Effect of ulinastatin on serum inflammatory factors in Asian patients with acute pancreatitis before and after treatment: a meta-analysis
.

OBJECTIVE: We applied a meta-analysis to explore the effect of ulinastatin (UTI) on the serum levels of C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α) in Asian patients with acute pancreatitis (AP). METHODS: Various databases were searched based on stringent inclusion and exclusion criteria to extract relevant cohort studies. Comprehensive Meta-analysis 2.0 (Biostat Inc., Englewood, NJ, USA) was applied for statistical analyses. RESULTS: A total of 113 relevant studies (67 in Chinese, 46 in English) were initially retrieved. Finally, 11 eligible studies were enrolled in our meta-analysis with 399 pancreatitis patients. Meta-analysis results showed that after being treated with UTI, the serum levels of CRP, IL-6, and TNF-α were evidently decreased (CRP: SMD = -2.697, 95% CI = -4.399 ~ -0.994, p = 0.002; IL-6: SMD = -5.268, 95% CI = -9.850 ~ -0.687, p = 0.024; TNF-α: SMD = -5.666, 95% CI = -11.083 ~ -0.249, p = 0.040). CONCLUSION: UTI can effectively reduce the serum levels of CRP, IL-6, and TNF-α in Asian patients with AP, suggesting that UTI has anti-inflammatory effect on Asian patients with AP.
.

[Electrophysiological effects of neurotransmitters on pacemaker cells in guinea pig left ventricular outflow tract].

This study was designed to explore the innervation of autonomic nervous system and the distribution of receptors on pacemaker cell membrane in guinea pig left ventricular outflow tract (aortic vestibule). By using conventional intracellular microelectrode technique to record action potentials, autonomic neurotransmitters and antagonists were used to investigate the electrophysiological features and regularities of spontaneous activity of left ventricular outflow tract cells. Electrophysiological parameters examined were: maximal diastolic potential (MDP), amplitude of action potential (APA), maximal rate of depolarization (V(max)), velocity of diastolic depolarization (VDD), rate of pacemaker firing (RPF), 50% and 90% of duration of action potential (APD(50) and APD(90)). The results are listed below: (1) Perfusion with 100 mumol/L isoprenaline (Iso) resulted in a significant increase in V(max) (P <0.05), VDD, RPF, and APA (P <0.01), a notable decrease in MDP (P<0.05), and also a marked shortening in APD(50) (P<0.01). Pretreatment with Iso (100 mumol/L), propranolol (5 mumol/L) significantly decreased RPF and VDD (P<0.01), decreased APA, MDP and V(max) (P<0.01) notably, prolonged APD(50) (P<0.01) and APD(90) (P<0.05) markedly. (2) Application of 100 mumol/L epinephrine (E) resulted in a significant increase in VDD (P<0.05), RPF (P<0.001), V(max) (P<0.05) and APA (P<0.001), and a notable shortening in APD(50) and APD(90) (P<0.05). (3) Perfusion with 100 mumol/L norepinephrine (NE) led to a significant increase in VDD, RPF, APA and V(max) (P<0.05), and a marked shortening in APD(50) (P<0.05). Pretreatment with NE (100 mumol/L), phentolamine (100 mumol/L) significantly decreased RPF and VDD, MDP and APA (P<0.01), decreased V(max) notably (P<0.05), prolonged APD(50) and APD(90) markedly (P<0.01). (4) During perfusion with 10 mmol/L acetylcholine (ACh), VDD and RPF slowed down notably (P<0.05), APA decreased significantly (P<0.001), V(max) slowed down notably (P<0.01), APD50 shortened markedly (P<0.05), Atropine (10 mmol/L) antagonized the effects of ACh (10 mumol/L) on APD(50) (P<0.05). These results suggest that there are probably alpha-adrenergic receptor (alpha-AR), beta-adrenergic receptor (beta-AR) and muscarinic receptor (MR) on pacemaker cell membrane of left ventricular outflow tract in guinea pig. The spontaneous activities of left ventricular outflow tract cells are likely regulated by sympathetic and parasympathetic nerves.

[Comparison of the electrophysiological features between the rhythmic cells of the aortic vestibule and the sinoatrial node in the rabbit].

The purpose of this study was to clarify the characteristics of the pacemaker cells in the left ventricular outflow tract (aortic vestibule) and compare them with those of the cells in the sinoatrial node (SAN). By using conventional intracellular microelectrode technique to record their action potentials, some ionic channel blockers were used to observe their electrophysiological effects on the two types of pacemaker cells in the rabbit, especially on the ionic movement during phase 0 and phase 4. The results obtained are as follows. (1) Perfusion with 1 micromol/L verapamil (VER) resulted in a significant reduction in the amplitude of action potential (APA), maximal rate of depolarization (V(max)), absolute value of the maximal diastolic potential (MDP), velocity of diastolic depolarization (VDD) and rate of pacemaker firing (RPF), and also a prolongation of the 90% of the duration of action potential (APD(90)) in the pacemaker cells of the SAN and aortic vestibule (P<0.05). (2) Perfusion with 180 micromol/L nickel chloride (NiCl2) resulted in a decrease in VDD in the two types of the pacemaker cells (P<0.01). APA, V(max) and RPF fell notably, and the APD(90) prolonged in the sinoatrial node cells (P<0.05). (3) 2 mmol/L 4-aminopyridine (4-AP) led to a increase in VDD in both types of pacemaker cells (P<0.01). At the same time the absolute values of MDP, APA and V(max) decreased significantly, and APD(90) prolonged notably (P<0.05). During the perfusion, RPF in SAN increased markedly, while RPF in aortic vestibule exhibited no significant change. (4) 2 mmol/L cesium chloride (CsCl) led to a decrease in VDD and RPF in the two types of the pacemaker cells (P<0.05).These results suggested: (1) the ion currents in phase 0 and phase 4 of depolarization and repolarization of slow-response activity in aortic vestibule are similar to those in dominant pacemaker cells of sinoatrial node; (2) for the pacemaker cells in the left ventricular outflow tract, Ca(2+) current is the main depolarizing ion current of the phase 0, K(+) current is the main factor responsible for the repolarization. Attenuation of K(+) current is responsible for the phase 4 spontaneous depolarization. In addition, it seems that I(Ca-T), I(Ca-L) and I(f ) play some role in the pacemaker currents.