Plasma Catecholamines and Carbohydrate Metabolism in Patients with Acute Myocardial Infarction

Christensen, Niels Juel; Videbæk, J

doi:10.1172/jci107763

Cited by 122 publications

(39 citation statements)

References 33 publications

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“…The plasma epinephrine concentrations resulting from these infusion rates have been measured previously in a group of 40 patients under circumstances similar to those in the present study and were found to fall within the range of plasma epinephrine concentrations that occurs during a wide variety of stresses in humans.1 Ten minutes of infusion are required to attain a steady-state plasma epinephrine concentration,5,6 and, therefore, to ensure that steady-state conditions had been achieved, epinephrine was infused for 14 minutes before its electrophysiologic effects were measured. There were no adverse reactions to the infusion of epinephrine.…”

Section: Infusion Of Epinephrinesupporting

confidence: 73%

Epinephrine-induced reversal of verapamil's electrophysiologic and therapeutic effects in patients with paroxysmal supraventricular tachycardia.

et al. 1989

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The purpose of our study was to determine whether an infusion of epinephrine reverses the electrophysiologic effects of verapamil and whether reversal of verapamil's effects on the induction of paroxysmal supraventricular tachycardia (PSVT) by epinephrine during electropharmacologic testing is predictive of stress-related recurrences of PSVT during long-term treatment with verapamil. The infusion rates of epinephrine used in this study were 25 and 50 ng/kg/min, which previously have been demonstrated to result in plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. The subjects of this study were 17 patients with recurrent PSVT who underwent an electrophysiologic study in the control state and after at least 2 days of treatment with 240-480 mg/day verapamil. After assessing the response to verapamil, epinephrine was infused and testing was repeated. Verapamil significantly slowed atrioventricular conduction and prolonged refractoriness in the atrium and atrioventricular node. The effects of the two infusion rates of epinephrine were generally similar in magnitude and, therefore, the results were pooled. Epinephrine partially or completely reversed all of verapamil's electrophysiologic effects. Verapamil suppressed the induction of sustained PSVT in 15 patients. Epinephrine facilitated the induction of PSVT in seven of these 15 patients. All 15 patients were treated on a long-term basis with verapamil. The eight patients in whom epinephrine did not facilitate the induction of PSVT had no recurrences of PSVT during 9-18 months of follow-up. In contrast, there were multiple recurrences of PSVT in six of the seven patients in whom epinephrine had facilitated the induction of PSVT, and in five of these patients the episodes of PSVT occurred exclusively during exertion or emotional stress. These five patients then were treated with verapamil and 50 mg/day atenolol. Three patients could not tolerate this combination; however, the remaining two patients had no further recurrences of PSVT. In conclusion, physiologic doses of epinephrine attenuate the electrophysiologic effects of verapamil and may reverse verapamil's effects on the induction of PSVT during electropharmacologic testing. Reversal by epinephrine of verapamil's effects on the induction of PSVT may accurately identify patients who are likely to experience stressrelated recurrences of PSVT and who may benefit from treatment with a f-blocker during long-term therapy with verapamil. (Circulation 1989;79:783-790) A physiologic increase in circulating epinephrine has been demonstrated to shorten atrial and atrioventricular (AV) nodal refractoriness and to accelerate AV nodal From

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Section: Infusion Of Epinephrinesupporting

confidence: 73%

Epinephrine-induced reversal of verapamil's electrophysiologic and therapeutic effects in patients with paroxysmal supraventricular tachycardia.

et al. 1989

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“…The possibility that WISP-1 may act early during the acute phase of myocardial injury is suggested not only by its responsiveness to TNF-␣ and IL-1␤ but also by the observation that cAMP induction by ␤-adrenergic agonists or forskolin treatment was shown to block CTGF expression (14). Catecholamines increase rapidly in the heart post-MI, leading to elevated cAMP levels that then decrease gradually over time (15,39,41). We observed rapid upregulation of WISP-1 in the heart post-MI where transcripts appeared as early as 6 h and protein levels were significantly elevated by 24 h. This induction occurred at a time when elevated cAMP levels would likely preclude CTGF expression.…”

Section: Discussionmentioning

confidence: 99%

Wnt-induced secreted protein-1 is a prohypertrophic and profibrotic growth factor

Colston¹,

Rosa²,

Koehler³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

102

127

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. Wnt-induced secreted protein-1 is a prohypertrophic and profibrotic growth factor. Am J Physiol Heart Circ Physiol 293: H1839-H1846, 2007. First published July 6, 2007; doi:10.1152/ajpheart.00428.2007.-Wnt1-induced secreted protein-1 (WISP-1) is a member of the cysteine-rich 61, connective tissue growth factor, and nephroblastoma overexpressed (CCN) family of growth factors and is expressed in the heart at low basal levels. The purpose of this study was to investigate whether WISP-1 is upregulated in postinfarct myocardium and whether WISP-1 exerts prohypertrophic and mitogenic effects stimulating myocyte hypertrophy, cardiac fibroblast (CF) proliferation, and collagen expression. Male C57Bl/6 (25 g) mice underwent permanent occlusion of the left anterior descending coronary artery. mRNA and protein levels were analyzed by Northern and Western blot analyses. Cardiomyocyte hypertrophy was quantified by protein and DNA synthesis. CF proliferation was quantified by CyQuant assay, and soluble collagen release by Sircol assay. A time-dependent increase in WISP-1 expression was detected in vivo in the noninfarct zone of the left ventricle, which peaked at 24 h (3.1-fold, P Ͻ 0.01). Similarly, biglycan expression was increased by 3.71-fold (P Ͻ 0.01). IL-1␤ and TNF-␣ expression preceded WISP-1 expression in vivo and stimulated WISP-1 expression in neonatal rat ventricular myocytes in vitro. WISP-1-induced cardiomyocyte hypertrophy was evidenced by increased protein (2.78-fold), but not DNA synthesis, and enhanced Akt phosphorylation and activity. Treatment of primary CF with WISP-1 significantly stimulated proliferation at 48 h (6,966 Ϯ 264 vs. 5,476 Ϯ 307 cells/well, P Ͻ 0.01) and enhanced collagen release by 72 h (18.4 Ϯ 3.1 vs. 8.4 Ϯ 1.0 ng/cell, P Ͻ 0.01). Our results demonstrate for the first time that WISP-1 and biglycan are upregulated in the noninfarcted myocardium in vivo, suggesting a positive amplification of WISP-1 signaling. WISP-1 stimulates cardiomyocyte hypertrophy, fibroblast proliferation, and ECM expression in vitro. These results suggest that WISP-1 may play a critical role in post-myocardial infarction remodeling.cysteine-rich 61, connective tissue growth factor, and nephroblastoma overexpressed family; myocardial infarction; myocardial remodeling; Akt; cardiomyocyte hypertrophy WNT1-INDUCED secreted protein-1 (WISP-1) is a member of the cysteine-rich 61, connective tissue growth factor (CTGF), and nephroblastoma overexpressed (CCN) family of growth factors shown to play a role in cellular growth, transformation, and survival (24,26,52,57). Because of the limited regenerative capacity of the heart, any structural adaptations of the myocardium occurring in response to chronic changes in hemodynamic loading conditions typically require alterations in the size of myocytes and composition of the interstitial components (46). When the stimulus is chronic pressure overload, as in hypertension or aortic stenosis, cardiac myocytes increase in diameter and there is increased deposition of interstitial col...

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“…We have shown (66) that these rates (the latter approximately equal to the former for a 70-kg subject) produce circulating norepinephrine levels in the range of 1,400-2,100 pg/ml, at which level we also saw an increase in plasma glycerol. Although this norepinephrine range is reached during exercise (61), and with illnesses such as ketoacidosis (63) and myocardial infarction (67), it is rarely approached under ordinary physiological circumstances. Thus, under usual conditions, it appears that the lipolytic actions of norepinephrine may be limited to its long recognized local effector role as sympathetic neurotransmitter at nerve endings in adipose tissue.…”

Section: Methodsmentioning

confidence: 99%

Epinephrine plasma thresholds for lipolytic effects in man: measurements of fatty acid transport with [l-13C]palmitic acid.

Galster¹,

Clutter²,

Cryer³

et al. 1981

J. Clin. Invest.

157

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A B S T R A C T To determine the plasma epinephrine thresholds for its lipolytic effects, 60-min epinephrine infusions at nominal rates of 0.1, 0.5, 1.0, 2.5, and 5.0 jg/min were performed in each of four normal young adult men while they also received a simultaneous infusion of [1-13C] 94-101.). Increments in plasma glycerol and free fatty acids and in the inflow and outflow transport of palmitate, however, occurred at lower plasma epinephrine thresholds in the range of 75 to 125 pg/ml. Palmitate clearance was unaffected at any steady-state epinephrine level produced. These data indicate that (a) the lipolytic effects of epinephrine occur at plasma levels approximately threefold basal values and (b) lipolysis is more sensitive than glycogenolysis to increments in plasma epinephrine.

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Plasma Catecholamines and Carbohydrate Metabolism in Patients with Acute Myocardial Infarction

Cited by 122 publications

References 33 publications

Epinephrine-induced reversal of verapamil's electrophysiologic and therapeutic effects in patients with paroxysmal supraventricular tachycardia.

Epinephrine-induced reversal of verapamil's electrophysiologic and therapeutic effects in patients with paroxysmal supraventricular tachycardia.

Wnt-induced secreted protein-1 is a prohypertrophic and profibrotic growth factor

Epinephrine plasma thresholds for lipolytic effects in man: measurements of fatty acid transport with [l-13C]palmitic acid.

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