Koronarreserve und maximaler Sauerstoffverbrauch des menschlichen Herzens

Tauchert, M.

doi:10.1007/bf01906424

Cited by 61 publications

(14 citation statements)

References 99 publications

(5 reference statements)

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“…Adenosine proved the ideal agent because in the dose used it produced maximal coronary vasodilation (often confirmed by reactive hyperemia responses) without affecting the blood pressure of the support dog, apparently because of rapid deamination in blood." The resistance values so obtained from normal hearts and from areas of normal blood flow in hearts with occluded coronary arteries were practically identical to those found by others in experimental animals 40 and in man, 41 with the electromagnetic flowmeter 40 and the Kety and Schmidt technique 41 using argon as a tracer. 42 Utley et al 4a and Downey et al, 44 who also used tracer microspheres in the dog heart at maximal vasodilation, found resistance values identical to or slightly lower than those reported here.…”

Section: Discussionsupporting

confidence: 84%

Quantification of collateral resistance in acute and chronic experimental coronary occlusion in the dog.

Schäper

Flameng

Winkler³

et al. 1976

Circulation Research

130

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SUMMARY The resistance to coronary blood flow in various parts of the myocardium was studied with the tracer mkrospberes technique before and immediately after an acute coronary occlusion and several weeks after a more slowly occurring coronary occlusion by Ameroid constrictor. All experiments were carried out in the isolated, metabolically supported, empty, beating dog heart at maximal coronary vasodilation induced with adenosine. Coronary resistance of the normal empty beating heart at maximal coronary vasodilation was 0.20 mm mm Hg/(ml/min) per 100 g of tissue (subepicardium) and 0.16 mm Hg/(ml/min) per 100 g of tissue (subendocardium). After acute coronary occlusion the perfusion of the subtended myocardium was maintained at a much lower level by way of collateral vessels, which snowed i resistance to flow of 3.52 mm Hg/(ml/miD) per 100 g. If coronary artery occlusion proceeded more slowly the collateral vessels became more functional and myocardial infarction was avoided. During collateral enlargement collateral resistance fell from 3.52 to 0.22 mm Hg/(ml/min) per 100 g within a period of 8 weeks after implantation of the constricting device. The degree of compensation by collaterals for the loss of the occluded native coronary artery was 33% of its former conductance.CORONARY ARTERY occlusion without myocardial infarction is a common finding at autopsy in humans; in reported cases'* collateral vessels had enlarged quickly enough and to a sufficient degree to prevent irreversible myocardial damage. Coronary arterial lesions, however, are not always compensated for by collateral enlargement, and clinical and technical limitations have made it impossible to study the collateral circulation quantitatively. Methodological limitations are also responsible for the fact that the collateral resistance in acute and chronic experimental coronary occlusion remained unknown.Until recently the time course of collateral development was estimated by the use of indirect indices because collateral flow proper, hence collateral resistance, could not be measured. The introduction of the tracer microsphere method into circulation research, 5 however, has changed this situation and we have tried to study the increase of collateral flow with time, using this method. Since the relationship between perfusion pressure and coronary collateral flow might not be linear and since zero flow must be assumed at positive pressures, i.e., the critical closing pressure,* collateral flows and pressures were measured over a wide physiological range. In this way the resistance of the collateral vessels as well as the degree of compensation for the loss of the native circulation, was quantitatively determined.

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Section: Discussionsupporting

confidence: 84%

Quantification of collateral resistance in acute and chronic experimental coronary occlusion in the dog.

Schäper

Flameng

Winkler³

et al. 1976

Circulation Research

130

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“…This has been demonstrated by others as well (1,2,22,36,46,58,59,73,74). The surprisingly high rise in flow observed by Hellems et at during moderate hypoxia of 10 vol % may be partially explained by the flow measuring technique applied, the nitrous oxide method (16,38,39), which overestimates high flow rates (71).…”

Section: Discussionmentioning

confidence: 81%

“…Oxygen contents were computed using 1.34 ml 02 per 1 g of hemoglobin. Arterial oxygen supply to the heart was expressed in mllmin· 100g by the product of arterial oxygen content and myocardial blood flow, efficiency of myocardial perfusion by the ratio of arterial oxygen supply to myocardial oxygen consumption, coronary flow reserve as previously described (9,28,30,71) and myocardial oxygen consumption per stroke by the ratio of myocardial oxygen consumption to heart rate. Heart rate was averaged from ECG recordings.…”

Section: Methodsmentioning

confidence: 99%

Studies on the regulation of myocardial blood flow in man II. Effects of acute arterial hypoxia

Heiß

Töpfer

Barmeyer

et al. 1978

Clinical Cardiology

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Summary:To determine whether adjustment of myocardial blood flow (MBF) , myocardial oxygen consumption (MVOl) and myocardial substrate uptake (MSU) to acute arterial hypoxia is influenced by training effects on the heart, 7 trained and 7 untrained healthy individuals were investigated. MBF (argon method), MV'Ol and MSU of glucose, lactate and free fatty acids were measured at rest during normoxia and two different stages of acute arterial hypoxia: a) 12.82 vol% Ol; b) 8.74 vol% Ol. Measurements were carried out during hemodynamic and respiratory steady state conditions.Myocardial flow and metabolism of athletes were significantly (p

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“…At rest, coronary blood flow was measured by the argon method (29). immediately thereafter basal hemodynamic parameters were obtained and simultaneous arterial and coronary sinus blood samples were taken for measurements of the oxygen saturation and hemoglobin concentration as well as plasma levels of CAMP and lactate.…”

Section: Methodsmentioning

confidence: 99%

Myocardial metabolism of cyclic 3,5‐adenosine monophosphate as influenced by dipyridamole and theophylline in patients with coronary heart disease

Hombach

Behrenbeck

Tauchert

et al. 1979

Clinical Cardiology

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Summary:In a total of 16 individuals, 4 females and I2 male patients ranging from 36 to 54 years, with proven coronary heart disease, hemodynamic parameters and coronary blood flow (argon method) were measured at rest and after administration of dipyridamole, 0.5 mg/kg body weight, and theophylline, 0.24 g i.v. Simultaneously, blood samples were taken from the arterial and coronary venous blood for determinations of oxygen content and concentrations of cyclic 33-adenosine monophosphate (CAMP) and lactate. Thus, myocardial oxygen consumption and uptake or release of cAMP and lactate could be calculated according to the Fick principle.After administration of dipyridamole, heart rate and cardiac index slightly increased together with a decrease in arterial pressure. Myocardial blood flow significantly increased, whereas myocardial oxygen consumption remained unchanged during the dipyridamole period. In nine patients myocardial release of cAMP and lactate could be observed during the dipyridamole action, whereas in the remaining seven patients there were only insignificant changes of release or uptake of cAMP and lactate in the dipyridamole and theophylline periods. Six of nine patients in the first group revealed specific anginal complaints corresponding to the release of cAMP and lactate, whereas only two patients in the non-CAMP-releasing individuals had characteristic angina pectoris.These data suggest that dipyridamole may induce myocardial ischemia with anginal complaints and that, under certain circumstances, myocardial release of CAMP as well as lactate might serve as biochemical correlates of these ischemic conditions.

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Koronarreserve und maximaler Sauerstoffverbrauch des menschlichen Herzens

Cited by 61 publications

References 99 publications

Quantification of collateral resistance in acute and chronic experimental coronary occlusion in the dog.

Quantification of collateral resistance in acute and chronic experimental coronary occlusion in the dog.

Studies on the regulation of myocardial blood flow in man II. Effects of acute arterial hypoxia

Myocardial metabolism of cyclic 3,5‐adenosine monophosphate as influenced by dipyridamole and theophylline in patients with coronary heart disease

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