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The effect of Chloroethylthiamin (CET), a structural analog of thiamin, on thiamin pyrophosphokinase (TPKase) activity of the supernatant of rat isolated enterocytes was compared with that on thiamin intestinal transport by rat everted jejunal sacs. Thiamin- thiazol-2(14C) was used as a substrate both for TPKase activity and for thiamin serosal transport and uptake. CET strongly inhibited TPKase activity of isolated enterocytes: at molar concentrations 10 or 100 times higher than labeled thiamin, the inhibition was 57 and 100% respectively. The inhibition was of the competitive type, with a Ki = 15 microM. At a molar concentration 10 times higher than labeled thiamin, CET lowered the thiamin serosal transport by 60%, and the sac wall content of free and phosphorylated thiamin by 54 and 42% respectively. At the 1:10 thiamin: CET molar ratio, the extent of the reductions of TPKase activity (57%) and of phosphorylated thiamin content of intestinal sac walls (42%) were of the same order. This indicates a relationship between the two events. Moreover, since TPKase activity inhibition alone resulted in the lowering of labeled thiamin serosal transport, thiamin phosphorylation and transport are probably two strictly related processes.

In order to estimate wave propagation "in vitro", aortic compliance has been studied by means of rings and stripes from 6 adult male Wistar rats. Lengthening and shortening maneuvres have been performed; the pulse transmission rate was evaluated by calculating the elastic modulus during the maneuvres. A Norepinephrine infusion has been done. Results obtained show that transmission rate is higher in shortening than in lengthening phases. Norepinephrine did not significantly affect the values. The rate values were not greatly different whether "in vitro" or "in vivo". By increasing specimen stress, the rate too was increased, but the amount was lower than "in vivo" values. Hence it was assumable that rate variations "in vivo", should be partially influenced by elastic modulus, and a vegetative intervention should be implied.

Pulse wave transmission rate has been measured "in vivo" in 6 male anaesthetized Wistar rats, by means of cannulae, inserted both in carotid and femoral arteries. The measure has been done by calculating the time delay of several corresponding levels in the two pressure pulses: at the foot, during the ascending phase, at the peak. Three different intervention have been carried out: Ach, NA, blood transfusion. The transmission rate outcame higher at the pulse foot than at the peak, in control animals and in Ach and blood transfusion interventions. The NA intervention inverted this behaviour, where the increase in transmission rate did not correspond to the rate of pressure growing. The possible influences of a vegetative component on arterial viscoelastic behaviour are discussed.