Changes in antioxidant status, protein concentration, acetylcholinesterase, (Na+,K+)-, and Mg2+ -ATPase activities in the brain of hyper- and hypothyroid adult rats.

It is a common knowledge that metabolic reactions increase in hyperthyroidism and decrease in hypothyroidism. The aim of this work was to investigate how the metabolic reactions could affect the total antioxidant status (TAS), protein concentration (PC) and the activities of acetylcholinesterase (AChE), (Na+,K+)-ATPase and Mg2+ -ATPase in the brain of hyper- and hypothyroid adult male rats. Hyperthyroidism was induced in rats by subcutaneous administration of thyroxine (25 microg/l00 g body weight) once daily for 14 days, while hypothyroidism was induced by oral administration of propylthiouracil (0.

Dronedarone administration prevents body weight gain and increases tolerance of the heart to ischemic stress: a possible involvement of thyroid hormone receptor alpha1.

Hypothyroid heart displays a phenotype of cardioprotection against ischemia and this study investigated whether administration of dronedarone, an amiodarone-like compound that has been shown to preferentially antagonize thyroid hormone binding to thyroid hormone receptor alpha1 (TRalpha1), results in a similar effect. Dronedarone was given in Wistar rats (90 mg/kg, once daily (od) for 2 weeks) (DRON), while untreated animals served as controls (CONT). Hypothyroidism (HYPO) was induced by propylthiouracil administration.

Trimetazidine protects isolated rat hearts against ischemia-reperfusion injury in an experimental timing-dependent manner.

The present study investigated the tolerance of the isolated rat heart to ischemia-reperfusion after administration of trimetazidine (TMZ) at different experimental phases, as well as the possible involvement of p38 MAPK and JNKs in this response. Isolated rat hearts were perfused in Langendorff mode. Untreated hearts after stabilization (S) were subjected to 20 min of zero-flow global ischemia (I) and 45 min of reperfusion (R), (NORM), n = 9.

Thyroid hormone and phenotypes of cardioprotection.

Thyroid hormone has multiple effects on the cardiovascular system with important physiological consequences. Several genes that encode important regulatory and structural proteins in the heart have been shown to be thyroid hormone responsive. More notably, certain effects of thyroid hormone have been exploited therapeutically.

Mepivacaine alters vascular responsiveness to vasoconstrictors in aortic rings from normal and aortic-banded rats.

The present study investigated the effects of mepivacaine on the response of rat aorta to vasoconstrictors in normal and aortic-banded animals. Cardiac hypertrophy was induced in Wistar rats by aortic banding, while sham-operated animals served as controls. Isolated aortic rings with or without endothelium were contracted with potassium chloride and phenylephrine in the presence of mepivacaine (10(-3) M).

Thyroxine pretreatment increases basal myocardial heat-shock protein 27 expression and accelerates translocation and phosphorylation of this protein upon ischaemia.

Thyroxine pretreatment increases the tolerance of the heart to ischaemia, and heat-shock protein 27 (HSP27) is considered to play an important role in cardioprotection. The present study investigated whether long-term thyroxine administration can induce changes in the expression, translocation and phosphorylation of HSP27 at baseline and upon ischaemic stress. L-Thyroxine (T(4)) was administered to Wistar rats (25 microg/100 g/day s.

Involvement of p38 MAPK and JNK in heat stress-induced cardioprotection.

The present study investigated whether heat stress-induced cardioprotection involves alterations in the pattern of p38 mitogen activated protein kinase (p38MAPK) and c-Jun NH2 - terminal kinase (JNK) activation during ischaemia - reperfusion in a model of isolated perfused rat heart. Wistar rats were subjected to whole-body hyperthermia at 42 degrees C for 15 min (HS), while untreated animals served as controls (CON). Twenty four hours later, CON and HS isolated hearts were perfused in a Langendorff mode and subjected to 20 min of zero-.

Loss of cardioprotection induced by ischemic preconditioning after an initial ischemic period in isolated rat hearts.

Background: The beneficial effect of ischemic preconditioning (PC) has been extensively studied in normal hearts but its effects on diseased hearts remain largely unknown. The effect of PC in the already ischemic myocardium has not been previously studied, although ischemia in varying intervals, which is difficult to assess, is often encountered in clinical practice.

Objective: To investigate whether the cardioprotective effect of PC is preserved when it is applied after a period of ischemia of varying duration.

Thyroid hormone and cardioprotection: study of p38 MAPK and JNKs during ischaemia and at reperfusion in isolated rat heart.

It has been recently shown that long-term thyroxine administration increases the tolerance of the heart to ischaemia. The present study investigated whether thyroxine induced cardioprotection involves alterations in the pattern of p38 mitogen activated protein kinase (p38MAPK) and c-Jun NH2-terminal kinases (JNKs) activation during ischaemia-reperfusion. L-thyroxine (T4) was administered in Wistar rats (25 microg/100 g/day, subcutaneously) for 2 weeks (THYR), while normal animals served as controls (NORM).

Dobutamine administration exacerbates postischaemic myocardial dysfunction in isolated rat hearts: an effect reversed by thyroxine pretreatment.

The present study has investigated the effects of dobutamine on postischaemic dysfunction in the setting of global ischaemia and reperfusion in a model of isolated heart preparation. Isolated rat hearts were subjected to 20 min of zero-flow global ischaemia followed by 45 min of reperfusion. Dobutamine administration (10 microg/kg/min) during the reperfusion period resulted in deterioration of functional recovery, which was abolished by propranolol administration.

Effects of dronedarone and amiodarone on plasma thyroid hormones and on the basal and postischemic performance of the isolated rat heart.

The present study investigated the effects of dronedarone and amiodarone on plasma thyroid hormones and the possible consequences on the response of the heart to ischemia. Amiodarone (30 mg/kg/day per os) or dronedarone (30 mg/kg/day per os) were administered for 2 weeks in normal and thyroxine-treated animals (25 microg/100 g body weight od sc, for 2 weeks), while animals without amiodarone and dronedarone served as controls. Isolated rat hearts were perfused in a Langendorff mode and subjected to 20 and 30 min of zero-flow global ischemia followed by 45 min of reperfusion.

Long-term thyroxine administration protects the heart in a pattern similar to ischemic preconditioning.

We have previously shown that long-term thyroxine administration can protect the heart against ischemia. In the present study, we investigated whether thyroxine-induced cardioprotection can mimic the pattern of protection that is afforded by a well-established cardioprotective means such as ischemic preconditioning. In a Langendorff-perfused rat heart preparation, after an initial stabilization, normal and thyroxine-treated hearts were subjected to 20 minutes of zero-flow global ischemia followed by 45 minutes of reperfusion.