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Cardiovascular Diabetology

, 10:26

First Online: 06 April 2011Received: 28 February 2011Accepted: 06 April 2011


BackgroundAlthough clinical diabetes mellitus is obviously a high risk factor for myocardial infarction MI, in experimental studies disagreement exists about the sensitivity to ischemic injury of an infarcted myocardium. Recently, our group demonstrated that diabetic animals presented better cardiac function recovery and cellular resistance to ischemic injury than nondiabetics. In the present study, we evaluated the chronic effects of MI on left ventricular LV and autonomic functions in streptozotocin STZ diabetic rats.

MethodsMale Wistar rats were divided into 4 groups: control C, n = 15, diabetes D, n = 16, MI I, n = 21, and diabetes + MI DI, n = 30. MI was induced 15 days after diabetes STZ induction. Ninety days after MI, LV and autonomic functions were evaluated 8 animals each group. Left ventricular homogenates were analyzed by Western blotting to evaluate the expression of calcium handling proteins.

ResultsMI area was similar in infarcted groups ~43%. Ejection fraction and +dP-dt were reduced in I compared with DI. End-diastolic pressure was additionally increased in I compared with DI. Compared with DI, I had increased Na-Ca exchange and phospholamban expression 164% and decreased phosphorylated phospholamban at serine 65% and threonine 70% expression. Nevertheless, diabetic groups had greater autonomic dysfunction, observed by baroreflex sensitivity and pulse interval variability reductions. Consequently, the mortality rate was increased in DI compared with I, D, and C groups.

ConclusionsLV dysfunction in diabetic animals was attenuated after 90 days of myocardial infarction and was associated with a better profile of calcium handling proteins. However, this positive adaptation was not able to reduce the mortality rate of DI animals, suggesting that autonomic dysfunction is associated with increased mortality in this group. Therefore, it is possible that the better cardiac function has been transitory, and the autonomic dysfunction, more prominent in diabetic group, may lead, in the future, to the cardiovascular damage.

List of abbreviationsBRbradycardic response

DAPdiastolic arterial pressure

+dP-dtmaximum rate of left ventricular pressure rise

-dP-dtmaximum rate of left ventricular pressure fall

EDTpeak E wave deceleration time

EFejection fraction

GAPDHglyceraldehyde-3-phosphate dehydrogenase

HRheart rate

IVRTleft ventricular isovolumetric relaxation time

LVleft ventricle

LV massleft ventricular mass corrected by body weight

LVEDDleft ventricular end-diastolic diameter

LVEDPleft ventricular end-diastolic pressure

LVSPleft ventricular systolic pressure

MAPmean arterial pressure

MImyocardial infarction

MPImyocardial performance index

NCXsodium calcium exchanger

phospho-ser16-PLNphosphorylated phospholamban at serine 16

phospho-thr17-PLNphosphorylated phospholamban at threonine 17

PIpulse interval

PLNdephosphorylated phospholamban

PP1phosphatase protein 1

SAPsystolic arterial pressure

SDstandard deviation

SEMstandard error of mean

SERCA2calcium pump ATPase of sarcoplasmic reticulum


TRtachycardic response

VCFvelocity of circumferential fiber shortening.

Electronic supplementary materialThe online version of this article doi:10.1186-1475-2840-10-26 contains supplementary material, which is available to authorized users.

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Author: Bruno Rodrigues - Kaleizu T Rosa - Alessandra Medeiros - Beatriz D Schaan - Patricia C Brum - Kátia De Angelis - Maria 

Source: https://link.springer.com/article/10.1186/1475-2840-10-26

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