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BACKGROUND: Palliative home-care teams often cooperate with general practitioners (GPs) and district nurses. Our aim was to evaluate a palliative home-care team from the viewpoint of GPs and district nurses. METHODS: GPs and district nurses received questionnaires at the start of home-care and one month later. Questions focussed on benefits to patients, training issues for professionals and cooperation between the home-care team and the GP/district nurse. A combination of closed- and open-ended questions was used. RESULTS: Response rate was 84% (467/553). Benefits to patients were experienced by 91%, mainly due to improvement in symptom management, 'security', and accessibility of specialists in palliative care. After one month, 57% of the participants reported to have learnt aspects of palliative care, primarily symptom control, and 89% of them found cooperation satisfactory. Dissatisfaction was caused mainly by lack of information from the home-care team to primary-care professionals. CONCLUSION: GPs and district nurses welcomed the palliative home-care team and most experienced benefits to patients. Strengthened communication, initiated by the home-care team would enhance cooperation. [ABSTRACT FROM AUTHOR]

In open-chest dogs transient occlusion of the left anterior descending coronary artery induced an immediate decline in the creatine phosphate content of the ischaemic area, a lesser decline of the ATP and total adenine nucleotide contents and a rise in S-T segments. Reperfusion after 15 min restored creatine phosphate level and intramyocardial electrograms to normal whereas ATP and total adenine nucleotide levels stayed down. None of these parameters were modified in the non-ischaemic area during the experiments. This study shows that there is no close relationship between electrical and biochemical events during either ischaemia or reflow. [ABSTRACT FROM PUBLISHER]

A voltage-dependent cationic channel of large conductance is observed in phospholipid bilayers formed at the tip of microelectrodes from proteoliposomes derived from mitochondrial membranes. This channel was blocked by a 13-residue peptide with the sequence of the amino terminal extremity of the nuclear-coded subunit IV of cytochrome c oxidase. The blockade was reversible, voltage- and dose-dependent. The peptide did not affect the activity of a Torpedo chloride channel observed under the same conditions. From experiments with phospholipid monolayers, it is unlikely that the peptide inserts into bilayers under the experimental conditions used. The blockade was observed from both sides of the membrane, being characterized by more frequent transitions to the lower conductance states, and a maximum effect was observed around 0 mV. Channels, the gating mechanism of which had been eliminated by exposure to trypsin, were also blocked by the peptide. For trypsinized channels, the duration of the closure decreased and the blockade saturated at potentials below -30 mV. These observations are consistent with a translocation of the peptide through the channel. Dynorphin B, which has the same length and charge as the peptide, had some blocking activity. Introduction of negative charges in the peptide by succinylation suppressed the activity. [ABSTRACT FROM AUTHOR]

The competition of ethacrynate with phosphate shown during oxidation of succinate by rat liver mitochondria [2] is confirmed by measuring [14C]ethacrynate incorporation into mitochondria: on increasing the phosphate present during preincubation, less ethacrynate is incorporated into the mitochondria and there is a decrease in the inhibition of succinate oxidation. Ethacrynate exhibits different effects according to the substrate used: a) with NAD-linked substrates, ethacrynate inhibits the oxidation, this inhibition being insensitive to phosphate and accompanied by complete oxidation of NADH to NAD+ ; b) with succinate, as already mentionned, the inhibition is sensitive to phosphate; if rotenone is present during preincubation with ethacrynate, there is oxidation, but it is an uncoupled oxidation, while, with phosphate plus ethacrynate, the oxidation is still coupled. Methylene blue added during preincubation with ethacrynate and rotenone prevents the uncoupling and reestablishes the inhibition of oxidation. As with NAD-linked substrates, the inhibition of oxidation by ethacrynate is accompanied by complete oxidation of NADH to NAD+ ; c) with TMPD + ascorbate (plus rotenone), ethacrynate completely uncouples oxidative phosphorylation; again phosphate prevents this effect. Ethacrynate inhibits the [32P]P1-ATP exchange reaction. The presence of Mg++ ions is required in order to get maximal effect of ethacrynate : the more Mg++ ions present, the greater is the inhibition (succinate oxidation measurement). The results presented in this paper are discussed on the basis that the primary action of etha- crynate is a phosphate-sensitive uncoupling action. The fact that inhibition of NAD-linked substrate oxidation is not sensitive to phosphate suggests that ethacrynate interferes in another way with these substrates. However, by depleting mitochondria of energy-rich compounds, the penetration of these substrates (assumed to be an energy requiring process) would be inhibited by ethacrynate and, consequently, the oxidation of these substrates would be impossible. As a thiol reagent, ethacrynate is believed to react with specific proteic thiol groups implicated in the formation of an energy-rich intermediate, and to compete with phosphate in the formation of a phosphorylated energy-rich compound from a non-phosphorylated energy-rich compound. [ABSTRACT FROM AUTHOR]