The neonatal resuscitation program consisted of three stages:pilot promotion, provinces promotion and grass-roots promotion in China. Neonatal resuscitation was easy to learn, training forms were various, the duration was different. There were regional differences in the pass rate of examination and standard recovery rate. The neonatal resuscitation training rate, the system execution rate and the equipment rate in primary hospitals was lower than secondary hospitals and tertiary hospitals. The primary hospitals would be the key link of the neonatal resuscitation program. We suggested to build neonatal resuscitation training and treatment system.

Objective: To evaluate the feasibility, technical characters and benefits of laparoscopic cholecystectomy (LC) in patients with cirrhotic portal hypertension(CPH). Methods:40 CPH patients, including 21 Child A class,26 Child B class and 3 Child C class were included. Data of the patients were collected and analyzed. Results: LC was successfully performed in 37 cases, and 3 patients were converted to open cholecystectomy (OC)for uncontrollled bleeding under laparoscopy and dense adhesion of Calot’s triangle. The convertion rate was 7.5%. The time of operation was (52.6? 15.2)min. The intraoperative blood loss was (75.5? 15.5)ml. The time to resume diet was (18.3?6.5)h. Seven postoperative complications occurred in 5 patients (13.2%). All patients discharged from hospital in (4.6?2.4) d after LC. Compared with LC in non cirrhotic patients, LC in patients with CPH has longer surgical time and hospital stay after operation, higher convertion rate and postoperative complication rate, more intraoperative blood loss. Conclusion: LC in patients with CPH has the advantages of minimal invasive surgery. It is feasible and relatively safe. But it has a higher convertion rate. Intraoperative blood loss is a prominent problem. The key step for a successful operation is to pay more attention to the perioperation managements and acquaint with the technical characters of this operation.

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the adult central nervous system (CNS), however, it causes excitation in the immature CNS neurons. The shift from GABA-induced depolarization to hyperpolarization in postnatal brain is primarily due to progressive decrease in the expression of the Na-K-2Cl symporter 1 (NKCC1) and increased expression of the K-Cl cotransporter 2 (KCC2). Unlike CNS neurons, both immature and mature neurons in the enteric nervous system (ENS) are depolarized by GABA. Molecular mechanisms by which GABA excites ENS neurons are unclear. It is understood, however, that the excitatory action depends on elevated intraneuronal Cl. We aimed to test a hypothesis that high intracellular Cl in ENS neurons is maintained by activity of the NKCCs. We found that NKCC2 immunoreactivity (IR) was expressed in the ENS of the rat colon on postnatal day 1 (P1). The expression level of NKCC2 continuously increased and reached a steady high level on P14 and maintained at that level in adulthood. NKCC1 IR appeared in ENS on P14 and maintained through adulthood. KCC2 IR was not detectable in the ENS in any of the developmental stages. Both NKCC1 IR and NKCC2 IR were co-expressed with GABA receptors in ENS neurons. Exogenous GABA (1 mmol/L) caused membrane depolarization in the ENS neurons. The reversal potential of GABA-induced depolarization was about -16 mV. Blockade of NKCC by bumetanide (50 μmol/L) or furosemide (300 μmol/L) suppressed the depolarizing responses to GABA. Bumetanide (50 μmol/L) shifted the reversal potential of GABA-induced depolarization in the hyperpolarizing direction. Neither the KCC blocker DIOA (20 μmol/L) nor the Cl/HCO exchanger inhibitor DIDS (200 μmol/L) suppressed GABA-evoked depolarization. The results suggest that ENS neurons continuously express NKCC2 since P1 and NKCC1 since P14, which contribute to the accumulation of Cl in ENS neurons and GABA-evoked depolarization in neonate and adult ENS neurons. These results provide the first direct evidence for the contribution of both NKCC2 and NKCC1 to the GABA-mediated depolarization.
Animals ; Bumetanide ; Neurons ; Rats ; Receptors, GABA-A ; Symporters ; gamma-Aminobutyric Acid