Effect of baroreceptor activation and systemic hypotension on plasma endothelin 1 and neuropeptide Y

1995 ◽  
Vol 73 (8) ◽  
pp. 1136-1143 ◽  
Author(s):  
C. F. Notarius ◽  
F. Erice ◽  
D. Stewart ◽  
S. Magder
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Neuropeptide Y ◽  
Carotid Sinus ◽  
Systemic Arterial Pressure ◽  
Systemic Hypotension ◽  
Endothelin 1 ◽  
Femoral Arteries ◽  
Anesthetized Dogs ◽  
Baroreceptor Activation

To determine whether endothelin (ET-1) and neuropeptide Y (NPY) release are controlled by the carotid sinus (CS) baroreceptor or local endothelial mechanisms, we isolated and pump perfused the CS in eight chloralose-anesthetized dogs and controlled systemic arterial pressure (SAP) with an elevated reservoir connected to both femoral arteries. This allowed the SAP to be kept constant while CS pressure was varied from 55.8 ± 2.0 (low CS) to 192 ± 1.9 (high CS) mmHg (1 mmHg = 133.3 Pa) or CS pressure to be kept constant while SAP was lowered to 53.9 ± 1.8 mmHg (low SAP). There was no significant change in ET-1 when CS pressure was varied (control, 2.08 ± 0.50; low CS, 2.18 ± 0.51; high CS, 2.11 ± 0.38 pg/mL), but ET-1 was significantly higher during low SAP (2.93 ± 0.49 pg/mL, p < 0.05). This increase was not observed with vagi and CS intact in six dogs or with vagi intact and CS constant in four dogs. In contrast, plasma NPY was significantly higher in the low CS condition (619.13 ± 66.87 pg/mL) versus high CS condition (528.88 ± 45.19 pg/mL, p < 0.05) and did not change during hypotension. In conclusion, NPY, but not ET-1, is affected by CS baroreceptor manipulation, and plasma ET-1 increases in response to hemorrhagic hypotension when modulating reflexes are abolished.Key words: endothelin 1, neuropeptide Y, carotid sinus baroreceptor, hemorrhage, cardiac output.

Influence of nitroglycerin on splanchnic capacity and splanchnic capacity-cardiac output relationship

1994 ◽  
Vol 76 (1) ◽  
pp. 112-119 ◽  
Author(s):  
M. A. Morse ◽  
D. L. Rutlen
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Carotid Sinus ◽  
Systemic Arterial Pressure ◽  
Intravascular Volume ◽  
Portal Flow ◽  
Portal Vein Pressure ◽  
Cervical Vagotomy

It has been postulated, but not tested directly, that nitroglycerin's venodilatory effects attenuate cardiac output. Thus, the present study examined the importance of changes in splanchnic capacity, as assessed by scintigraphy, in the regulation of cardiac output during nitroglycerin administration in 16 anesthetized pigs under conditions of carotid sinus denervation and cervical vagotomy. With nitroglycerin administration (0.5 mg/min i.v.) for 5 min, systemic arterial pressure decreased from 115 +/- 7 to 95 +/- 7 mmHg (P < 0.0001), portal vein pressure decreased from 9.0 +/- 0.5 to 8.5 +/- 0.5 mmHg (P < 0.0001), portal flow increased from 637 +/- 49 to 668 +/- 60 ml/min (P = 0.09), and transhepatic resistance decreased from 7.5 +/- 1.5 to 6.5 +/- 1.0 mmHg.min.l-1 (P < 0.01), but cardiac output was unchanged (1,929 +/- 126 to 1,890 +/- 138 ml/min). Total splanchnic intravascular volume (VI) increased 1.6 +/- 1.0% (P < 0.05, 14 +/- 10 ml). This increase was due to an increment in extrahepatosplenic (mesenteric) VI (12.9 +/- 1.9%, P < 0.0001), since splenic VI decreased (9.6 +/- 2.8%, P < 0.0001) and hepatic VI did not change. After splenectomy, nitroglycerin infusions at doses of 0.5 and 2 mg/min were associated with increases in total splanchnic VI of 3.7 +/- 1.2% (P < 0.0001, 30 +/- 10 ml) and 7.6 +/- 1.7% (P < 0.001, 59 +/- 10 ml) due entirely to increases in mesenteric volume of 9.9 +/- 2.7% (P < 0.0001) and 16.5 +/- 1.9% (P < 0.0001), respectively, but cardiac output was unchanged at the end of infusion at either dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of carotid sinus baroreflex in attenuating systemic arterial pressure variability studied in anesthetized dogs

1994 ◽  
Vol 266 (2) ◽  
pp. H720-H729 ◽  
Author(s):  
T. Yoshida ◽  
Y. Harasawa ◽  
T. Kubota ◽  
H. Chishaki ◽  
T. Kubo ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Amplitude Spectrum ◽  
Low Frequency ◽  
Systemic Arterial Pressure ◽  
Open Loop ◽  
Frequency Range ◽  
Carotid Sinus Baroreflex ◽  
Anesthetized Dogs

Attenuation of systemic arterial pressure (SAP) variability by the carotid sinus baroreflex (CSBR) was quantified in nine anesthetized, vagotomized dogs. SAP amplitude spectrum was compared between open-loop [SAPo(f)] and closed-loop [SAPc(f)] operation of the CSBR. At 0.002 Hz, SAPc amplitude was 3.5 +/- 2.2 (SD) mmHg, and SAPo was 9.6 +/- 3.5 mmHg (P < 0.01). At 0.02 Hz, SAP(c) amplitude was 2.8 +/- 1.2 mmHg, and SAPo was 4.3 +/- 1.2 mmHg (P < 0.05). At higher frequencies, SAPo(f) was indistinguishable from SAPc(f). With the opened CSBR, intracarotid sinus pressure (CSP) was pseudorandomly varied, and the resulting SAP responses were recorded to determine the transfer function from CSP to SAP [HCSP.SAP(f)]. From SAPo(f) and the determined HCSP.SAP(f), we estimated SAP(f) if the CSBR was closed [SAPc,est(f)] and compared it with SAPc(f). These two spectra were similar in each dog over a frequency range of 0.002–0.15 Hz, the differences between SAPo(f) and SAPc(f) being reconcilable with HCSP.SAP(f). Although the anesthetized state and vagotomy may have distorted the transfer characteristics of the CSBR from those in conscious (with the intact vagi) states, the results of the present study indicate that the CSBR attenuated SAP variability mainly in a low-frequency range below 0.02 Hz and that this attenuation was attributable to the transfer properties of the CSBR.

Chronic isolation of carotid sinus baroreceptor region in conscious normotensive and hypertensive rats

1998 ◽  
Vol 275 (1) ◽  
pp. H322-H329 ◽  
Author(s):  
Kelly P. McKeown ◽  
Artin A. Shoukas
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Baroreceptor Reflex ◽  
Hypertensive Rats ◽  
Conscious Rat ◽  
Sd Rats ◽  
The Right ◽  
Reflex System

We have developed a chronic technique to isolate the carotid sinus baroreceptor region in the conscious rat model. Our technique, when used in conjunction with other methods, allows for the study of the control of arterial pressure, heart rate, and cardiac output by the carotid sinus baroreceptor reflex in conscious, unrestrained rats. The performance of our technique was evaluated in two strains: normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Each rat was instrumented with an aortic flow probe and a catheter placed in the right femoral artery to monitor cardiac output and arterial pressure, respectively. The cervical sympathetic trunk and aortic depressor nerve were ligated and cut bilaterally, leaving vagus nerves intact. The right and left carotid sinuses were isolated using our new technique. We tested the open-loop function of the carotid sinus baroreceptor reflex system in the conscious rat after recovery from the isolation surgery. We found that changes in nonpulsatile carotid sinus pressure caused significant changes in arterial pressure, heart rate, and total peripheral resistance in both rat strains. However, the cardiac output responses differed dramatically between strains. Significant changes were seen in the cardiac output response of SHR, whereas no significant changes were observed in normotensive SD rats. We have found this technique to be a highly reliable tool for the study of the carotid sinus baroreceptor reflex system in the conscious rat.

Carotid sinus control of pulsatile hemodynamics in halothane-anesthetized dogs

1980 ◽  
Vol 238 (3) ◽  
pp. H294-H299
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Open Loop ◽  
Hydraulic Power ◽  
Set Point ◽  
Hemodynamic Variables ◽  
Vascular Impedance ◽  
Mean Pressure ◽  
Anesthetized Dogs ◽  
Sinus Pressure

The open-loop characteristics of the carotid sinus baroreceptor reflex control of pulsatile arterial pressure-flow relations were studied in halothane-anesthetized dogs. Pressures and flows were measured in the ascending aorta, the celiac, mesenteric, renal, and iliac arteries and were used to compute values of regional vascular impedance and hydraulic power. The carotid sinuses were bilaterally isolated and perfused under conditions of controlled mean pressure with a constant sinusoidal component. Measurements were made with the vagi intact and after bilateral vagotomy. Maximum values of open-loop gain averaged -0.78 +/- 0.08 before and -1.42 +/- 0.20 after vagotomy. Vagotomy produced significant increases in the variation of all hemodynamic variables with carotid sinus pressure that were nonuniformly affected in the various regional vascular beds. Aortic and regional vascular impedance showed significant variations with carotid sinus pressure that were augmented by vagotomy. Aortic impedance exhibited a minimum at the normal set point. These results indicate that a) carotid sinus baroreflexes are well preserved with halothane anesthesia, b) thoracic baroreceptor-mediated reflexes exert significant hemodynamic effects on systemic hemodynamics around normal set point values of arterial pressure, c) systemic baroreceptors exert control over large as well as small vessel properties, and d) the baroreceptor-mediated reflexes produce significant influences on hydraulic power and its components.

Mechanism and pharmacology of endotoxin shock in sheep

1963 ◽  
Vol 18 (3) ◽  
pp. 544-552 ◽  
Author(s):  
D. F. J. Halmagyi ◽  
B. Starzecki ◽  
G. J. Horner
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Arterial Oxygen Saturation ◽  
Lung Compliance ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Arterial Oxygen ◽  
Marked Rise ◽  
Pulmonary Arterial ◽  
Pressure Fall

The cardiopulmonary consequences of coli-lipopolysaccharide and staphylococcus toxin administration were studied in sheep. Circulatory changes consisted mainly of a marked rise in pulmonary arterial and pulmonary arterial wedge pressure (with left atrial pressure unchanged), and a fall in cardiac output and in systemic arterial pressure. Fall in the latter closely followed the onset of pulmonary hypertension. The respiratory response consisted mainly of a severe fall in lung compliance produced by terminal airway closure. Continued perfusion of the nonventilated alveoli resulted in venous admixture. Premedication with antihistaminic, antiserotonin, or adrenolytic agents failed to affect the response. Norepinephrine or hypertensin administered after toxin injection had virtually no effect while isoproterenol treatment reduced pulmonary arterial pressure, increased cardiac output, arterial oxygen saturation, and, in cases of endotoxin shock, promptly raised systemic arterial pressure. Endotoxin-resistant sheep proved nonresponsive to minor pulmonary embolism and to incompatible blood transfusion. It is suggested that a common mediator agent is responsible for the similar cardiopulmonary consequences of these three diverse conditions. Submitted on November 26, 1962

Baroreflex attenuation after hypotension induced by vena caval occlusion in anesthetized dogs

1995 ◽  
Vol 268 (4) ◽  
pp. R859-R864
Author(s):  
F. Sawano ◽  
T. Shibamoto ◽  
T. Hayashi ◽  
Y. Saeki
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Systemic Hypotension ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Cardiopulmonary Receptors ◽  
Pressure Fall

We determined effects of vena caval occlusion-induced systemic hypotension of 50 mmHg lasting 10 min (VCO) on efferent sympathetic nerve activity (SNA) and sympathetic baroreflex responsiveness. We recorded simultaneously SNA to the kidney (RNA), heart (CNA), spleen (SpNA), and liver (HNA) in anesthetized dogs. Baroreflex sensitivity was assessed using the ratio of a reflex SNA increase to a mean arterial pressure fall, which was also induced by caval occlusion. During VCO, SNA initially and equivocally increased, followed by recovery toward baseline. Cervical vagotomy attenuated the VCO-induced initial sympathoexcitation and subsequently maintained SNA at higher levels than those of intact animals, a finding basically similar to hemorrhagic hypotension [S. Koyama, F. Sawano, Y. Matsuda, Y. Saeki, T. Shibamoto, T. Hayashi, Jr., Y. Matsubayashi, and M. Kawamoto. Am. J. Physiol. 262 (Regulatory Integrative Comp. Physiol. 31): R579-R585, 1992]. At 5 min after releasing VCO, the baroreflex responsiveness was significantly attenuated: RNA, 79 +/- 11%; CNA, 78 +/- 8%; HNA, 60 +/- 16%; SpNA, 81 +/- 13% of the corresponding baseline. Fifteen minutes after VCO, this attenuation disappeared. Either vagotomy or pretreatment with intravenous vasopressin V1 receptor antagonist abolished this baroreflex attenuation. In conclusion, systemic hypotension to 50 mmHg for 10 min causes transient attenuation of sympathetic baroreflex sensitivity due to circulating vasopressin released by unloading of cardiopulmonary receptors during hypotension.

Rho kinase and Ca2+ entry mediate increased pulmonary and systemic vascular resistance in l-NAME-treated rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1306-L1313 ◽  
Author(s):  
Jasdeep S. Dhaliwal ◽  
David B. Casey ◽  
Anthony J. Greco ◽  
Adeleke M. Badejo ◽  
Thomas B. Gallen ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Rho Kinase ◽  
Systemic Arterial Pressure ◽  
Intravenous Injections ◽  
Pulmonary Arterial ◽  
Dose Dependent

The small GTP-binding protein and its downstream effector Rho kinase play an important role in the regulation of vasoconstrictor tone. Rho kinase activation maintains increased pulmonary vascular tone and mediates the vasoconstrictor response to nitric oxide (NO) synthesis inhibition in chronically hypoxic rats and in the ovine fetal lung. However, the role of Rho kinase in mediating pulmonary vasoconstriction after NO synthesis inhibition has not been examined in the intact rat. To address this question, cardiovascular responses to the Rho kinase inhibitor fasudil were studied at baseline and after administration of an NO synthesis inhibitor. In the intact rat, intravenous injections of fasudil cause dose-dependent decreases in systemic arterial pressure, small decreases in pulmonary arterial pressure, and increases in cardiac output. l-NAME caused a significant increase in pulmonary and systemic arterial pressures and a decrease in cardiac output. The intravenous injections of fasudil after l-NAME caused dose-dependent decreases in pulmonary and systemic arterial pressure and increases in cardiac output, and the percent decreases in pulmonary arterial pressure in response to the lower doses of fasudil were greater than decreases in systemic arterial pressure. The Ca++ entry blocker isradipine also decreased pulmonary and systemic arterial pressure in l-NAME-treated rats. Infusion of sodium nitroprusside restored pulmonary arterial pressure to baseline values after administration of l-NAME. These data provide evidence in support of the hypothesis that increases in pulmonary and systemic vascular resistance following l-NAME treatment are mediated by Rho kinase and Ca++ entry through L-type channels, and that responses to l-NAME can be reversed by an NO donor.

Effect of PEEP on discharge of pulmonary C-fibers in dogs

1985 ◽  
Vol 59 (4) ◽  
pp. 1085-1089 ◽  
Author(s):  
M. P. Kaufman ◽  
G. A. Ordway ◽  
T. G. Waldrop
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Impulse Activity ◽  
Vena Cava ◽  
Laboratory Animals ◽  
Positive End Expiratory Pressure ◽  
Firing Rates ◽  
C Fibers ◽  
Anesthetized Dogs ◽  
Stimulation Of

Although positive end-expiratory pressure (PEEP) is believed to depress cardiac output and arterial pressure by compressing the vena cava and the heart, it is unclear whether PEEP also depresses these variables by a reflex arising from an inflation-induced stimulation of pulmonary C-fibers. We therefore recorded the impulse activity of 17 pulmonary C-fibers in barbiturate-anesthetized dogs with closed chests, while we placed the expiratory outlet of a ventilator under 5–30 cmH2O. Increasing PEEP in a ramp-like manner stimulated 12 of the 17 pulmonary C-fibers, with activity increasing from 0.0 +/- 0.1 to 0.9 +/- 0.2 imp/s when end-expiratory pressure equaled 15 cmH2O. When PEEP was increased in a stepwise manner to 15–20 cmH2O and maintained at this pressure for 15 min, pulmonary C-fibers increased their firing rates, but the effect was small averaging 0.2–0.3 imp/s after the 1st min of this maneuver. We conclude that pulmonary C-fibers are unlikely to be responsible for causing much of the decreases in cardiac output and arterial pressure evoked by sustained periods of PEEP in both patients and laboratory animals. These C-fibers, however, are likely to be responsible for causing the reflex decreases in these variables evoked by sudden application of PEEP.

Modulation of carotid sinus baroreceptor reflex by sciatic nerve stimulation

1975 ◽  
Vol 228 (5) ◽  
pp. 1535-1541 ◽  
Author(s):  
M Kumada ◽  
K Nogami ◽  
K Sagawa
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Baroreceptor Reflex ◽  
Equilibrium Pressure ◽  
Sciatic Nerve Stimulation

In anethetized, immobilized, and vagotomized cats we analyzed the effect of sciatic nerve stimulation (SNS) on the relationships between intrasinus pressure (ISP) and arterial pressure (AP) and between ISP and heart rate (HR). At each of seven ISP levels between 60 and 240 mmHg, AP and HR before and 20 s after the onset of SNS were plotted against ISP to obtain the ISP-AP and ISP-HR relationships before and during SNA. SNA caused increases in AP, HR, and total peripheral resistance (TPR) and a decrease in cardiac output (CO). SNS raised the equilibrium pressure (the value of AP at which AP equaled ISP), but it significantly (P smaller than 0.005) decreased the slope (or gain) of the ISP-AP relationship at ISP's between 90 and 150 mmHg. SNS also significantly (P smaller than 0.05) diminished the gain of ISP-HR relationship at ISP's between 120 and 210 mmHg. Modulation of the gain of ISP-AP relationship was ascribable to that of CO but not of TPR. We conclude that in vagotomized cats 1) SNS attenuates the sensitivity of AP and HR responses in the carotid sinus baroreceptor reflex, and 2) the inhibition of the reflex AP response was caused by modulation of the reflex CO response.

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation

1975 ◽  
Vol 39 (3) ◽  
pp. 411-416 ◽  
Author(s):  
D. Heistad ◽  
F. M. Abboud ◽  
A. L. Mark ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Ventilatory Response ◽  
Carotid Bifurcation ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Baroreceptor Activation ◽  
Stimulation Of

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

Sign in / Sign up

Export Citation Format

Share Document