Direct Release of Myocardial Catecholamines Into the Left Heart Chambers

Lammerant, J; Herdt, P. de; Schryver, Christian De

doi:10.3109/13813456509081856

Cited by 8 publications

(9 citation statements)

References 13 publications

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“…The re-2 sponse of plasma-free fatty acids to propranolol was similar to that observed for the catecholamines. After the acute reduction following intravenous proof the in-pranolol, plasma-free fatty acids remained essentially rug adminis5 unchanged during days 1 and 2 and showed a second ontents de-in 4 and in-decrease on day 3; this change was significant when ,epinephrine compared with the results of day 1 (P < 0.01). In the result of the placebo group plasma-free fatty acids remained elevated at least during the 1st d of infarction.…”

Section: Methodsmentioning

confidence: 72%

“…Raab (1) as early as 1943 reported an increase in epinephrine and 1-norepinephrine contents during exercise in patients with angina pectoris. Subsequent studies revealed high plasma catecholamine concentrations in myocardial infarction (2,3) and release of catecholainines locally from ischemic myocardium (4). Serial determinations of plasma catecholamines during early myocardial infarction in man demonstrated that high catecholamine contents correlated with clinical status (5) and hemodynamic findings (6).…”

Section: Introductionmentioning

confidence: 99%

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Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Mueller¹,

Ayres²

1980

J. Clin. Invest.

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Section: Methodsmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Mueller¹,

Ayres²

1980

J. Clin. Invest.

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“…Areas of higher number or activity would have higher 02 consumptions and this may explain the heterogeneity of myocardial venous 02 saturations in normal heart (23). It has been suggested that coronary artery occlusion promotes increased circulating (35) and local myocardial (36) catecholamines. This could explain the marked heterogeneity of arterial and venous 02 saturation seen in an ischemic zone (11).…”

Section: Discussionmentioning

confidence: 99%

Role of Propranolol in Improvement of the Relationship between O2 Supply and Consumption in an Ischemic Region of the Dog Heart

Conway¹,

Weiss²

1982

J. Clin. Invest.

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A B S T R A C T Several aspects of the myocardial 02 supply/consumption relationship were determined after coronary artery occlusion and subsequent /l-adrenergic blockade in 16 anesthetized open-chest dogs. Small artery and vein 02 saturations, and hence extraction, were obtained microspectrophotometrically and combined with radioactive microsphere blood flow determinations to calculate regional myocardial 02 consumption. Eight dogs remained untreated after coronary artery ligation while another group was given 2 mg/kg propranolol, 10 min after occlusion. Untreated occlusion resulted in decreased arterial and especially venous 02 saturations, indicating an increased 02 extraction. Ischemic 02 consumption was reduced and the subendocardial/subepicardial consumption ratio was reversed (1.26 vs. 0.37) due to the pattern of occluded area flow. Calculated 02 supply/ consumption also decreased. Propranolol produced no significant changes in volume or distribution of flow within the ischemic region while reducing flow, extraction, and consumption in the unoccluded region. The heterogeneity of arterial and particularly venous 02 saturations within the ischemic region decreased dramatically. Venous 02 saturations were elevated relative to the control group resulting in a reduced 02 extraction. The decrease in heterogeneity of arterial and venous 02 saturations suggest that propranolol eliminates microregions of relatively high 02 extraction, consumption, and/or a majority of vessels with extremely low flow. This leads to a significant improvement in the 02 supply/consumption ratio in the ischemic myocardium of the dog. This may be due to a reduction in the heterogeneity and level of nj-adrenergic receptor activity within the heart.

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“…In the early 1960s, Raab and associates (69) suggested that myocardial ischemia in coronary artery disease is frequently triggered by catecholamine release, rather than by a sudden alteration in coronary perfusion alone. More recent studies, showing catecholamine release by ischemic myocardium (34,51,76,83), and other studies, demonstrating deterioration of ischemic myocardium with isoproterenol (24,42,48,49). emphasize that enhanced sympathetic nervous activity can be harmful.…”

Section: Introductionmentioning

confidence: 99%

Propranolol during the evolution and subsequent ten days of myocardial infarction in man: Hemodynamic, initial cardiac energetic, and neurohumoral responses

Müeller

Rao

Fletcher

et al. 1979

Clinical Cardiology

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Summary: During the evolution of transmural myocardial infarction an intensive sympathetic hyperactivity was observed. Plasma I-norepinephrine and epinephrine contents were strikingly increased, the mean values to 2.04fl .I0 (SD) and 0.94f0.48 pg/l, respectively. Propranolol(O.1 mg/kg) was administered intravenously within an average of 8.8 h of transmural myocardial infarction to 55 patients who did not show significant left ventricular failure. The drug was continued orally with an average dose of 56f20 (SD) mg q6h for 10 d. Mean plasma propranolol levels during the first 5 d ranged between 89 and 162 ng/ml. Cardiac index, left ventricular ejection fraction, and, to a lesser degree, blood pressure significantly decreased. Mean pulmonary capillary wedge pressure remained unchanged. Decreases in coronary blood flow and myocardial oxygen consumption were associated with improvement of myocardial lactate metabolism, suggesting reduced myocardial oxygen requirements. Plasma free fatty acid contents significantly decreased. Myocardial glucose extraction and respiratory quotient increased, indicating enhanced carbohydrate utilization. Prior to propranolol administration, plasma glucose and glucagon contents were increased and plasma insulin levels were inappropriately low. Initial glucagon and initial I-norepinephrine and epinephrine contents were correlated (r = 0.54 and 0.50, p <0.01). Beta-adrenergic blockade decreased plasma insulin contents in spite of hyperglycemia and abolished the correlation between glucagon and catecholamines. Propranolol was tolerated well by all patients; none of them developed acute left ventricular failure.The study demonstrates that propranolol can be safely administered during the evolution and early phase of transmural myocardial infarction, if selection criteria for patients are carefully considered. Propranolol, dampening the response to acute ischemic stress, diminishes energy requirements and thus appears to be a promising drug for preservation of ischemic myocardium.

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Direct Release of Myocardial Catecholamines Into the Left Heart Chambers

Cited by 8 publications

References 13 publications

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Propranolol decreases sympathetic nervous activity reflected by plasma catecholamines during evolution of myocardial infarction in man.

Role of Propranolol in Improvement of the Relationship between O2 Supply and Consumption in an Ischemic Region of the Dog Heart

Propranolol during the evolution and subsequent ten days of myocardial infarction in man: Hemodynamic, initial cardiac energetic, and neurohumoral responses

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