Carotid sinus baroreceptor reflex control and the role of autoregulation in the systemic and pulmonary arterial pressure-flow relationships of the dog.

Shoukas, Artin A.; Brunner, M. J.; Frankle, A E; Greene, Andrew S.; Kallman, Clayton H.

doi:10.1161/01.res.54.6.674

Cited by 36 publications

(23 citation statements)

References 22 publications

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“…Shoukas et al 10 have reported that large changes in carotid sinus pressure may produce small shifts in the pulmonary vascular pressure-flow relationship. The changes in blood pressure that we observed after opening the fistulas in each condition or after hydralazine therapy were small, and would not be expected to have altered the PA-CO plots.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism.

Ducas¹,

Girling²,

Schick³

et al. 1986

Circulation

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Pulmonary arterial pressure (PAP)-flow coordinates were obtained in 14 anesthetized dogs before and after pulmonary hypertension was induced with autologous blood clots. Cardiac output (CO) was altered by systemic arteriovenous fistulas. The PAP-CO coordinates were always rectilinear. Before emboli, the mean vascular closing or outflow pressure (the pressure intercept of the PAP-CO line) was 8. THE ACTION of vasoactive drugs in pulmonary hypertensive disorders has been the focus of extensive investigation. Several clinical reports'-' and a recent canine study4 have documented an increase in cardiac output (CO) and a decrease in pulmonary vascular resistance with hydralazine. In these studies, pulmonary vascular resistance, calculated as (mean pulmonary arterial pressure [PAP] -left atrial pressure) + CO is assumed to reflect the flow-resistive properties of the pulmonary vasculature. This approach forces one to make assumptions about the vascular effects of the drug on the basis of single pressure-flow measurements before and during therapy. When these data are used to define a "resistance," as derived from Poiseuille's law, it is implied that the relationship between pressure and flow in the pulmonary circulation is linear, and that flow begins (zone III) when the upstream pressure (PAP) exceeds the apparent downstream left

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Section: Discussionmentioning

confidence: 99%

Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism.

Ducas¹,

Girling²,

Schick³

et al. 1986

Circulation

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“…Evidence primarily derived from animal experiments suggests that the carotid sinus baroreflex also affects respiratory function (7,26,45,48). Rapidly increasing blood pressure causes decreased ventilation, whereas decreasing blood pressure causes increased ventilation.…”

Section: Baroreceptors; Ventilation; Blood Pressurementioning

confidence: 99%

Ventilatory baroreflex sensitivity in humans is not modulated by chemoreflex activation

Stewart

Rivera²,

Clarke³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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IL, Ocon AJ, Taneja I, Terilli C, Medow MS. Ventilatory baroreflex sensitivity in humans is not modulated by chemoreflex activation. Am J Physiol Heart Circ Physiol 300: H1492-H1500, 2011. First published February 11, 2011 doi:10.1152/ajpheart.01217.2010.-Increasing arterial blood pressure (AP) decreases ventilation, whereas decreasing AP increases ventilation in experimental animals. To determine whether a "ventilatory baroreflex" exists in humans, we studied 12 healthy subjects aged 18 -26 yr. Subjects underwent baroreflex unloading and reloading using intravenous bolus sodium nitroprusside (SNP) followed by phenylephrine ("Oxford maneuver") during the following "gas conditions:" room air, hypoxia (10% oxygen)-eucapnia, and 30% oxygen-hypercapnia to 55-60 Torr. Mean AP (MAP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), expiratory minute ventilation (V E), respiratory rate (RR), and tidal volume were measured. After achieving a stable baseline for gas conditions, we performed the Oxford maneuver. V E increased from 8.8 Ϯ 1.3 l/min in room air to 14.6 Ϯ 0.8 l/min during hypoxia and to 20.1 Ϯ 2.4 l/min during hypercapnia, primarily by increasing tidal volume. V E doubled during SNP. CO increased from 4.9 Ϯ .3 l/min in room air to 6.1 Ϯ .6 l/min during hypoxia and 6.4 Ϯ .4 l/min during hypercapnia with decreased TPR. HR increased for hypoxia and hypercapnia. Sigmoidal ventilatory baroreflex curves of V E versus MAP were prepared for each subject and each gas condition. Averaged curves for a given gas condition were obtained by averaging fits over all subjects. There were no significant differences in the average fitted slopes for different gas conditions, although the operating point varied with gas conditions. We conclude that rapid baroreflex unloading during the Oxford maneuver is a potent ventilatory stimulus in healthy volunteers. Tidal volume is primarily increased. Ventilatory baroreflex sensitivity is unaffected by chemoreflex activation, although the operating point is shifted with hypoxia and hypercapnia.baroreceptors; ventilation; blood pressure In intact animals (dogs) hyperpnea follows occlusion of the common carotid arteries; it is wholly reflex in origin because the effect is the same even though all branches of the carotids have been previously tied excepting only the lingual arteries, and because section of the sinus nerves completely abolishes the reaction.Carl F. Schmidt (45) DETECTION OF ARTERIAL BLOOD PRESSURE (AP) by the arterial baroreceptors causes changes in heart rate (HR), sympathetic vasoconstriction, adrenal function, and renal sympathetic activity (2, 5). Evidence primarily derived from animal experiments suggests that the carotid sinus baroreflex also affects respiratory function (7,26,45,48). Rapidly increasing blood pressure causes decreased ventilation, whereas decreasing blood pressure causes increased ventilation. While these ventilatory effects were at one time attributed to increased or decreased perfusion of the arterial chemoreceptors (26, 32), s...

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“…Some factors, such as catecholamines, which can modify Q, may also act on HPV [24]. However, although no catecholamines were used in this study, no variations in fC or SAP were found before or after dextran infusion.…”

Section: Discussionmentioning

confidence: 81%

The effect of hypertonic saline dextran solutions on hypoxic pulmonary vasoconstriction in anaesthetised piglets

Bellezza¹,

Kerbaul²,

Roussel³

et al. 2002

European Respiratory Journal

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The effect of hypertonic saline dextran solutions on hypoxic pulmonary vasoconstriction in anaesthetised piglets. M. Bellezza, F. Kerbaul, L. Roussel, M. Imbert, C. Guidon. #ERS Journals Ltd 2002. ABSTRACT: Hypoxic pulmonary vasoconstriction (HPV) is a regulatory mechanism by which blood is diverted from poorly ventilated to better ventilated areas of the lung. The aim of the present study was to assess the extent to which hypertonic saline dextran and dextran solutions modify the magnitude of HPV during isovolumic haemodilution in intact acutely instrumented piglets.Eighteen large white piglets were anesthetised and assigned to two groups. Mean pulmonary arterial pressure (PAP) and cardiac output (Q), systemic arterial pressure and left arterial pressure (LAP) were measured. A decrease in Q was obtained by reducing venous return. This enabled measurement of transpulmonary pressures (mean PAP minus LAP) at four levels of Q in hyperoxia (inspiratory oxygen fraction (Fi,O 2 )=0.4), then in hypoxia (Fi,O 2= 0.1) in the two groups before blood soustraction (10 mL?kg -1 ) and after loading with sodium chloride (NaCl) 7.5% and dextran 6% or with dextran 6% alone. Dextran alone led to a decrease in mean PAP-LAP/Q values, and NaCl with dextran was associated with a significant shift of mean PAP-LAP/Q plots to higher pressures in hypoxia.Hypertonic saline dextran solution, as replacement fluid in isovolaemic haemodilution increased the magnitude of hypoxic pulmonary vasoconstriction, whereas dextran solution reduced it. Fluid expanders are usually used for the resuscitation of intraoperative hypovolaemia or haemorragia. They act on different parts of the cardiovascular system, mainly the heart and vascular resistances. Therefore, the vascular resistance response differs with the solution used and the vascular bed of the organ studied [1,2].Hypertonic saline solution (sodium chloride (NaCl) 7.5%) with dextran 6% has been shown to increase volaemia ten-times more than dextran 6% by an osmotic effect (transfer of water from the interstitial to vascular space), this, in turn, increases cardiac output (Q) and decreases systemic vascular resistance [3,4]. However, the effect of this hypertonic saline and dextran solution on pulmonary circulation remains unknown. Dextran used alone can also reduce pulmonary vascular resistance (PVR) resulting in a reduction of blood viscosity.Therefore, the effect of these two different plasma expanders on pulmonary vascular circulation was studied, focusing on the hypoxic pulmonary vascular response using pressure (P)/Q relationships in intact anaesthetised piglets submitted to normovolaemic haemodilution. It was hypothesised that these two different plasma expanders would have different effects on hypoxic pulmonary vasoconstriction (HPV), and thereby modify gas exchange. Piglets were chosen because they exhibit the greatest pulmonary vasoconstriction response to hypoxia [5]. In this study, pulmonary haemodynamics were evaluated by multipoint P/Q (mean pulmonary arterial pressure (PAP)-LAP/Q) ...

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Carotid sinus baroreceptor reflex control and the role of autoregulation in the systemic and pulmonary arterial pressure-flow relationships of the dog.

Cited by 36 publications

References 22 publications

Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism.

Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism.

Ventilatory baroreflex sensitivity in humans is not modulated by chemoreflex activation

The effect of hypertonic saline dextran solutions on hypoxic pulmonary vasoconstriction in anaesthetised piglets

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