Simultaneous Determination of the Pulmonary and Systemic Circulation Times in Man and of a Figure Related to the Cardiac Output

Hamilton, W. F.; Moore, John W.; Kinsman, J. M.; Spurling, R. Glen

doi:10.1152/ajplegacy.1928.84.2.338

Cited by 170 publications

(52 citation statements)

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“…He also performed dye injection with color recording in the retinal vessels at the eye fundus [52,53,54,55,56,57]. Hamilton et al improved the concept of time±concentration curves [58,59,60,61]. Meier and Zierler then applied the model developed by Stewart and Hamilton to the measurement of regional blood flows [62,63,64].…”

Section: Central Volume Principlementioning

confidence: 99%

Quantitative assessment of regional cerebral blood flows by perfusion CT studies at low injection rates: a critical review of the underlying theoretical models

et al. 2001

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IntroductionBrain metabolism is provided almost exclusively by glucose oxidation. The high metabolic demand of the brain, associated with its inability to store energy, requires an important and stable cerebral perfusion, in order to guarantee a normal cerebral function. Mean cerebral blood flow (CBF) values range around 50 cc per 100 g and per minute. They are, however, higher in young people and lower in the elderly. Regional cerebral blood flows (rCBF) are twice or thrice superior in the gray matter, compared with those in the white matter. rCBF are increased in activated cerebral areas. The rCBF changes relating to cerebral activity modifications may reach 10±20 %, and up to 40 % in case of extreme metabolic conditions, such as coma or convulsion [1, 2].Complex autoregulation processes ensure both the adjustment of rCBF to local energetic needs, determined by the activity level of local neurons and the stability of CBF despite changes in systemic arterial pressure. This rCBF autoregulation is controlled by intricate neurobiochemical mechanisms, involving sensitivity to blood pressure, blood pCO 2 and pH. Brain vascular autoregulation notably allows for a vascular dilatation when the systemic pressure tends to lower, in order to keep a constant CBF. This vascular dilatation leads in turn to an increased cerebral blood volume (CBV) [3, 4].The rCBF alterations are encountered in a variety of pathological conditions, the most frequent being strokes. Strokes affect 500,000 patients every year in the United States and represent the third cause of death in Eur. Radiol. (2001) Abstract Viability of the cerebral parenchyma is dependent on cerebral blood flow (CBF), which is usually kept in a very narrow range due to efficient autoregulation processes and can be altered in a variety of pathological conditions. An accurate method allowing for a quantitative assessment of regional cerebral blood flows (rCBF) and available for the routine clinical practice would, for sure, greatly contribute to improving the management of patients with cerebrovascular diseases. Different imaging techniques are now available to evaluate rCBF: positron emission tomography; single photon emission CT; stable-xenon CT; perfusion CT; and perfusion MRI. Each of these imaging techniques uses an indicator, with specific biological properties, and is supported by a model, which consists of a few simplifying assumptions, necessary to state and solve the equations giving access to rCBF. The obtained results are more or less reliable, depending on whether modeling hypotheses are fulfilled by the used indicator. The purpose of this article is to review the various supporting models in the assessment of rCBF, with special emphasis on perfusion CT studies at low injection rates and on iodinated contrast material used as an indicator.

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Section: Central Volume Principlementioning

confidence: 99%

Quantitative assessment of regional cerebral blood flows by perfusion CT studies at low injection rates: a critical review of the underlying theoretical models

et al. 2001

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“…Five mg of indocyanine green dye was injected into either the inferior or superior vena cava, and blood was sampled from the indwelling arterial needle through a densitometer. The results were calculated from the dye-dilution curve according to the method of Hamilton, Moore, Kinsman, and Spurling (20). Since individual values agreed closely, the mean value was reported when two or three estimations were made.…”

mentioning

confidence: 99%

Renal Circulation in Cirrhosis: Observations Based on Catheterization of the Renal Vein*

Baldus¹,

Summerskill²,

Hunt³

et al. 1964

J. Clin. Invest.

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“…4 Hamilton and associates 8 determined the size of the dog's heart by x-ray during epinephrine infusion and concluded that the heart is responsible for a great part of the increase in the "central blood volume" which occurs during the infusion of this drug. 6 Medullary stimulation with thrombin or fibrinogen increases the weight of the lungs, inferential evidence of a volume increase in this organ, and this weight increase can be abolished with a ganglionic blocking agent, RO 2-2222.…”

mentioning

confidence: 99%

“…8 In twenty-one of the twenty-eight determinations, mean transit time was corrected for the passage time through the sampling catheter. The volume of the sampling catheter was 1.3 e c , and the arterial samples were collected at a known rate (1-2 cc.…”

mentioning

confidence: 99%

Effect of l-Arterenol Infusion on "Central Blood Volume" in the Dog

Shadle

Moore

Billig

1955

Circulation Research

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Infusion of 1-arterenol into anesthetized dogs increased the volume of blood in the heart and lungs, as indicated by an increase in "central blood volume," estimated lung volume and pressure changes in the heart and lungs. An analysis of pressure and flow data in the systemic venous bed during infusion of the drug suggests that important sources of the shifted blood are the peripheral veins and venules.F OWLER AND COWORKERS have demonstrated that both pulmonary artery and "pulmonary capillary pressures" increase during the continuous infusion of 1-arterenol, in the human.1 These workers concluded that the pulmonary hypertension was secondary to an increased pulmonary venous pressure; however, the mechanism of this pressure rise was not investigated. With a constant cardiac output, changes in pulmonary vascular pressures occurring during 1-arterenol infusion could be due to either vasomotor activity in the pulmonary vascular bed, or a volume increase in the pulmonary circuit due to the shift of blood from the systemic circuit. Since the resistance across the pulmonary vascular bed did not change in any consistent manner during 1-arterenol infusion, Fowler concluded that the rise in pulmonary artery pressure was not due to constriction of the pulmonary arteries. These data, together with the general lack of evidence for active pulmonary vasomotor changes, make the second possibility the more likely explanation for the increased pulmonary artery pressure.2 '' Work from various laboratories indicates that systemic vasomotor activity can change the volume of blood contained in the heart and lungs. Johnson observed a decrease in this

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Simultaneous Determination of the Pulmonary and Systemic Circulation Times in Man and of a Figure Related to the Cardiac Output

Cited by 170 publications

References 0 publications

Quantitative assessment of regional cerebral blood flows by perfusion CT studies at low injection rates: a critical review of the underlying theoretical models

Quantitative assessment of regional cerebral blood flows by perfusion CT studies at low injection rates: a critical review of the underlying theoretical models

Renal Circulation in Cirrhosis: Observations Based on Catheterization of the Renal Vein*

Effect of l-Arterenol Infusion on "Central Blood Volume" in the Dog

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