Mean Circulatory Filling Pressure Measured Immediately After Cessation of Heart Pumping

Guyton, Arthur C.; Polizo, Dimitri; Armstrong, George G.

doi:10.1152/ajplegacy.1954.179.2.261

Cited by 210 publications

(129 citation statements)

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“…The fact that ventricles could be restarted by an increase of pressure (Fig. 4), together with evidence that the venous pressure can be raised by sudden exposure to cold (Bondurant, Hickam & Isley, 1957;Keatinge & McCance, 1957), and that vasoconstriction will raise the mean circulatory filling pressure even after the circulation has stopped (Guyton, Polizo & Armstrong, 1954) suggests that sudden exposure to cold, in the form of a bucket of cold water, might be a useful first-aid measure for Stokes-Adams attacks in man. The observations on the effect of intraluminal pressure on heart block provide an explanation for the clinical observation that bundle-branch block may disappear if the degree of heart failure is reduced (Cecil & Loeb, 1955).…”

Section: Discussionmentioning

confidence: 94%

The effect of increased filling pressure on rhythmicity and atrioventricular conduction in isolated hearts

Keatinge¹

1959

The Journal of Physiology

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Section: Discussionmentioning

confidence: 94%

The effect of increased filling pressure on rhythmicity and atrioventricular conduction in isolated hearts

Keatinge¹

1959

The Journal of Physiology

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“…The increased cardiac filling must occur despite the shortened filling time that results from the postprandial tachycardia, and must therefore stem from increased venous return. The overall haemodynamic state dictating venous return can be assessed from measurements of mean circulatory filling pressure (MCFP), the pressure within the cardiovascular system that prevails when the heart is stopped, which reflects a combination of blood volume and venous tone (Guyton et al, , 1954.…”

Section: Introductionmentioning

confidence: 99%

Improved cardiac filling facilitates the postprandial elevation of stroke volume inPython regius

Enok

Leite

et al. 2016

Journal of Experimental Biology

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To accommodate the pronounced metabolic response to digestion, pythons increase heart rate and elevate stroke volume, where the latter has been ascribed to a massive and fast cardiac hypertrophy. However, numerous recent studies show that heart mass rarely increases, even upon ingestion of large meals, and we therefore explored the possibility that a rise in mean circulatory filling pressure (MCFP) serves to elevate venous pressure and cardiac filling during digestion. To this end, we measured blood flows and pressures in anaesthetized Python regius. The anaesthetized snakes exhibited the archetypal tachycardia as well as a rise in both venous pressure and MCFP that fully account for the approximate doubling of stroke volume. There was no rise in blood volume and the elevated MCFP must therefore stem from increased vascular tone, possibly by means of increased sympathetic tone on the veins. Furthermore, although both venous pressure and MCFP increased during volume loading, there was no evidence that postprandial hearts were endowed with an additional capacity to elevate stroke volume. In vitro measurements of force development of paced ventricular strips also failed to reveal signs of increased contractility, but the postprandial hearts had higher activities of cytochrome oxidase and pyruvate kinase, which probably serves to sustain the rise in cardiac work during digestion.

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“…MCFP is the pressure measured in the vasculature immediately after cardiac arrest, after pressures in all parts of the circulation are made to equilibrate, and represents the effective driving force for venous return to the heart. 24 The major determinants of MCFP are compliance of the venous system and blood volume, 25 and MCFP is considered the best methodology for determination of body venous tone. 26 …”

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confidence: 99%

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

2007

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Abstract-Chronic angiotensin II (Ang II) infusion, in rats fed high salt, engages the sympathetic nervous system to increase venomotor tone. The splanchnic sympathetic nervous system is the most important regulator of venous tone, indicating that splanchnic sympathetic nervous system activity may be increased in Ang II salt hypertension. We hypothesized that celiac ganglionectomy (CGx), to selectively disrupt sympathetic innervation to the splanchnic circulation, would attenuate arterial pressure (AP), and venous tone increases in Ang II salt hypertension. Rats fed 2% or 0.4% NaCl were instrumented to allow AP measurement by radiotelemetry at the same time as surgical CGx or sham operation. Ang II was delivered by minipump (150 ng/kg per minute) for 14 days. CGx reduced AP independent of salt diet during control. CGx markedly attenuated Ang II hypertension in rats on 2% NaCl but had little effect in rats fed 0.4% NaCl. To test the possibility that CGx exerted its effects via renal denervation, rats were subjected to the same protocol but received selective bilateral renal denervation. Renal denervation decreased AP during control but had no protective effect on Ang II hypertension and actually tended to exacerbate the pressor response. Finally, separate groups of rats underwent CGx or sham operation and were instrumented to allow repeated measures of mean circulatory filling pressure, an index of venous tone. In addition to attenuating Ang II salt hypertension, CGx completely prevented Ang II salt-induced increases in mean circulatory filling pressure and substantially attenuated depressor responses to acute ganglion blockade. We conclude that, in the presence of high salt, Ang II activates the splanchnic sympathetic nervous system to increase venomotor tone and AP. Key Words: angiotensin II Ⅲ sympathetic nervous system Ⅲ splanchnic circulation Ⅲ venomotor tone Ⅲ renal denervation W e have shown recently, using repeated measures of mean circulatory filling pressure (MCFP) in conscious undisturbed rats, that chronic infusion of angiotensin II (Ang II), only when administered in combination with a high-salt diet, activates the sympathetic nervous system (SNS) to increase venomotor tone. 1 This increase in venomotor tone may contribute to the pathogenesis of Ang II salt hypertension by increasing central blood volume, resulting in a translocation of blood from the highly compliant venous system to the less compliant arterial circulation. 1 This redistribution of blood volume and the well-documented impairment of renal excretory function caused by Ang II 2 would be major factors in increasing arterial pressure (AP) in this model. [3][4][5] Splanchnic veins and venules account for most of the active capacitance responses in the circulation and are richly innervated by the SNS. 6 -8 In fact, it has been estimated that innervation to the nonhepatic splanchnic organs accounts for half of the total norepinephrine (NE) released in the entire body. 9 Therefore, our recent observations in Ang II salt hypertension of neurog...

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Mean Circulatory Filling Pressure Measured Immediately After Cessation of Heart Pumping

Cited by 210 publications

References 0 publications

The effect of increased filling pressure on rhythmicity and atrioventricular conduction in isolated hearts

The effect of increased filling pressure on rhythmicity and atrioventricular conduction in isolated hearts

Improved cardiac filling facilitates the postprandial elevation of stroke volume inPython regius

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

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