A Study of Coronary Flow Under Conditions of Hemorrhagic Hypotension and Shock

Opdyke, David F.; Foreman, Robert C.

doi:10.1152/ajplegacy.1947.148.3.726

Cited by 46 publications

(12 citation statements)

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“…The resulting "stagnant anoxemia" also has been repeatedly described (29,30). The data reported in this paper are in partial agreement with those of Opdyke and Foreman (6). Their experiments indicated that during the period of hypotension, the actual coronary flow was seriously curtailed; immediately following infusion, however, the coronary flow appeared adequate.…”

Section: Metabolic Changes During Normovolemic Shocksupporting

confidence: 90%

“…Such a decrease in coronary vascular resistance would not seem fortuitous in replenishing the ischemic myocardium. In contrast, Opdyke and Foreman, using a coronary artery perfusion set in open chest dogs, observed a marked decrease in coronary resistance following reinfusion (6).…”

Section: Metabolic Changes During Normovolemic Shockmentioning

confidence: 84%

“…It was assumed that the trigger mechanism for myocardial depression was a decrease in the coronary flow with resulting myocardial ischemia. Opdyke and Foreman (6) indicated that during the period of hypotension, the actual coronary flow was seriously curtailed, providing ample opportunity for myocardial changes. Immediately following reinfusion, however, the coronary flow appeared adequate.…”

mentioning

confidence: 99%

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Studies on Myocardial Metabolism. III. Coronary Blood Flow, Myocardial Oxygen Consumption and Carbohydrate Metabolism in Experimental Hemorrhagic Shock12

Edwards¹,

Siegel²,

Bing³

1954

J. Clin. Invest.

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Section: Metabolic Changes During Normovolemic Shocksupporting

confidence: 90%

Section: Metabolic Changes During Normovolemic Shockmentioning

confidence: 84%

mentioning

confidence: 99%

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Studies on Myocardial Metabolism. III. Coronary Blood Flow, Myocardial Oxygen Consumption and Carbohydrate Metabolism in Experimental Hemorrhagic Shock12

Edwards¹,

Siegel²,

Bing³

1954

J. Clin. Invest.

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“…The reason for this is obscure. The general tendency for coronary arterial resistance to fall during haemorrhage in the experiments described in this paper resembles the results obtained by Opdyke & Foreman (1947).…”

supporting

confidence: 88%

The circulation of the thoracic cage in the dog and its reaction to haemorrhage

Mott¹

1953

The Journal of Physiology

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The experiments to be described in this paper arose from curiosity about the role of the azygos vein, which is such a prominent feature of the mammalian chest. The vessels of the thoracic wall have received little attention from physiologists. Anrep, Cerqua & Samaan (1934) measured the rate of blood flow into the diaphragm of dogs using a hot-wire anemometer and showed that flow decreased during muscular contraction. Rous & Gilding (1929) injected diffusible dyes intravenously immediately before killing rabbits and found that the diaphragm, intercostal and lingual muscles were especially well stained in normal animals. In rabbits bled under local anaesthesia, the respiratory movements were exaggerated and these muscles stained nearly as well as normal. They concluded that the blood supply to these muscles was well maintained.The vast literature on haemorrhage has been largely concerned with the problems of prognosis and prophylaxis, and few detailed observations have been made on the quantitative changes in blood flow. Nevertheless, there is a large body of evidence, much of it recently summarized by Franklin (1951), that the distribution of the cardiac output is altered during haemorrhage. This paper describes the quantitative changes in blood flow to various parts of the circulation which occurred as the result of haemorrhage in dogs. METHODSDogs varying in weight from 3 to 13 kg were used, and were anaesthetized with ether followed by intravenous chloralose, 70 mg/kg, or sodium pentobarbitone, 32 mg/kg. The impression was gained that chloralose tends to promote vasoconstriction in the peripheral circulation unduly soon. Mean arterial blood pressure was measured in a carotid or femoral artery using a mercury manometer. One jugular vein was cannulated. In some experiments respiratory movements were measured by a modification of Gaddum's (1941) method; in others the body plethysmograph described by Dawes, Mott & Widdicombe (1951) was used.The following methods of measuring blood flow were used.(1) Collection of venous outflow. The apparatus permitted the venous return to take its normal

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“…Not only will myocardial infarction and pulmonary embolism directly alter cardiac performance, but hemorrhagic, traumatic, and septic shock also may be accompanied by hemodynamic evidence of myocardial deterioration (1)(2)(3)(4)(5). Cardiac failure in shock has been variously attributed to a reduction of coronary blood resulting from lowered aortic pressure (6)(7)(8)(9), to the myocardial depressant effect of humoral substances (9,10), and to derangements in acid-base balance (11,12).…”

Section: Introductionmentioning

confidence: 99%