Cardiac Output and Related Functions Under Basal and Postprandial Conditions

Gladstone, Sidney A.

doi:10.1001/archinte.1935.00160220003001

Cited by 22 publications

(7 citation statements)

References 15 publications

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“…It is observed since many years that intake of food, especially carbohydrate, is followed by some cardiovascular changes (Gladstone 1935, Welle et al 1981, Fagan et al 1986), and more recently a rise in plasma noradrenaline is well established (Welle et al 1981, Heseltine et al 1990, Sidery et al 1991). In 1981 it was reported that different levels of hyperinsulinaemia during euglycaemic clamp evoked an increase in plasma noradrenaline, indicating a sympathetic activation (Rowe et al 1981).…”

Section: Hyperinsulinaemia and Feedingmentioning

confidence: 99%

Sympathetic nerve activity in metabolic control – some basic concepts

Fagius

2003

Acta Physiologica Scandinavica

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A role for the sympathetic nervous system in hypertension has been looked for in relation to the 'metabolic syndrome' with associations between body weight, insulin sensitivity and hypertension. By use of microneurography human sympathetic responses to hypoglycaemia, normoglycaemic hyperinsulinaemia and food intake have been studied. A strong but differentiated influence of insulin-induced hypoglycaemia comprises increase in muscle sympathetic nerve activity (MSNA) and the sudomotor part of skin sympathetic nerve activity (SSNA), whereas vasoconstrictor SSNA is inhibited. Responses to infusion of 2-deoxy-D-glucose are identical, suggesting central nervous system glucopenia and not insulin to be the causative factor. Insulin infusion during normoglycaemia evokes a moderate increase in MSNA; SSNA and blood pressure does not change. After glucose ingestion MSNA displays a sustained increase, which is only partly elicited by insulin. A significant albeit weaker increase occurs after pure protein or fat meals, and after glucose ingestion in C-peptide-negative diabetic patients, with no insulin secretion. In healthy elderly people the MSNA response to food intake is weak, because of a high outflow already at rest; this is suggested to explain postprandial hypotension in the elderly, a paradoxical mechanism behind clinical autonomic failure. A pathophysiological role of MSNA in the metabolic syndrome with hypertension has been speculated. An association between obesity and elevated level of MSNA at rest is established; observed relationships to chronic insulin levels and hypertension are less unanimous. The adipose tissue regulating hormone leptin has become one focus of interest in ongoing attempts to elucidate a possible role of the human sympathetic nervous system in the 'metabolic syndrome' and hypertension.

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Section: Hyperinsulinaemia and Feedingmentioning

confidence: 99%

Sympathetic nerve activity in metabolic control – some basic concepts

Fagius

2003

Acta Physiologica Scandinavica

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“…1988, Waaler et al . 1990), which also initiates an increase in CO (Grollman 1929, Gladstone 1935, Waaler et al . 1990).…”

mentioning

confidence: 99%

Circulatory responses to a meal in patients with a newly transplanted heart

Waaler¹,

Hisdal²,

Eriksen³

2002

Acta Physiologica Scandinavica

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It is well established that consumption of a meal releases a gradually developing and quite marked increase in blood flow to the gastrointestinal organs and a similar and simultaneous increase in cardiac output (CO). It is not known through which mechanism the pumping of the heart adjusts so accurately to the gastrointestinal flow increase. We have approached this problem by serving a standardized, mixed meal to five patients with recently transplanted and thus denervated hearts and to five sex- and age-matched controls. Pre- and postprandial levels of CO and blood flow in the superior mesenteric artery (SMA) were recorded with Doppler ultrasound technique. The patients with transplanted hearts had significantly higher preprandial levels of heart rate (HR) and CO than the controls. With a timing similar to that seen in the controls did all five patients develop considerable and synchronous postprandial increases in superior mesenteric arterial flow and in CO. Increases in superior mesenteric arterial flow were significantly greater than the controls. Also, COs, high even before meals were given, increased further and to the same relative extent as in the control persons. The marked postprandial increase in CO, probably secondary to the increase in intestinal blood flow, could hardly come about through any sort of nervous reflex to the recently transplanted and denervated hearts. It appears more likely that a humoral connection of some sort exists between the two circulatory events.

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“…The moderate albeit inconsistent increases in heart rate and cardiac output may constitute part of an increased sympathomimetic activity associated with the ingestion of food as has been postulated by some investigators who noted the absence of such a response in catecholamine-depleted dogs (Fronek and Stahlgren, 1968). A postprandial increase rather than a decrease or no change in arterial blood pressure has been noted previously in normal subjects (Grollman, 1929;Gladstone, 1935;Dagenais et al, 1966) and in patients with coronary artery disease (Morrison and Swalm, 1940;Berman et al, 1950). It should be emphasised, however, that in these studies measurements were taken at least 45 to 60 rather than 20 minutes after the completion of a meal, which, in addition, had a very much greater caloric content.…”

Section: Discussionmentioning

confidence: 71%

Haemodynamic and electrocardiographic accompaniments of resting postprandial angina.

Figueras¹,

Singh²,

Ganz³

et al. 1979

Heart

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SUMMARY The early postprandial changes in 10 patients with angiographically proven coronary artery disease and history ofpostprandial angina were studied by the continuous recording on magnetic tape of the electrocardiogram and haemodynamic variables. The significant changes 20 minutes after a meal not followed by angina included increases in cardiac index and stroke index, with a decrease in systemic vascular resistance. When angina developed after a meal, there were significant increases in mean systemic arterial blood pressure, heart rate, pulmonary capillary wedge pressure, and systemic vascular resistance with decreases in stroke index at the onset of pain rather than at the onset of ischaemic electrocardiographic abnormalities. The first haemodynamic variable to change was pulmonary capillery wedge pressure which tended to increase coincident in time with the electrocardiographic abnormalities. In all cases, postprandial angina occurred within 25 minutes after a meal. In every instance, there was little or no change in the product of heart rate and systolic arterial blood pressure at the onset of the ischaemic electrocardiographic abnormalities at a time when the pulmonary capillary wedge pressure had begun to rise. Postprandial angina, like many cases of rest angina, may arise on the basis of a primary decrease in myocardial perfusion, the nature ofwhich is unclear but merits further investigation.

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Cardiac Output and Related Functions Under Basal and Postprandial Conditions

Cited by 22 publications

References 15 publications

Sympathetic nerve activity in metabolic control – some basic concepts

Sympathetic nerve activity in metabolic control – some basic concepts

Circulatory responses to a meal in patients with a newly transplanted heart

Haemodynamic and electrocardiographic accompaniments of resting postprandial angina.

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