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Updated: Jul 31, 2026
Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Triiodothyronine concomitantly inhibits calcium overload and postischemic myocardial stunning in diabetic rats
Y Oshiro1, M Shimabukuro, N Takasu
1Second Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Nishihara, Okinawa, Japan.
Abstract:
Acute effects of triiodothyronine (T3) on postischemic myocardial stunning and intracellular Ca2+ contents were studied in the isolated working hearts of streptozotocin-induced diabetic rats and age-matched controls. After two weeks of diabetes, serum T3 and T4 levels were decreased to 62.5% and 33.9% of control values. Basal preischemic cardiac performance did not differ between diabetic and control rats. In contrast, during reperfusion after 20-min ischemia, diabetic rats exhibited an impaired recovery of heart rate (at 30-min reperfusion 57.5% of baseline vs. control 88.5%), left ventricular (LV) systolic pressure (44.1% vs. 89.5%), and cardiac work (23.1% vs. 66.0%). When 1 and 100 nM T3 was added before ischemia, heart rate was recovered to 77.2% and 81.8% of baseline, LV systolic pressure to 68.3% and 81.9%, and cardiac work to 50.8% and 59.0%, respectively. Diabetic rat hearts showed a higher Ca2+ content in the basal state and a further increase after reperfusion (4.96+/-1.17 vs. control 3.78+/-0.48 micromol/g, p<0.01). In diabetic hearts, H+ release was decreased after reperfusion (5.24+/-2.21 vs. 8.70+/-1.41 mmol/min/g, p<0.05). T3 administration caused a decrease in the postischemic Ca2+ accumulation (lnM T3 4.66+/-0.41 and 100 nM T3 3.58+/-0.36) and recovered the H+ release (lnM T3 16.2+/-3.9 and 100 nM T3 11.6+/-0.9). T3 did not alter myocardial O2 consumption. Results suggest that diabetic rat hearts are vulnerable to postischemic stunning, and T3 protects the myocardial stunning possibly via inhibiting Ca2+ overload.
Insights
Triiodothyronine (T3) treatment improves recovery in diabetic rat hearts after ischemia by reducing calcium overload. This finding suggests T3 may protect against postischemic myocardial stunning in diabetes.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Metabolic Diseases
Background:
- Diabetes mellitus is associated with impaired cardiac function and increased vulnerability to ischemia.
- Thyroid hormones, like triiodothyronine (T3), play a crucial role in cardiac metabolism and function.
- Diabetic cardiomyopathy can exacerbate myocardial stunning following ischemic events.
Purpose of the Study:
- To investigate the acute effects of triiodothyronine (T3) on postischemic myocardial stunning in diabetic rat hearts.
- To assess the impact of T3 on intracellular calcium (Ca2+) handling during ischemia-reperfusion in diabetes.
- To determine if T3 administration can mitigate impaired cardiac performance in diabetic hearts subjected to ischemia.
Main Methods:
- Isolated working hearts from streptozotocin-induced diabetic rats and age-matched controls were used.
- Hearts were subjected to 20 minutes of global ischemia followed by reperfusion.
- Triiodothyronine (T3) was administered at 1 nM and 100 nM concentrations before ischemia.
- Cardiac performance (heart rate, left ventricular systolic pressure, cardiac work) and intracellular Ca2+ content were measured.
Main Results:
- Diabetic rat hearts showed significantly impaired recovery of cardiac function and increased intracellular Ca2+ content after ischemia-reperfusion compared to controls.
- T3 administration (1 nM and 100 nM) significantly improved the recovery of heart rate, left ventricular systolic pressure, and cardiac work in diabetic hearts.
- T3 treatment reduced postischemic Ca2+ accumulation and normalized altered H+ release in diabetic hearts.
- T3 did not affect myocardial oxygen consumption in either group.
Conclusions:
- Diabetic rat hearts are highly susceptible to postischemic stunning due to impaired recovery and altered Ca2+ handling.
- Acute administration of triiodothyronine (T3) confers significant protection against myocardial stunning in diabetic hearts.
- T3 likely exerts its protective effects by inhibiting intracellular Ca2+ overload during reperfusion, thereby improving cardiac performance.
