PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
August 1, 1990Journal of Clinical Investigation125 citationsOpen Access

Abnormal cardiac function in the streptozotocin-diabetic rat. Changes in active and passive properties of the left ventricle.

SLSheldon E. LitwinHeart Failure / CardiomyopathyTRT E RayaUniversity of ArizonaPAPeter G. AndersonUniversity of Alabama at Birmingham

Structured PICO

Does streptozotocin-induced diabetes alter left ventricular systolic and diastolic function in rats, and are these changes reversible with insulin?

P
Population
Rats (n=40 total: 14 given streptozotocin 65 mg/kg i.v., 15 untreated age-matched controls, 11 treated with insulin after streptozotocin)
I
Intervention
Streptozotocin (STZ) 65 mg/kg i.v. to induce diabetes, with a subgroup receiving insulin treatment
C
Comparator
Untreated age-matched controls
O
Outcome
Changes in systolic and diastolic function (conscious hemodynamics and ex vivo left ventricular passive-elastic properties)surrogate

Streptozotocin-induced diabetes in rats causes early hemodynamic and passive-elastic changes indicative of dilated cardiomyopathy, which can be reversed by insulin therapy.

Abstract

To provide an integrated assessment of changes in systolic and diastolic function in diabetic rats, we measured conscious hemodynamics and performed ex vivo analysis of left ventricular passive-elastic properties. Rats given streptozotocin (STZ) 65 mg/kg i.v. (n = 14) were compared with untreated age-matched controls (n = 15) and rats treated with insulin after administration of STZ (n = 11). After 7 d, diabetic rats exhibited decreases in heart rate and peak developed left ventricular (LV) pressure during aortic occlusion. After 26 d of diabetes there were significant decreases in resting LV systolic pressure, developed pressure, and maximal +dP/dt, whereas LV end-diastolic pressure increased and the time constant of LV relaxation was prolonged. The passive LV pressure-volume relationship was progressively shifted away from the pressure axis, and the overall chamber stiffness constant was decreased. However, "operating chamber stiffness" calculated at end-diastolic pressure was increased at 7 d, and unchanged at 26 d. LV cavity/wall volume and end-diastolic volume were increased after 26 d of diabetes. Myocardial stiffness was unchanged at both time intervals. All of the above abnormalities were reversed by the administration of insulin. We conclude that the hemodynamic and passive-elastic changes that occur in diabetic rats represent an early dilated cardiomyopathy which is reversible with insulin.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Litwin et al. (1990) studied this question.

synapsesocial.com/papers/6a23f0ad1c36a2d27b9ef42dhttps://doi.org/10.1172/jci114734
Ask AI
Helpful
Bookmark
Share
View Full Paper