1. We investigated the mechanisms regulating acid extrusion in cultured fetal rat hippocampal neurones loaded with 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein.2. In the absence of HCO3-, removal of external Nae by substitution with N-methyl-Dglucamine caused a sustained intracellular acidification that was not observed when Na+ was replaced by Li+, but neither steady-state intracellular pH (pH1) nor the rate of pH, recovery from an imposed acid load were influenced by amiloride analogues or HOE 694, inhibitors of Na+-H+ exchange in other cell types. In the presence of HC03-, removal of external Na+ or Cl-evoked an intracellular acidification and a 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid-sensitive (DIDS-sensitive) intracellular alkalinization, respectively.Applied alone, however, DIDS elicited a fall in steady-state pHi at room temperature but not at 37 'C. The DIDS-evoked fall in steady-state pHi and the 0 CF-evoked intracellular alkalinization observed in the presence of HC03-at room temperature were dependent on external Na+. 3. At room temperature (18-22°C), but not at 37°C, the transition from HC03-free to HC03--containing medium at a constant pH. produced a net alkalinization that was dependent on external Nae and was inhibited by DIDS or the depletion of internal CF. 4. Recovery of pH, from an acid load imposed in the absence of HC03-was dependent on external Nae. Addition of HC03-to the perfusion medium increased the rate of pH1 recovery from an acid load at room temperature but not at 37 'C. In the presence of HCO3-, DIDS slowed the rate of recovery of pHi from an acid load at both room temperature and at 37°C.5. Recovery of pH1 following an imposed intracellular acidification to pH < 6-5 could occur in the absence of external Na+, providing that HC03-was present in the perfusate. This slow, Nae-independent recovery of pHi from very low levels of intracellular pH was sensitive to DIDS. 6. The results indicate that acid extrusion in cultured fetal rat hippocampal neurones involves primarily two Nae-dependent mechanisms, one HC03-dependent and the other HC03-independent (possibly a Na+-H+ exchanger). Although both mechanisms participate in the maintenance of steady-state pH1 at room temperature, only the HCO3--independent mechanism does so at 37°C.

1. The effects of changes in extra-and intracellular pH (pHï and pHé, respectively) on depolarization-evoked rises in intracellular free Ca¥ concentration ([Ca¥]é) and the activity of a Ca¥-dependent K¤ channel were investigated in cultured fetal rat hippocampal neurones. 2. In neurones loaded with 2',7'-bis-(2-carboxyethyl)_5-(and _6)-carboxyfluorescein (BCECF), changes in pHï evoked changes in pHé. At room temperature, the ratio ÄpHé : ÄpHï (the slope of the regression line relating pHé to pHï) was 0·37 under HCOצÏCOµ-buffered conditions and 0·45 under Hepes-buffered conditions; corresponding values at 37°C were 0·71 and 0·79, respectively. The measurements of changes in pHé evoked by changes in pHï were employed in subsequent experiments to correct for the effects of changes in pHé on the Kd of fura_2 for Ca¥. When changes in pHé similar to those observed during the application of weak acids or bases were elicited by changing pHï, reductions in pH inhibited rises in [Ca¥]é evoked by 50 mÒ K¤ whereas increases in pH enhanced them. 5. The effects of changes in pH on the kinetic properties of a BK-type Ca¥-dependent K¤ channel were investigated. In inside-out patches excised from neurones in sister cultures to those used in the microspectrofluorimetric studies, with internal [Ca¥] at 20 ìÒ, channel openings at an internal pH of 6·7 were generally absent whereas at pH 7·3 (or 7·8) the open probability was high. In contrast, channel activity in outside-out patches was not affected by reducing the pH of the bath (external) solution from 7·3 to 6·7. In inside-out patches with internal [Ca¥] at 0·7 ìÒ, a separate protocol was applied to generate transient activation of the channel at a potential of 0 mV following a step from a holding level of −80 mV. In this case open probabilities were 0·81 (at pH 7·8), 0·57 (pH 7·3), 0·19 (pH 7·0) and 0·04 (pH 6·7). Channel conductance was not affected by changes in internal pH. 6. The results indicate that, in fetal rat hippocampal neurones, depolarization-evoked rises in[Ca¥]é mediated by the influx of Ca¥ ions through dihydropyridine-sensitive and -resistant voltage-activated Ca¥ channels are modulated by changes in pHï. The effects of pHï cannot be accounted for by changes in pHé consequent upon changes in pHï. However, changes in pHé affect the unitary properties of a Ca¥-dependent K¤ channel. The results support the notion that pHï andÏor pHé transients may serve a modulatory role in neuronal function.

Anastomotic complications after enteroenterostomy or primary repair for trauma are uncommon regardless of the technique, but surgeons must be especially cautious during or after damage control. Primary repairs are desirable, but when anastomosis is unavoidable, the method of repair should reflect that with which the surgeon is the most comfortable.

Patients aged 65 to 79 years and >80 years had inferior primary, primary assisted, and secondary patency and maturation compared with those <65 years. When stratified by configuration, radiocephalic accesses demonstrated lower patency and maturation compared with brachiocephalic accesses for patients aged 65 to 79 years and >80 years and were an independent predictor of secondary patency loss.

I The block by ifenprodil of voltage-activated Ca2+ channels was investigated on increases in intracellular free calcium concentration ([Ca2+]

In this preliminary study, the RUDI demonstrated similar patency, symptom resolution, and survival compared with the DRIL for patients with severe ARHI. All-cause mortality after any procedure for severe steal syndrome is high, and the particular intervention for management of steal must account for anatomic-, patient-, and disease-related considerations.

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