Assessment of inotropic and vasodilating effects of milrinone lactate in patients with dilated cardiomyopathy and severe heart failure

Bregagnollo, Edson Antônio; Fortes, Adjair Humberto; Cicogna, Antônio Carlos

doi:10.1590/s0066-782x1999000200003

Cited by 6 publications

(4 citation statements)

References 27 publications

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“…Epidemiological and animal studies indicate that exposure to concentrated ambient air or ultrafine particles (size <0.1 mm) up-regulates the mRNA and protein expression of pro-inflammatory cytokines, such as TNF-a, IL-1 and IL-6 (Totlandsdal et al 2010;Wilson et al 2010); alters the white blood cell profile; and results in systemic inflammation (Liao et al 2008). In human and animal studies, elevation of circulatory inflammatory mediators, particularly TNF-a, IL-1 and IL-6 have reduced the left ventricular ejection fraction (LVEF), a typical clinical sign that occurs in patients with heart failure (Bregagnollo et al 1999), through p38 MAPK-dependent or non-dependent pathways. An in vitro study confirmed that TNF-a and IL-1 can induce cardiac dysfunction by activation of p38 MAPK via the p38 MAPK upstream protein MKK3/6.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Kan

Young

et al. 2011

Nanotoxicology

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The inhalation of engineered nanoparticles stimulates the development of atherosclerosis and impairs vascular function. However, the cardiac effects of inhaled engineered nanoparticles are unknown. Here, we investigate the effects of ultrafine titanium dioxide (UFTiO(2)) on the heart, and we define the possible mechanisms underlying the measured effects. Pulmonary exposure of rats to UFTiO(2) increased the phosphorylation levels of p38 mitogen-activated protein kinase and cardiac troponin I, but not Akt, in the heart and substance P synthesis in nodose ganglia. Circulatory levels of pro-inflammatory cytokines, and blood cell counts and differentials were not significantly changed after pulmonary exposure. Separately, the incubation of cardiac myocytes isolated from naïve adult rat hearts in vitro with UFTiO(2) did not alter the phosphorylation status of the same cardiac proteins. In conclusion, the inhalation of UFTiO(2) enhanced the phosphorylation levels of cardiac proteins. Such responses are likely independent of systemic inflammation, but may involve a lung-neuron-regulated pathway.

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Section: Discussionmentioning

confidence: 99%

Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Kan

Young

et al. 2011

Nanotoxicology

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“…Considering both milrinone and dobutamine produce similar improvements in cardiac output, dobutamine is advisable for septic shock patients with myocardial dysfunction and severe renal failure, while milrinone should be used with caution. On the other hand, milrinone is preferred when dealing with the presence of pulmonary hypertension and right ventricular failure due to its greater effect on reducing pulmonary vascular resistance (PVR) [16], as well as for patients with simultaneous use of betablockers.…”

Section: Phosphodiesterase III Inhibitor (Milrinone)mentioning

confidence: 99%

Inotropic drugs in septic shock

Yolsiriwat,

Tongyoo

2024

Clin Crit Care

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Septic shock is a life-threatening condition characterized by a complex underlying mechanism that requires a multidimensional treatment approach. Sepsis-induced cardiomyopathy plays a significant role in the development of multiple organ failure. The focus of this review is to determine the evidence-based data of the commonly used inotropic drugs in the management of septic shock during clinical hypoperfusion and reduced myocardial performance. Current guidelines recommend adding dobutamine to norepinephrine or using epinephrine alone in septic-induced cardiomyopathy, while suggesting against the use of levosimendan. Although dobutamine increases cardiac contractility and heart rate, it also decreases systemic vascular resistance. Epinephrine has a greater potency than dobutamine but does not demonstrate a clinical difference in hemodynamic improvement. Milrinone is preferred for cases involving pulmonary hypertension and right ventricular failure but should be avoided in the presence of renal dysfunction. Levosimendan improves cardiac performance and promotes coronary blood flow, but later evidence mentioned significant arrhythmia compared to other inotropic agents. Due to the narrow therapeutic window of these agents, precise therapeutic targets are crucial.

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“…It is important to mention that congestive heart failure (translated as myocardial infarction) can induce cardiomyocyte cell death and result in a decrease of cardiac work [3 -5]. Some drugs are used for the treatment of this clinical pathology, such as angiotensin-converting-enzyme inhibitors [6], β 1 -adrenergic agonist or β 1 -adrenergic blockers [7], diuretics [8], angiotensin-receptor inhibitors [9], calcium sensitizer [10], phosphodiesterase III inhibitors [11], ATP-ase inhibitors [12] and others. However, some of these drugs can produce adverse effects [13 -18]; therefore, in the search for a new drug for the treatment of heart failure and ischemia-reperfusion injury, several drugs have been developed such as MK-7145 (potassium channel inhibitor) [19], some heteroaryl-substituted naphthalenes (CYP11B2 inhibitors) [20,21], BAY-1021189 (guanylate cyclase stimulator) [22], N-benzylcarboxamide (G-protein-coupled receptor kinase 2 inhibitor) [23], a naphthalene-prazosin derivative (calcium channels activation) [24], a guanidine analog (sodiumhydrogen exchanger isoform inhibitor) and others.…”

Section: Introductionmentioning

confidence: 99%

New Amino-steroid-anthracenone with Biological Activity Against Ischemia-reperfusion Injury in a Wistar Rat Model

Figueroa‐Valverde¹,

Marcela²,

Virginia³

et al. 2018

TOPHARMJ

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Objective: The main objective of this study was to evaluate the biological activity of an ASA (Amino-Steroid-Anthracenone derivative) against heart failure caused by the ischemia- reperfusion injury (translated as infarct area). Methods: Biological activity exerted by ASA (0.001-100 nM) on infarct area was determined using an ischemia-reperfusion injury model. In addition, to characterize the molecular mechanism involved in the effect exerted by ASA on left ventricular pressure, some drugs such as estrone (0.001-100 nM), tamoxifen (1 nM), butoxamine (1 nM) and ZM-241385 (1 nM) were used. Results: The experimental data showed that ASA decreased the infarction area significantly (p = 0.05) compared to estrone. Other results indicated that ASA decreased left ventricular pressure and this effect was inhibited by ZM-241385. In addition, ASA increased cAMP levels in a time-dependent manner compared to control conditions. Conclusion: The results showed that ASA decreases ischemia-reperfusion injury (translated as infarct area) via A2 adenosine receptor activation and these phenomena involve changes in cAMP levels.

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Assessment of inotropic and vasodilating effects of milrinone lactate in patients with dilated cardiomyopathy and severe heart failure

Abstract: Milrinone lactate is an inotropic dilating drug that, when administered intravenously, has beneficial effects on cardiac performance and myocardial contractility. It also promotes reduction of SVR and PVR in patients with DCM and NYHA class III and IV of heart failure.

Cited by 6 publications

References 27 publications

Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Inotropic drugs in septic shock

New Amino-steroid-anthracenone with Biological Activity Against Ischemia-reperfusion Injury in a Wistar Rat Model

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