scholarly journals Metabolic effects of phosphodiesterase III inhibitors: another reason to promote their use?

Critical Care ◽  
2007 ◽  
Vol 11 (3) ◽  
pp. 139 ◽  
Author(s):  
Vladislava Simkova ◽  
Peter Radermacher ◽  
Eberhard Barth
Keyword(s):  
Metabolic Effects ◽  
Phosphodiesterase Iii Inhibitors ◽  
Phosphodiesterase Iii

Positive inotropes

2018 ◽  
Author(s):  
Mattia Arrigo ◽  
Alexandre Mebazaa
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Mechanisms Of Action ◽  
Inotropic Agents ◽  
Organ Perfusion ◽  
Cardiac Myosin ◽  
Inappropriate Use ◽  
Calcium Sensitizers ◽  
Phosphodiesterase Iii Inhibitors ◽  
Phosphodiesterase Iii

Inotropic agents are substances used to improve cardiac output and end-organ perfusion in severe forms of acute heart failure. However, inappropriate use of inotropic agents may be associated with severe adverse effects and death. Despite clear indications to restrict their use to acute heart failure patients presenting with signs of end-organ hypoperfusion, the current use of inotropes is very frequent and often unnecessary. This chapter reviews mechanisms of action of current and future inotropes (including catecholamines, phosphodiesterase-III inhibitors, calcium sensitizers, cardiac myosin activators, and istaroxime) and discusses their clinical use in acute heart failure.

Positive inotropes

ESC CardioMed ◽  
2018 ◽  
pp. 184-187
Author(s):  
Mattia Arrigo ◽  
Alexandre Mebazaa
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Mechanisms Of Action ◽  
Inotropic Agents ◽  
Clinical Use ◽  
Organ Perfusion ◽  
Heart Failure Patients ◽  
Inappropriate Use ◽  
Phosphodiesterase Iii Inhibitors ◽  
Phosphodiesterase Iii

Inotropic agents are substances used to improve cardiac output and end-organ perfusion in severe forms of acute heart failure. However, inappropriate use of inotropic agents may be associated with severe adverse effects and death. Despite clear indications to restrict their use to acute heart failure patients presenting with signs of end-organ hypoperfusion, the current use of inotropes is very frequent and often unnecessary. This chapter reviews mechanisms of action of current and future inotropes (including catecholamines, phosphodiesterase-III inhibitors, calcium sensitizers, cardiac myosin activators, and istaroxime) and discusses their clinical use in acute heart failure.

scholarly journals Differentiating Spontaneous from Drug-Induced Vascular Injury in the Dog

2003 ◽  
Vol 31 (1_suppl) ◽  
pp. 25-31 ◽  
Author(s):  
Frances A.S. Clemo ◽  
Winston E. Evering ◽  
Paul W. Snyder ◽  
Mudher A. Albassam
Keyword(s):  
Coronary Arteries ◽  
Vascular Injury ◽  
Clinical Signs ◽  
Vascular Pathology ◽  
Endothelin Receptor ◽  
Drug Induced ◽  
Arterial Lesion ◽  
Arterial Lesions ◽  
Phosphodiesterase Iii Inhibitors ◽  
Phosphodiesterase Iii

When vascular injury is observed in dogs used in preclinical toxicology studies, careful evaluation of the lesions is warranted, especially when differentiating drug-induced vascular changes from spontaneous findings, such as idiopathic canine polyarteritis. The clinical signs as well as the nature and distribution of lesions can often be distinguishing, as is the case with vasoactive drugs, including vasodilators and/or positive inotropes (hydralazine, minoxidil, endothelin receptor antagonists, and phosphodiesterase III inhibitors). For most types of vasodilator-induced vascular injury, the lesion is often restricted to coronary arteries, whereas in idiopathic canine polyarteritis, arterial lesions not only involve coronary arteries, but also medium to small arteries of other organs. In addition, the nature of the changes in vessels yields important clues. Medial and adventitial hemorrhage is generally associated with vasodilator-induced arterial lesion, whereas hemorrhage is generally absent in idiopathic polyarteritis. Although idiopathic canine polyarteritis can generally be differentiated from vasoactive-induced vascular injury in dogs, there are increasing incidences of this type of polyarteritis in dogs receiving any 1 of a number of unrelated classes of compounds, suggestive of an exacerbation of the spontaneous disease. Therefore, in order to differentiate drug-induced injury from idiopathic canine polyarteritis, it is critical that examination of the vascular pathology be conducted with good understanding of clinical, pharmacological, and mechanistic data associated with the drug.

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