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Ciliary neurotrophic factor (CNTF) participates in the survival of motor neurons and reduces the denervation-induced atrophy of skeletal muscles. Experiments performed in rats show a decrease in peripheral CNTF synthesis during aging, associated with an overexpression of its alpha-binding receptor component by skeletal muscles. Measurement of sciatic nerve CNTF production and of the muscular performance developed by the animals revealed a strong correlation between the two studied parameters (r = 0.8; p < 0.0003). Furthermore, the twitch and tetanic tensions measured in the isolated soleus skeletal muscle in 24-month-old animals increased 2. 5-fold by continuous in vivo administration of CNTF. Analyses of the activation level of leukemia inhibitory factor receptor beta- and signal transducer and activator of transcription 3-signaling molecules in response to exogenous CNTF revealed an increased tyrosine phosphorylation positively correlated with the twitch tension developed by the soleus muscle of the animals.

We investigated, at first in low-flow global ischemia and then with ischemic preconditioning, the effects of a compound, (4-isopropyl-3-methylsulphonylbenzoyl)guanidine hydrochloride (HOE 642), known to inhibit the Na+/H+ exchange in rat cardiomyocytes. In rat isolated hearts, perfused on a Langendorff apparatus with Krebs-Henseleit carbonate buffer, the action potentials and the contractile function were measured during a 25-min period of global low-flow ischemia (coronary flow, 0.3 mL.min-1) followed by a 30-min reperfusion. In hearts previously preconditioned, two intermittent periods of total ischemia for 5 min each, separated by 5 min reflow, were performed before low-flow ischemia. Treated hearts received HOE 642 (3.0 x 10(-8) mol.min-1) exclusively during low-flow ischemia. Treatment with HOE 642 during low-flow ischemia improves cardiac performance and lowers the rise in diastolic tension during reperfusion. Concomitantly HOE 642 shortens the action potential, and has striking effects on ventricular arrhythmias during reperfusion as well. These results support the concept that Na+/H+ exchange activation is a contributing factor to low-flow ischemia-reperfusion injuries. HOE 642 exhibited minor effects when combined with the preconditioning protocol, but a lengthening in action potential was observed and ventricular arrhythmias were mostly affected. Preconditioned hearts demonstrated marked glycogen depletion compared with controls. These results support the hypothesis that preconditioning could decrease glycogenolysis and therefore subsequently limit acidification during low-flow ischemia.

In this work, we compared the electrophysiological and metabolic parameters of a volume overload model of cardiac hypertrophy (aorto-caval fistula) with those of two other models of hypertrophy (aortic stenosis and isoproterenol pretreatment). In these last models, a prolongation of action potential and a decrease of myocardial ATP content are observed. However, these alterations are not shown in the aorto-caval fistulated animals while their heart are well hypertrophied. The amplitude increase of phase 3 AP seemed to be a common factor of these models of cardiac hypertrophy.

Thymic ectopies are under study in 45 Pangolin's thyroids (Manis tricuspis Rafinesque). Their frequency seems to be independent of the sex of the animal but this frequency also appears to be in relation to the age of the animal. The topographic and morphological studies suggest a close relationship between these inclusions made out of thymic tissue and the presence of parathyroid islets included into the thyroid capsule. Some pictures, showing a connection between parathyroid cells and thymis parenchym elements, plead in favour of a functional interelation between these different structures as the Mc Manus experiments suggest it.