Heart Rate Independence of Catecholamine-Induced Myocardial Damage in the Newborn Pig

Caspi, Joseph; Coles, John G.; Benson, Lee; Herman, S L; Act, Janet Augustine; Wilson, Gregory J.

doi:10.1203/00006450-199407001-00008

Cited by 13 publications

(9 citation statements)

References 20 publications

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“…On the other hand, cardiomyocyte injury are induced by excess of catecholamine [56] and prognosis after myocardial infarction [57] or congestive heart failure [58] correlates with plasma catecholamine level. It is therefore possible that PAMP has a compensatory function that offsets the further development of cardiogenic disease both by decreasing blood pressure and by sympatho-inhibition, and thus may be a useful therapeutic agent.…”

Section: Clinical Implications Of Pampmentioning

confidence: 99%

Adrenomedullin and its Related Peptide

Shimosawa

Fujita

2005

Endocr J

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MORE than 100 years have passed since Riva-Rocci [1] modified the sphygmograph by Marey [2], Mahomed [3] and Von Basch [4] to make conventional blood pressure measurements possible. Two years after the method was established, existence of hypertensive agents, now known as renin, was reported [5]. Since then laboratory investigations as well as clinical and epidemiological studies in hypertension research have been advancing at an exponential rate [6]. Since the 1950s, several circulation-regulating peptides, both hypertensive and hypotensive, were discovered. Among them, a novel vasodilative peptide, adrenomedullin (AM) was isolated from pheochromocytoma tissue in 1993 [7]. Another processing site in a propeptide of AM was found and a new hypotensive peptide, named proadrenomedullin N-terminal 20 peptide (PAMP), was isolated from human plasma and urine [7,8].Blood circulates throughout the body by the pressure force generated by cardiac output and peripheral resistance. Each of these primary determinants of blood pressure is determined by the interaction of an exceedingly complex series of factors. Thus it is crucial to determine this complex of interactions in order to better understand the physiological role of these newly found factors. AM and PAMPAs mentioned above, AM, originally isolated from pheochromocytoma cell, is also produced and secreted in endothelial cells [7,19], and has been shown to exhibit hypotensive action by direct vasodilation via both the elevation of intracellular cAMP and alteration of calcium sensitivity in vascular smooth muscle cells [20]. Besides these actions, recent studies have shown that AM increases nitric oxide synthesis in endothelial cell by elevating intracellular calcium [21][22][23][24]. Studies on the physiological action of AM have also revealed that AM increases intracellular cAMP [22] [28]. Moreover, AM inhibits smooth muscle cell migration and proliferation [29, 30]. AM also shares a slight homology with CGRP and the above mentioned physiological effects are inhibited by CGRP antagonist CGRP(8-37) [21]. Together with the evidence that AM production is increased in failing heart [31, 32], it is speculated that

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Section: Clinical Implications Of Pampmentioning

confidence: 99%

Adrenomedullin and its Related Peptide

Shimosawa

Fujita

2005

Endocr J

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“…Downregulation of the receptors in the signal transduction pathway may also occur (30) but is not likely in the time period covered by this study. The myocardial toxicity which has been demonstrated with prolonged inotropic infusions could also contribute to the decrease in CI during prolonged infusions (31).…”

mentioning

confidence: 99%

Systemic, pulmonary and mesenteric perfusion and oxygenation effects of dopamine and epinephrine.

Cheung

Barrington²,

Pearson³

et al. 1997

Am J Respir Crit Care Med

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The response of the systemic, pulmonary, hepatic and portal circulations to infusion of dopamine and epinephrine was studied in newborn piglets 1 to 3 d of age. Anesthetized animals were instrumented to measure cardiac index (CI), hepatic arterial flow, and portal venous blood flow. Catheters were inserted for measurement of systemic arterial pressure (SAP), pulmonary arterial pressure (PAP), and for sampling of arterial, portal venous, and mixed venous oxygen saturations and plasma lactate levels. Systemic, pulmonary and mesenteric vascular resistance indices (SVRI, PVRI, MVRI), and systemic and mesenteric oxygen extraction were calculated. Dopamine and epinephrine were infused in doses of 2, 10, 32 microg/kg/min and 0.2, 1.0, 3.2 microg/kg/min respectively, given in random order. Significant increases in SAP, PAP, and CI were demonstrated with 32 microg/kg/min of dopamine and the two higher doses (1.0 and 3.2 microg/kg/min) of epinephrine. There were no significant changes in SVRI and PVRI with dopamine infusions. Epinephrine at 3.2 microg/kg/min significantly elevated SVRI and PVRI. The SAP/PAP ratio was decreased with 32 microg/kg/min of dopamine whereas epinephrine did not affect the ratio. Dopamine had no significant effect on hepatic arterial flow, portal venous flow, or mesenteric vascular resistance. Epinephrine infusion at 3.2 microg/kg/min decreased portal venous blood flow, total hepatic blood flow, and hepatic oxygen delivery with an increase in calculated mesenteric vascular resistance. Systemic and mesenteric oxygen extraction were not affected by dopamine or epinephrine infusions. Plasma lactate levels were significantly elevated with epinephrine infusion 3.2 microg/kg/min. The differential responses of dopamine and epinephrine on pulmonary and mesenteric circulations may be significant in the pathophysiology and management of persistent fetal circulation and necrotizing enterocolitis.

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“…Suggested causes are reduced sequestration of calcium within the SR, failure of the ATP calcium relaxation mechanism, and free radical generation from catecholamine oxidation. It may also be related to the exhaustion of energy supply with falling levels of ATP after catecholamine treatment (19). This observation was also seen in a comparative study of neonatal and mature sheep where heart work was increased to similar levels of oxygen consumption using an epinephrine infusion (20).…”

Section: Heart and Vascular Responses To Inotropesmentioning

confidence: 75%

Limitations and vulnerabilities of the neonatal cardiovascular system: considerations for anesthetic management

Wolf

Humphry

2013

Pediatric Anesthesia

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Development of the cardiovascular system through the last trimester of pregnancy and the subsequent neonatal period is profound. Morphological changes within the myocardium make the heart vulnerable to challenges such as fluid shifts and anesthetic drugs. The sensitivity of the myocardium to metabolic challenges and potential harm of drugs needed to maintain adequate blood pressure and cardiac output are highlighted. Traditional monitoring under anesthesia has focussed on maintaining oxygenation and heart rate in the neonate with less attention paid to blood pressure, cardiac output, and more importantly organ well-being. There is now a better understanding of the limitations of blood pressure homeostasis in the neonate and the potential consequences of marginal hypoperfusion. This article highlights some of these vulnerabilities particularly as they relate to anesthesia and surgery in the very young.

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Heart Rate Independence of Catecholamine-Induced Myocardial Damage in the Newborn Pig

Cited by 13 publications

References 20 publications

Adrenomedullin and its Related Peptide

Adrenomedullin and its Related Peptide

Systemic, pulmonary and mesenteric perfusion and oxygenation effects of dopamine and epinephrine.

Limitations and vulnerabilities of the neonatal cardiovascular system: considerations for anesthetic management

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