Mitochondria-associated yeast mRNAs and the biogenesis of molecular complexes.

The coherence of mitochondrial biogenesis relies on spatiotemporally coordinated associations of 800-1000 proteins mostly encoded in the nuclear genome. We report the development of new quantitative analyses to assess the role of local protein translation in the construction of molecular complexes. We used real-time PCR to determine the cellular location of 112 mRNAs involved in seven mitochondrial complexes. Five typical cases were examined by an improved FISH protocol. The proteins produced in the vicinity of mitochondria (MLR proteins) were, almost exclusively, of prokaryotic origin and are key elements of the core construction of the molecular complexes; the accessory proteins were translated on free cytoplasmic polysomes. These two classes of proteins correspond, at least as far as intermembrane space (IMS) proteins are concerned, to two different import pathways. Import of MLR proteins involves both TOM and TIM23 complexes whereas non-MLR proteins only interact with the TOM complex. Site-specific translation loci, both outside and inside mitochondria, may coordinate the construction of molecular complexes composed of both nuclearly and mitochondrially encoded subunits.

[Failure of an intravenous locoregional anesthesia in a hypertensive patient]. / Echec d'une anesthésie locorégionale intraveineuse chez une hypertendue.

A case is reported of a congested arm occurring during intravenous regional anaesthesia with a double cuff tourniquet in a female elderly patient suffering from hypertension. The proximal cuff was apparently inflated adequately to 300 mmHg. Recent studies showed that the use of only the proximal tourniquet was associated with a risk of venous leakage. In elderly hypertensive patients, when intravenous regional anaesthesia was necessary, one would be justified in inflating the two cuffs before injection of the local anaesthetic.

[Prolongation of spinal anesthesia with hyperbaric bupivacaine by adrenaline and clonidine in the elderly]. / Prolongation de la rachianesthésie à la bupivacaïne hyperbare par l'adrénaline et la clonidine chez le vieillard.

So as to determine the effects of vasoconstriction on the duration of hyperbaric bupivacaine spinal anaesthesia, a prospective controlled study was carried out on 80 ASA class II or III patients, aged 75 years or more, who were scheduled for spinal anaesthesia for lower limb surgery. They were randomly allocated to four groups, and were each given 3 ml (15 mg) of 0.5% bupivacaine in plain solution with 0.5 ml of 30% dextrose solution, together with 1 ml normal saline in group I, 0.15 mg clonidine in group II, 0.2 mg adrenaline in group III, and 0.4 mg adrenaline in group IV. All patients therefore received 4.5 ml of 0.33% bupivacaine solution in 3.3% dextrose solution. The injection was made in the lateral position, and the patients turned supine immediately afterwards. The segmental level of sensory loss was tested using forceps. The time course required for maximal spread of the sensory blockade did not differ in the four groups. No difference was observed between median highest levels of sensory analgesia. Adding 0.15 mg clonidine or 0.4 mg adrenaline significantly prolonged mean times for two- and four-segment regression and mean times for regression to L2 level. The addition of 0.2 mg adrenaline only prolonged the mean regression time to L2 level. Regression times tended to increase more with 0.4 mg than with 0.2 mg adrenaline. Significant prolongation of motor block was also associated with the addition of vasoconstrictors. It is concluded that addition of 0.15 mg clonidine or 0.4 mg adrenaline may be useful to increase duration of hyperbaric bupivacaine spinal anaesthesia in elderly patients.

Effect of adding sodium bicarbonate to bupivacaine for spinal anesthesia in elderly patients.

The effect of added sodium bicarbonate on plain bupivacaine spinal anesthesia is unknown. Forty patients aged 75 years or older, ASA II or III, undergoing orthopedic lower limb surgery under spinal anesthesia were randomly classified into two groups. Just before injection, either 0.2 ml normal saline (group I) or 0.2 ml 0.42% NaHCO3 solution (group II) was added to 20 ml 0.5% bupivacaine hydrochloride. All patients then received intrathecally 3 ml (14.85 mg) of the bupivacaine solution in the lateral decubitus position. The segmental level of sensory loss was tested using forceps. The median time required to achieve maximal height of the sensory blockade and the median highest level of sensory anesthesia did not differ in the two groups. Alkalinized bupivacaine increased significantly the median times for regression to the T12 and L2 segments by 15 and 25 minutes, and the duration of complete motor block by 15 minutes, as compared to the hydrochloride salt. The clinical importance of such modest prolongations seems limited.