[Determination of urinary NAG to detect renal ischemia-reperfusion injury and the protective effect of Allopurinol]. / Ischaemia-reperfusiós vesekárosodás és az Allopurinol védo hatásának kimutatása vizelet NAG követésével.

We analysed the effect of ischemia-reperfusion injury to renal parenchyma after unilateral renal artery clamping using urinary N-acetyl-beta-D-glucosaminidase (NAG) that is a sensitive parameter of early renal tubular injury. In the study 60 mongrel dogs were divided into 3 groups: in the 1st group the left renal artery was clamped for 45 minutes, in the 2nd group Allopurinol was administered before the clamping, the 3rd was the control group, where only laparotomy and closure of the abdomen was performed. Urinary NAG activity referring to urinary creatinine (NAG index) was determined before the operation, at the beginning of the reperfusion, in the 60th and 120th minute of the reperfusion then 1, 2, 3 and 5 days after the operation. The highest NAG indices relating to injury of the proximal tubuli were found at the beginning of the reperfusion, in the 60th and 120th minutes of the reperfusion, then NAG returned to preoperative level in each group. Significantly higher NAG indices were found in the ischemia-reperfusion group compared to the group with Allopurinol pretreatment. Renal ischemia-reperfusion injury and the protective effect of Allopurinol could be detected by lysosomal NAG enzyme. The injury of the tubular function was reversible so it could be a change in tubular function.

Characterization of rebound depolarization in hippocampal neurons.

Rebound depolarization (RD) following hyperpolarizing pulses is found in several neuronal cell types where it takes part in the regulation of neuronal firing behavior. During whole-cell current and voltage clamp recordings in slice preparations, we investigated the modulation of RD by different stimulation patterns and its underlying ionic currents in rat CA1 pyramidal cells. RD was mainly carried by the hyperpolarization-activated cation current I(h) (about two-third) and T-type calcium currents (about one-third), respectively. RD increased with increasing hyperpolarizing amplitude and stimulation frequency, whereas RD substantially decreased with longer pulse duration and, less pronounced, with increasing pulse number. The pulse duration-related decrease of RD was due to a decrease of the driving force of I(h). In conclusion, we showed that RD is differentially modulated by precedent hyperpolarization. Since RD amplitude was high enough to generate action potentials, RD may serve, even under physiologic conditions, as an inhibition-excitation converter.