Decreased mortality in a rat model of acute postinfarction heart failure

Råmunddal, Truls; Lorentzon, Mattias; Ömerovic, Elmir

doi:10.1016/j.bbrc.2005.12.198

Cited by 5 publications

(2 citation statements)

References 18 publications

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“…Two days later, rats underwent echocardiography, and were randomized on confirmation of MI and demonstration of similar MI size based upon fractional shortening and wall motion score index [ 21 ] and followed for a further 7 weeks before being terminated. All procedures were performed in the research vivarium under anesthesia using 2.5% isoflurane supplemented with 100% O 2 as previously undertaken and shown to effectively reduce consciousness without impairing cardiac function [ 22 ]. Urine was obtained for measurement of glucose concentration just prior to termination by cervical dislocation under isoflurane anesthesia.…”

Section: Methodsmentioning

confidence: 99%

Dual inhibition of sodium–glucose linked cotransporters 1 and 2 exacerbates cardiac dysfunction following experimental myocardial infarction

Connelly

Zhang

Desjardins

et al. 2018

Cardiovasc Diabetol

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BackgroundInhibiting both type 1 and 2 sodium–glucose linked cotransporter (SGLT1/2) offers the potential to not only increase glucosuria beyond that seen with selective SGLT2 inhibition alone but to reduce glucose absorption from the gut and to thereby also stimulate glucagon-like peptide 1 secretion. However, beyond the kidney and gut, SGLT1 is expressed in a range of other organs particularly the heart where it potentially assists GLUT-mediated glucose transport. Since cardiac myocytes become more reliant on glucose as a fuel source in the setting of stress, the present study sought to compare the effects of dual SGLT1/2 inhibition with selective SGLT2 inhibition in the normal and diseased heart.MethodsFischer F344 rats underwent ligation of the left anterior descending coronary artery or sham ligation before being randomized to receive the dual SGLT1/2 inhibitor, T-1095, the selective SGLT2 inhibitor, dapagliflozin or vehicle. In addition to measuring laboratory parameters, animals also underwent echocardiography and cardiac catheterization to assess systolic and diastolic function in detail.ResultsWhen compared with rats that had received either vehicle or dapagliflozin, T-1095 exacerbated cardiac dysfunction in the post myocardial infarction setting. In addition to higher lung weights, T-1095 treated rats had evidence of worsened systolic function with lower ejection fractions and reduction in the rate of left ventricle pressure rise in early systole (dP/dtmax). Diastolic function was also worse in animals that had received T-1095 with prolongation of the time constant for isovolumic-pressure decline (Tau) and an increase in the end-diastolic pressure volume relationship, indices of the active, energy-dependent and passive phases of cardiac relaxation.ConclusionsThe exacerbation of post myocardial infarction cardiac dysfunction with T-1095 in the experimental setting suggests the need for caution with the use of dual SGLT1/2 inhibitors in humans.

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Section: Methodsmentioning

confidence: 99%

Dual inhibition of sodium–glucose linked cotransporters 1 and 2 exacerbates cardiac dysfunction following experimental myocardial infarction

Connelly

Zhang

Desjardins

et al. 2018

Cardiovasc Diabetol

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show abstract

“…Further research procedures were performed in the rats 4 weeks after the myocardial infarction, because this was the time needed to develop HF …”

Section: Methodsmentioning

confidence: 99%

The role of apelin in central cardiovascular regulation in rats with post‐infarct heart failure maintained on a normal fat or high fat diet

Czarzasta

Cudnoch‐Jędrzejewska

Szczepañska‐Sadowska

et al. 2016

Clin Exp Pharma Physio

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Based on the available literature, it can be assumed that in cases of post-infarct heart failure (HF) and obesity, a significant change in the central regulation of the cardiovascular system takes place with, among others, the involvement of the apelinergic system. The main objective of the present study was to clarify the role of apelin-13 in the central regulation of the cardiovascular system in Sprague Dawley rats with HF or sham operated (SO) and fed on a normal fat (NFD) or a high fat diet (HFD). The study was divided into two parts: Part I, hemodynamic studies; and Part II, biochemical and molecular studies. The animals were subjected to the following research procedures. Part I and II: feeding NFD or HFD; experimental induction of HF or SO; Part I: intracerebroventricular (ICV) infusion of the examined substances, monitoring of mean arterial blood pressure (MABP) and heart rate (HR); Part II: venous blood and tissue samples collected. ICV infusion of apelin-13 caused significantly higher changes in ΔMABP in the SO NFD group. No changes were noted in ΔHR in any of the studied groups. Apelin and apelin receptor (APJ) mRNA expression in the brain and adipose tissues was higher in the HF rats. HFD causes significant increase in expression of apelin and APJ mRNA in the left ventricle. In conclusion, HF and HFD appear to play an important role in modifying the activity of the central apelinergic system and significant changes in mRNA expression of apelin and APJ receptor.

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Antiarrhythmic effects of growth hormone—in vivo evidence from small-animal models of acute myocardial infarction and invasive electrophysiology

Råmunddal

Gizurarson

Lorentzon

et al. 2008

Journal of Electrocardiology

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Decreased mortality in a rat model of acute postinfarction heart failure

Cited by 5 publications

References 18 publications

Dual inhibition of sodium–glucose linked cotransporters 1 and 2 exacerbates cardiac dysfunction following experimental myocardial infarction

Dual inhibition of sodium–glucose linked cotransporters 1 and 2 exacerbates cardiac dysfunction following experimental myocardial infarction

The role of apelin in central cardiovascular regulation in rats with post‐infarct heart failure maintained on a normal fat or high fat diet

Antiarrhythmic effects of growth hormone—in vivo evidence from small-animal models of acute myocardial infarction and invasive electrophysiology

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