[National survey on cardiovascular emergencies. Modalities of admission to cardiologic intensive care units (Paris excluded)]. / Enquête nationale sur les urgences cardio-vasculaires. Modalités d'admission en unité de soins intensifs cardiologiques (à l'exclusion de Paris).

In a national investigation carried out between December 10, 1985 and March 31, 1986, the modalities of admission of 19 Cardiology Intensive Care Units (Paris excluded) of 738 cardiovascular emergency patients were evaluated. Detail of the pre-medical phase duration and of the dispatching phase duration was obtained for each patient. Each of these two phases was then analyzed according to the geographical location of the Intensive Care Unit (ICU), to the symptoms experienced by the patient, to the type of medical aid initially sought (general practitioner, cardiologist, "emergency doctor") and to the medical itinerary followed. The median duration of the pre-medical phase was 1 h 45 min, that of the dispatching phase 2 h, 15 min and that of the total time elapsed before admission 5 hours, there being no clear-cut differences due to the location of the ICU. The duration of the pre-medical phase was essentially determined by the awareness of a vital risk or otherwise, or by the relation established by the patient between his symptoms and a possible heart disease. The median duration of the dispatching phase was about 2 hours when only one doctor intervened and 4 h, 35 min when a second doctor was consulted. The role of the cardiologist in the dispatching of these cardiovascular emergency cases was very limited (7 p. 100 of the patients) and not very expeditive, the median duration of admission being 6 h, 30 min when he intervened initially and 12 hours when he intervened at the request of the patient's general practitioner.(ABSTRACT TRUNCATED AT 250 WORDS)

Gastric microsomal NADH-cytochrome b5 reductase: characterization and solubilization.

NADH-cytochrome b5 reductase from hog gastric microsomes was studied with respect to substrate dependence, optimum pH, thermal denaturation as well as anti-cytochrome b5 antibodies and different ions. The reduction of potassium ferricyanide by the enzyme was specific for NADH. Using potassium ferricyanide or trypsin-solubilized liver cytochrome b5 (Tb5) as substrates, enzyme activity was inhibited by ADP and to a lesser extent by ATP. Tb5- (but not ferricyanide-) reductase was activated by ionic strength up to 0.05 ion equivalent per liter and inhibited at higher strengths whatever the ion used (Cl-, Na+, Ca2+, Mg2+). Enzyme solubilization occurred with Triton X100. The solubilization increased the Tb5- (but not the ferricyanide-) reductase activity up to a Triton:protein ratio of 15. We therefore suggest that gastric microsomes contain a Triton soluble membrane-bound NADH cytochrome b5 reductase which is in many respects similar to the liver and red cell enzymes.

Cytochrome b5-dependent delta 9 desaturation of fatty acids in gastric microsomes.

Stearyl-CoA was shown to stimulate the reoxidation rate of cytochrome b5 of gastric microsomes and to decrease the reduction rate of trypsin-purified hog liver cytochrome b5 by the NADH-cytochrome b5 reductase of these microsomes. This latter effect was (1) proportional to microsome concentration and to stearyl-CoA concentration with an apparent Km of 3.3 . 10(-6) M and a Vmax of 71 nmol per min and per mg microsomal protein, (2) insensitive to ATP and inhibited by 1.4 mM KCN, (3) mimicked by palmityl-CoA but not by stearic nor palmitic acid. Direct assays carried out using [14C]stearyl- and [14C]palmityl-CoA as substrates showed a production of 0.12 nmol of oleic and palmitoleic acid, respectively, per min per mg of microsomal protein. In the presence of Tb5 antibodies the reaction was inhibited by 40%. These results support the occurrence of cytochrome b5-dependent fatty acid delta 9 desaturation in gastric microsomes.

C1-transport in gastric micorsomes. An ATP-dependent influx sensitive to membrane potential and to protein kinase inhibitor.

Uptakes of radioactive C1- or 1- by gastric microsomal vesicles were stimulated 2- to 8-fold by AtP. The sensitivity of those uptakes to a C1- in equilibrium OH- ionophore and to osmotic swelling suggested they were due to transport rather than to binding. The ATP effect was labile, but dithiothreitol and methanol improved its stability. The stimulation of anion transport required magnesium; GTP and UTP were less potent than ATP whereas ADP and AMP had no effect. The apparent Km for ATP was estimated to be 2 X 10(-4) M at 22 degrees C. The rate of the ATP-dependent transport showed saturation-type kinetics, with half-maximal uptake at 10 mM for I- and 15 mM for C1-. Nonradioactive C1-, I-, and SCN- competed with 125I- uptake while SO42- did not. K+ valinomycin increased the ATP-dependent C1- uptake. The thermostable inhibitor of cAMP-dependent protein kinases inhibited the effect of ATP. These results suggest the existence of an anion conductance, permeant to C1-, I-, and SCN- and nonpermeant to SO42-, which could be linked to a cAMP-dependent protein kinase.