Why the study?
Does triiodothyronine or insulin treatment prevent cardiac dysfunction in diabetic renovascular hypertensive rats?
Does triiodothyronine or insulin treatment prevent cardiac dysfunction in diabetic renovascular hypertensive rats?
In a rat model of diabetic renovascular hypertension, T3 treatment prevented cardiac dysfunction nearly as effectively as insulin, suggesting hypothyroidism contributes to diabetic cardiomyopathy.
Answers are grounded in this paper and cite their sources.
T3 may mitigate cardiac dysfunction in diabetic RVH models; extends hypothyroidism hypothesis but leaves clinical translation open.
The influences of hypertension and hypothyroidism on diabetic cardiomyopathy are not clear. We studied this problem further by characterizing the effects of chronic triiodothyronine (T 3 ) treatment on cardiac performance of diabetic renovascular hypertensive (RVH) rats. Hypertension was effected by clipping the left renal artery of Wistar–Kyoto (WKY) rats, and diabetes was induced 2 weeks later by streptozotocin (STZ; 55 mg/kg i.v.). The WKY strain was selected because it is relatively resistant to the cardiodepressant effects of diabetes, so that the influence of superimposed hypertension would be more apparent. Performance of working Krebs–Henseleit buffer perfused hearts was quantified by measuring left ventricular pressure and flow characteristics. The results showed that renovascular clipping caused a marked hypertension and left ventricular hypertrophy (LVH) but had no effect on perfused heart performance after 10 weeks. They also showed that diabetes during the final 8 weeks (i) caused a marked impairment in the performance of perfused hearts ex vivo of hypertensive rats but had no measurable effect in the normotensive WKY, (ii) had no effect on arterial pressure of either the normotensive or the hypertensive rats but reduced heart rate of hypertensive animals in vivo, and (iii) caused equivalent hyperglycemia, hypoinsulinemia, and hypothyroidism (depressed serum T 3 and T 4 levels) of hypertensive and normotensive rats. Treatment of diabetic RVH rats with T 3 (10 μg∙kg −1 ∙day −1 ) in vivo was nearly as effective as insulin therapy (10 U∙kg −1 ∙day −1 ) in preventing the cardiac dysfunction ex vivo and was as effective as insulin therapy in preventing the bradycardia in vivo and the decline in serum T 3 levels, even though it intensified the hyperglycemia and body weight loss. The results provide support for a synergistic effect of diabetes and hypertension on heart function. They also add support to the hypothesis that attendant hypothyroidism contributes significantly to diabetic cardiomyopathy in the hypertensive rat.
No takes yet. Share an insight, caveat, or question.
Rodgers et al. (1991) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: