Arterial Blood ◽  
Cervical Vagotomy ◽  
The Moment ◽  
Cardiopulmonary Receptors

Mean arterial blood pressure, heart rate, and cardiac output were monitored at rest and during exercise of two grades of severity in conscious dogs under control conditions and after progressive interruption of the baroreflexes. Aortic arch denervation and vascular isolation and pressurization of the carotid sinuses were used to interrupt arterial baroreflexes. Subsequent interruption of cardiopulmonary afferents was produced by acute bilateral cervical vagotomy. The results indicate that 1) with the cardiopulmonary receptors alone operative, the arterial blood pressure response to exercise is abnormal, 2) cardiopulmonary receptors do not contribute to the moment-to-moment modulation of arterial pressure, and 3) the carotid sinuses, aortic arch, and cardiopulmonary receptors are all involved in determining the mean level of arterial blood pressure. It is concluded that vagally innervated cardiopulmonary receptors do not have a significant role in regulating arterial blood pressure during exercise but are involved in establishing the general level of arterial blood pressure.

Electrical stimulation of cervical vagal afferents. II. Central relays for behavioral antinociception and arterial blood pressure decreases

1990 ◽  
Vol 64 (4) ◽  
pp. 1115-1124 ◽  
Author(s):  
A. Randich ◽  
K. Ren ◽  
G. F. Gebhart
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Nucleus Tractus Solitarius ◽  
Cardiovascular Response ◽  
Ibotenic Acid ◽  
Vagal Afferents ◽  
Ventrolateral Medulla ◽  
Tail Flick ◽  
Threshold Intensity ◽  
Arterial Blood

1. Supraspinal substrates mediating vagal afferent stimulation (VAS)-induced inhibition of the nociceptive tail-flick reflex were examined by the use of the soma-selective neurotoxin ibotenic acid and the nonselective local anesthetic lidocaine. Fifty rats were studied in the lightly anesthetized state maintained with pentobarbital sodium. 2. The threshold intensity of VAS required to inhibit the tail-flick reflex to a cut-off latency of 10 s was established in all rats. Ibotenic acid (5 or 10 micrograms, 0.5 microliter) or lidocaine (4%, 0.5 microliter) was then microinjected into various regions of the brain stem followed by reestablishment of the intensity of VAS required to produce inhibition of the tail-flick reflex. 3. Microinjections of ibotenic acid into the ipsilateral nucleus tractus solitarius (NTS), medial rostroventral medulla (principally the nucleus raphe magnus; NRM), or bilaterally into the dorsolateral pons (principally the locus coeruleus/subcoeruleus; LC/SC), significantly increased the threshold intensity of VAS required to inhibit the tail-flick reflex. Microinjections of ibotenic acid into either the rostral or caudal ventrolateral medulla (RVLM or CVLM, respectively) ipsilateral to the vagus nerve stimulated or ipsilateral LC/SC did not significantly affect the inhibition produced by VAS. Arterial blood pressure decreases produced by VAS were significantly attenuated or eliminated after microinjections of ibotenic acid into the NTS, RVLM, CVLM, or NRM. Lidocaine microinjected into the ipsilateral CVLM also significantly increased the intensity of VAS required to inhibit the tail-flick reflex. 4. These outcomes obtained with behavioral measures are consistent with the outcomes of the preceding study using electrophysiological measures in establishing that cells in the NTS, LC/SC, and NRM regions and fibers of passage in the CVLM are important in mediating the inhibitory effects of VAS. The present studies confirm previous reports of the importance of the RVLM and CVLM in VAS-produced depressor responses but also demonstrate that the NRM is critical for this cardiovascular response.

The Study of Dynamic Response to Acute Hemorrhage by Pulse Spectrum Analysis

2006 ◽  
Vol 34 (03) ◽  
pp. 449-460 ◽  
Author(s):  
Yu Hsin Chang ◽  
Chia I Tsai ◽  
Jaung Geng Lin ◽  
Yue Der Lin ◽  
Tsai Chung Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Spectrum Analysis ◽  
Pulse Spectrum ◽  
Acute Hemorrhage ◽  
Arterial Blood ◽  
Percentage Difference ◽  
Before And After

Traditional Chinese Medicine (TCM) holds that Blood and Qi are fundamental substances in the human body for sustaining normal vital activity. The theory of Qi, Blood and Zang-Fu contribute the most important theoretical basis of human physiology in TCM. An animal model using conscious rats was employed in this study to further comprehend how organisms survive during acute hemorrhage by maintaining the functionalities of Qi and Blood through dynamically regulating visceral physiological conditions. Pulse waves of arterial blood pressure before and after the hemorrhage were taken in parallel to pulse spectrum analysis. Percentage differences of mean arterial blood pressure and harmonics were recorded in subsequent 5-minute intervals following the hemorrhage. Data were analyzed using a one-way analysis of variance (ANOVA) with Duncan's test for pairwise comparisons. Results showed that, within 30 minutes following the onset of acute hemorrhage,the reduction of mean arterial blood pressure was improved from 62% to 20%. Throughout the process, changes to the pulse spectrum appeared to result in a new balance over time. The percentage differences of the second and third harmonics, which were related to kidney and spleen, both increased significantly than baseline and towards another steady state. Apart from the steady state resulting from the previous stage, the percentage difference of the 4th harmonic decreased significantly to another steady state. The observed change could be attributed to the induction of functional Qi, and is a result of Qi-Blood balancing activity that organisms hold to survive against acute bleeding.

scholarly journals Interrelationships between pulse arrival time and arterial blood pressure during postural transitions before and after spaceflight

2019 ◽  
Vol 127 (4) ◽  
pp. 1050-1057
Author(s):  
Katelyn N. Wood ◽  
Danielle K. Greaves ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Arrival Time ◽  
Standing Posture ◽  
Pulse Arrival Time ◽  
Arterial Blood ◽  
Increased Risk ◽  
Before And After ◽  
Acute Changes ◽  
Pulse Arrival

We tested the hypothesis that acute changes in arterial blood pressure (BP) when astronauts moved between supine and standing posture before and after spaceflight can be tracked by beat-to-beat changes in pulse arrival time (PAT). Nine male crewmembers (45 ± 7 yr of age; mean mission length: 165 ± 13 days) participated in a standardized supine-to-sit-to-stand test (5 min-30 s-3 min) before flight and 1 day following return to Earth with continuous monitoring of ECG and finger arterial BP. PAT was determined from the R-wave of the ECG to the foot of the BP waveform. On average, modest cardiovascular deconditioning was detected by ~10 beats/min increase in heart rate in supine and standing posture after spaceflight ( P < 0.05). When looking across the full data collection period, the r2 values between inverse of PAT (1/PAT) and systolic (SBP) and diastolic BP (DBP) varied considerably between individuals (SBP preflight 0.142 ± 0.186, postflight 0.262 ± 0.243). Individual variability was consistent during periods of transition (SBP preflight 0.284 ± 0.324, postflight 0.297 ± 0.269); however, when SBP dropped >20 mmHg, r2 was significant in 5 of 5 preflight tests and 5 of 7 postflight tests. The standard error of the estimate based on a simple linear model during both pre- and postflight testing was 9–11 mmHg for SBP and 6–7 mmHg for DBP. Overall, the results support the hypothesis that PAT tracked dynamic changes in BP. PAT as a noninvasive, nonintrusive surrogate for changes in BP could be developed as an indicator of risk for syncope on return from spaceflight or other Earth-based applications. NEW & NOTEWORTHY Astronauts returning to Earth’s gravity are at increased risk of low blood pressure on standing. Arterial pulse arrival time tracked the decrease in arterial blood pressure on moving from supine to upright posture. Nonintrusive technology providing indicators sensitive to acute changes in blood pressure could act as an early warning system to identify risk for hypotension that place astronauts, or people on Earth, at risk of impaired cognitive performance, fainting, and falls.

scholarly journals Cerebral Blood Flow Changes during Cortical Spreading Depression are Not Altered by Inhibition of Nitric Oxide Synthesis

1994 ◽  
Vol 14 (6) ◽  
pp. 939-943 ◽  
Author(s):  
Zheng Gang Zhang ◽  
Michael Chopp ◽  
Kenneth I. Maynard ◽  
Michael A. Moskowitz
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Arterial Blood ◽  
Nos Inhibitors ◽  
Before And After ◽  
Male Wistar Rats

CBF increases concomitantly with cortical spreading depression (CSD). We tested the hypothesis that CBF changes during CSD are mediated by nitric oxide (NO). Male Wistar rats (n = 23) were subjected to KCl-induced CSD before and after administration of nitric oxide synthase (NOS) inhibitors N-nitro-l-arginine (L-NNA) or N-nitro-l-arginine methyl ester (L-NAME) and in nontreated animals. CBF, CSD, and mean arterial blood pressure were recorded. Brain NOS activity was measured in vitro in control, L-NNA, and L-NAME-treated rats by the conversion of [3H]arginine to [3H]citrulline. Our data show that the NOS inhibitors did not significantly change regional CBF (rCBF) during CSD, even though cortical NOS activity was profoundly depressed and systemic arterial blood pressure was significantly increased. Our data suggest that rCBF during CSD in rats is not regulated by NO.

Ouabain prevents loss of autoregulation in rat pial arterioles caused by reoxygenation after a brief hypoxic episode

1989 ◽  
Vol 67 (5) ◽  
pp. 423-427 ◽  
Author(s):  
J. Kettler ◽  
B. Y. Ong ◽  
D. Bose
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Protective Effects ◽  
Cranial Window ◽  
Arterial Blood ◽  
Hypoxic Episode ◽  
Electrogenic Sodium Pump ◽  
Before And After ◽  
Pressure Changes ◽  
Arteriolar Diameter

Pial arteriolar diameter changes inversely with changes in systemic arterial blood pressure. Such changes are consistent with autoregulatory functions. These responses are reduced by a brief period of hypoxia followed by reoxygenation. By using an open cranial window preparation we assessed the changes in pial arteriolar diameters during blood pressure changes in rats induced by hemorrhage and reinfusion of blood, before and after a brief period of hypoxia. The slopes of the changes in pial arteriolar diameter as a function of mean arterial blood pressure were −0.47 ± 0.26 μm/mmHg (mean ± SD; 1 mmHg = 133.3 Pa) before hypoxia and −0.11 ± 0.23 μm/mmHg after hypoxia in the untreated rats. In ouabain-treated rats, corresponding slopes were −0.42 ± 0.24 and −0.46 ± 0.22 μm/mmHg. The observed protective effects of ouabain might be a blockade of the Na–K pump in the sarcolemma of the vascular smooth muscle.Key words: vascular smooth muscle, electrogenic sodium pump, metabolic inhibition.

scholarly journals Changes in Peripheral Arterial Blood Pressure After Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) in Non-traumatic Cardiac Arrest Patients

2021 ◽  
Author(s):  
Jostein Rødseth Brede ◽  
Eivinn Skjærseth ◽  
Pål Klepstad ◽  
Trond Nordseth ◽  
Andreas Jørstad Krüger
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Balloon Occlusion ◽  
Aortic Occlusion ◽  
Compression Phase ◽  
Adjunct Treatment ◽  
Relaxation Phase ◽  
Arterial Blood ◽  
Before And After ◽  
Peripheral Arterial

Abstract Background Resuscitative endovascular balloon occlusion of the aorta (REBOA) may be an adjunct treatment to cardiopulmonary resuscitation (CPR). Aortic occlusion may increase aortic pressure and increase the coronary perfusion pressure and the cerebral blood flow. Peripheral arterial blood pressure is often measured during or after CPR, however, changes in peripheral blood pressure after aortic occlusion is insufficiently described. This study aimed to assess changes in peripheral arterial blood pressure after REBOA in patients with out of hospital cardiac arrest.Methods An observational study performed at the helicopter emergency medical service in Trondheim (Norway). Eligible patients received REBOA as adjunct treatment to advanced cardiac life support. Peripheral invasive arterial blood pressure and end-tidal CO2 (EtCO2) was measured before and after aortic occlusion. Differences in arterial blood pressures and EtCO2 before and after occlusion was analysed with Wilcoxon Signed Rank test.Results Five patients were included to the study. The median REBOA procedural time was 11 minutes and median time from dispatch to aortic occlusion was 50 minutes. Two patients achieved return of spontaneous circulation. EtCO2 increased significantly 60 seconds after occlusion, by a mean of 1.16 kPa (p = 0.043). Before occlusion the arterial pressure in compression phase were 43.2 (12 – 112) mmHg, the mean pressure 18.6 (4 – 27) mmHg and pressure in the relaxation phase 7.8 (-7 – 22) mmHg. Two minutes after aortic occlusion the corresponding pressures were 114.8 (23 – 241) mmHg, 44.6 (15 – 87) mmHg and 14.8 (0 – 29) mmHg. The arterial pressures were significant different in the compression phase and as mean pressure (p = 0.043 and p = 0.043, respectively) and not significant in the relaxation phase (p = 0.223).Conclusion This study is, to our knowledge, the first to assess the peripheral invasive arterial blood pressure response to aortic occlusion during CPR in the pre-hospital setting. REBOA application during CPR significantly increase the peripheral artery pressures. This likely indicates improved central aortic blood pressure and warrants studies with simultaneous peripheral and central blood pressure measurement during aortic occlusion.Trial registration The study is registered in ClinicalTrials.gov (NCT03534011).

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