Leak detector in medical gas delivery systems

We describe an original device developed by the biomedical technicians of the University Hospital of Nancy for checking tightness and measuring the capacity of medical gas pipeline network. A leak can be assessed either as a loss of pressure or as a loss of volume per unit of time (cmH2O.min-1 and mL.min-1 respectively). To assess the latter, the capacity of the explored pipeline must have been measured when it still was gas-tight. With the device, a leak can be assessed within a few minutes whereas the official procedure requires a delay between 1 and 24 hours. The device still has to undergo bench evaluation and validation.     

Recovery of slow skeletal muscle after injury in the senescent rat

We studied the contractile, histological and biochemical characteristics of regenerating slow (soleus) muscles of aged rats and the effect of IGF-1 treatment on these parameters. Regenerating soleus muscles were studied 21 days after myotoxic injury. In senescent rats (24 month old), the in situ isometric maximal tetanic force (P0), resistance to fatigue (T20%P0) and shortening speed with an afterload of 20%P0 (SS20%P0) were lower (p<0.05) in regenerating soleus muscles as compared to uninjured controlateral soleus muscles. Moreover, the expression of type 1 myosin heavy chain (MHC-1) was decreased by injury in the soleus muscles of senescent rats (p<0.05). Furthermore, a single injection of IGF-1 (3 microg) into the soleus of senescent rats only slightly increased the level of sarcoplasmic reticulum type 2 Ca(2+)-ATPase in regenerating soleus muscles (p<0.01). Contrary to senescent animals, regenerating soleus of adult rats (10 month old) did not present significantly lower P0 and MHC-1 expression than uninjured controlateral muscles (p>0.05). In conclusion, the regeneration of a slow muscle is more uncompleted 3 weeks after myotoxic injury in senescent rats than in adult rats. It cannot be made more effective by a single injection of IGF-1 into the senescent slow muscle.     

Exercise training improves functional post-ischemic recovery in senescent heart

The incidence of ischemic cardiac diseases increases with age and elderly subjects are more vulnerable to myocardial infarction. Endurance exercise (e.g. treadmill training) provides cardioprotection against an ischemia and reperfusion (IR) event in adult heart but such a potential beneficial effect of regular exercise has never been evaluated during aging. Therefore, this study investigated the effects of moderate running training on post-ischemic recovery of contractile function and coronary perfusion in senescent myocardium. Isolated hearts of sedentary (24 mo-sedentary; n=10) and trained senescent (24 mo-trained; n=11; moderate running: 1h/day, 5 days/week for 12 weeks) rats were submitted to 45min low-flow ischemia (15% of initial coronary flow (CF)) followed by 30min reperfusion. Active tension (AT) and CF were recorded at baseline and after 1, 3, 5, 10, 15, 20, 25 and 30min of reperfusion. Left ventricular protein carbonylation, and both heat-shock-protein 70 (HSP70) and endothelial nitric oxide synthase (eNOS) contents were determined by Oxyblotting and Western blotting, respectively. Regular physical exercise improves impairment of functional post-ischemic recovery (AT and CF) of aged hearts during reperfusion and this cardioprotection is associated to limited protein oxidation and increased HSP70 and eNOS myocardial contents.     

Differential modification of myosin heavy chain expression by tenotomy in regenerating fast and slow muscles of the rat

We have examined the effect of tenotomy on the expression of myosin heavy chains (MyHC) in regenerating fast and slow skeletal muscles. Degeneration/regeneration of the left soleus and plantaris of Wistar male rats was induced by an injection into the muscle belly of a myotoxin (snake venom: Notechis scutatus scutatus). MyHC isoform content of regenerating plantaris and soleus muscles were studied 21 days after muscle injury using an electrophoretic technique. Tenotomy of the regenerating plantaris (mechanical underload) did not alter its MyHC expression (P > 0.05). In contrast, tenotomy of the regenerating soleus increased its relative levels of MyHC-2b (P < 0.05) and MyHC-2x/d (P < 0.01), and decreased its relative level of MyHC-1 (P < 0.01). Tenotomy of the synergistic gastrocnemius (overload) tended to decrease the relative level of MyHC-2b in regenerating plantaris (P < 0.07). The effect of tenotomy of the synergistic gastronecmius on the regenerating soleus was different: a decrease in the relative levels of MyHC-1 (P < 0.05) and an increase in the relative level of MyHC-neonatal (P < 0.01). In conclusion, and in contrast to a regenerating slow muscle, a change of mechanical loading by tenotomy did not seem to markedly alter the expression of mature MyHC phenotype in a fast regenerating muscle.     

Effect of anabolic/androgenic steroids on myosin heavy chain expression in hindlimb muscles of male rats

We have examined the effect of male sex hormones on the myosin heavy chain (MHC) expression of the soleus and extensor digitorum longus (EDL) muscles. Young male adult Wistar rats were treated over a 25-day period with either oil (CON, n = 8), nandrolone (nortestosterone decanoate, NAN, n = 8), nandrolone combined with endurance exercise (treadmill running, NAN+EXE, n = 8), or were castrated (CAS, n = 8). The MHC composition of the soleus and EDL muscles was measured by electrophoresis. Castration and treatment with nandrolone had no effect (P > 0.05) on the relative levels of MHC in the soleus and EDL. In contrast, in NAN+EXE rats, the relative level of MHC-1 increased [slow isoform; mean (SD) 97.6 (4.7)% in NAN+EXE rats, versus 86.5 (7.5)% in CON rats] and MHC-2a decreased [fast isoform; 2.4 (4.7)% in NAN+EXE, versus 13.5 (7.5)% in CON rats], only in the soleus (P < 0.05). In conclusion, it appears that endogenous anabolic/androgenic steroids are not essential for the maintenance of the MHC expression of fast- and slow-twitch muscles in the young adult male rat. In addition, nandrolone combined with endurance exercise induced a shift from a fast to a slower MHC phenotype of the slow-twitch muscle. Accepted: 27 July 1999