Effect of sepsis on the action potential and cardiac serotonin response in rats.

The current study aimed to investigate the effect of sepsis on rat serotonin (5-HT) responses and cardiac action potentials. A total of 20 rats were randomly divided into a sepsis and control group (each, n=10). Rat hearts were harvested and perfused using the Langendorff method 18-h after the induction of sepsis, which was assessed using cecal puncture. Cardiac action potential was subsequently measured using a multichannel electrophysiology instrument. Immunohistochemistry and quantitative analysis were performed to identify the effect of sepsis on myocardial 5-HT expression. The results revealed that mitochondrial changes were present in septic rat hearts. Heart rate (361.10±12.29 bpm vs. 348.60±12.38 bpm; P<0.05) was significantly higher, atrial action potential duration (106.40±2.95 ms vs. 86.60±4.12 ms; P<0.01) was significantly longer and the area (0.62±0.06 µm2 vs. 0.39±0.05 µm2; P<0.05) and number (0.92±0.02/field vs. 0.46±0.01/field; P<0.01) of myocardial cells were significantly higher in the septic compared with the control group. These results demonstrated that 5-HT prolongs the atrial action potential, increases heart rate and aggravates myocardial injury, indicating that it may therefore be one of the factors that leads to cardiac dysfunction in sepsis.

[Spectral Characteristics and Catalytic Performances of SO2-4/Ce-TiO2 with Visible Light Response].

Ce doped TiO2 was prepared via sol-gel method. The as-prepared Ce doped TiO2 was impregnated with diluted H2SO4 to obtain a H2SO4-treated Ce doped TiO2. In succession, the characterizations of X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), pyridine adsorption-FTIR (Py-FTIR), ultraviolet-visible spectroscopy (UV-vis) and X-ray photoelectron spectroscopy (XPS) were carried out to analyze the reasons for the improvement of the light response performance. The visible light photocatalytic degradation of Rhodamine B (RhB) in an aqueous solution was used as a probe reaction to evaluate the photocatalytic activity of the obtained samples. According to the XRD analysis, Ce doping created the lattice defects in TiO2 and minimized the particle size, which promoted the transfer of photo-generated electrons and then improved catalyst activity. The bridged bidentate coordination mode of SO2-4 was proposed based on the FTIR spectra. The pyridine FTIR spectra showed that both Lewis and Brnsted acid sites were formed on the sample surface. The characteristic absorption band as Lewis acid was more intense than that of the Brnsted acid, exhibiting the major Lewis acidity. The presence of the Lewis acid sites resulted in the transfer of photogenerated electrons to the Lewis acid center because of the electron deficiency of the Lewis acid sites, which contributed greatly to the transport of the photogenerated electrons, inhibiting the recombination of the photogenerated electron/hole pairs and leading to the enhancement of the photocatalytic activity of samples. From UV-Vis results, Ce-doping introduced an impurity energy level in the band gap, narrowing the TiO2 band gap. The impurity energy level could capture the photogenerated electrons on the conduct band and photogenerated holes on the valence band, reducing the recombination probability of photogenerated carriers and exciting the electrons captured on the impurity energy band by the photons with lower energy, thus expanding the light response range of TiO2. The XPS results indicated that the doped Ce existed as a mixture of Ce3+/Ce4+ states, which facilitated the efficient separation of the photo-generated electrons and holes because of the electron transfer, enhancing the system's quantum efficiency. The sulfated Ce doped TiO2 catalysts were very active for the visible photocatalytic degradation of RhB. Results showed that the synergetic effects of Ce doping and acid-treatment improved the visible light response for sulfated Ce-doped TiO2, enhancing the visible photocatalytic activity.

Investigation of the alterations in cellular electrophysiology underlying ventricular arrhythmia in dogs with the multiple organ dysfunction syndrome.

BACKGROUND: Multiple organ dysfunction syndrome (MODS)-specific cellular electrophysiological changes have so far not been reported and it seemed unlikely that they were related to arrhythmogenesis. METHODS AND RESULTS: Twelve dogs, weight 12 +/- 2 kg, were divided into a control group (n = 6) and an MODS group (n = 6). MODS lasting for 72 h was induced by the 'two-hit' method in 6 dogs. Ventricular myocytes were enzymatically isolated. Early afterdepolarizations (EADs), action potential duration (APD) and L-type calcium currents (ICa,L) were assessed. Sinus arrhythmias in all MODS dogs (100%; 6 of 6) and premature ventricular beats in 4 MODS dogs (66%; 4 of 6) were recorded, while no arrhythmias were found in the control animals. The prolongation of the APD was associated with a decreased ICa,L, and frequently provoked EADs were the typical electrophysiological alterations in the myocytes of MODS dogs. The action potential prolongation was shortened, the ICa,L blocked and EAD suppressed by using verapamil (100 micromol/l) in the myocytes of MODS dogs (66%; 4 of 6). CONCLUSION: The changes in cellular electrophysiology within 72 h in the heart of MODS dogs are APD prolongation, markedly decreased ICa,L as well as frequently provoked EAD, the most common types of arrhythmia being sinus arrhythmia and premature ventricular beats. This study suggests that verapamil appears to be an effective agent in reversing alterations in cellular electrophysiology at the early stage of MODS.

[Microelectrode arrays mapped tissue field action potential duration changes of thoracic spinal cord 1 - 5 nerves and heart in chronic stress rat model].

OBJECTIVE: To investigate chronic stress induced tissue action potential and pathological changes of thoracic spinal cord 1 - 5 nerves and heart in SD rats. METHODS: SD rats (weighing 180 - 250 g) were randomly divided into depressive group and control group (n = 10 each). Depressive model (unpredicted chronic mild stress) was established according to Gronli's protocol. The heart rhythm, tissue field action potential duration (FAPD) of thoracic spinal cord 1 - 5 nerves, atrium and ventricle were mapped by microelectrode arrays (MEA) technique. Heart was sectioned and stained with Massion and HE for pathological analysis. RESULTS: After 3 weeks chronic stress, P wave [(35.09 +/- 7.92) ms vs. (25.43 +/- 3.38) ms, P<0.05] and Q-T interval [(114.64 +/- 35.08) ms vs. (81.93 +/- 16.35) ms, P<0.01] were significantly increased, FAPD of thoracic spinal cord 1 - 5 nerves and heart was significantly prolonged, atrial field action potential duration dispersion (FAPDd) was significantly increased, atrial premature beats (n = 2) and ventricular premature beats ( n = 3) were also recorded in rats from depressive group. Moreover, increased collagen deposition was evidenced in Massion stained myocardium and increased inflammatory cell infiltration in the heart was found by both HE stain and electron microscope from depressive rats. CONCLUSION: Chronic mild stress could activate sympathetic nerves system, promote inflammatory cell myocardial infiltration and myocardial fibrosis, induce arrhythmias by prolonging FAPD and increasing FADPd in thoracic spinal cord 1 - 5 nerves and/or heart tissue.

ACh-evoked membrane hyperpolarization in smooth muscle cells of rat vas deferens in vitro: involvement of K(+) channels and NO.

To explore the underlying mechanism of acetylcholine (ACh)-evoked membrane hyperpolarizing response in isolated rat vas deferens smooth muscle cells (SMCs), intracellular microelectrode recording technique and intracellular microelectrophoresis fluorescent staining technique were used to study ACh-evoked membrane hyperpolarizing response in SMCs freshly isolated from Wistar rat vas deferens. By using microelectrodes containing fluorescent dye 0.1% propidium iodide (PI), 37 and 17 cells were identified as SMCs in outer longitudinal and inner circular muscular layers, respectively. The resting membrane potentials of SMCs were (-53.56+/-3.88) mV and (-51.62+/-4.27) mV, respectively. The membrane input resistances were (2245.60+/-372.50) MOmega and (2101.50+/-513.50) MOmega, respectively. ACh evoked membrane hyperpolarizing response in a concentration-dependent manner with an EC(50) of 36 micromol/L. This action of ACh was abolished by both a non-sepcific muscarinic (M) receptor antagonist atropine (1 mumol/L) and a selective M(3 ) receptor antagonist diphenylacetoxy-N-methylpiperidine-methiodide (DAMP, 100 nmol/L). ACh-evoked membrane hyperpolarization was also abolished by a nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME, 300 micromol/L) and suppressed by an ATP-sensitive potassium (K(ATP)) channel blocker glipizide (5 micromol/L) and an inward rectifier potassium (K(ir)) channel inhibitor bariumion (50 micromol/L). A combination of glipizide and bariumion abolished ACh-evoked membrane hyperpolarizing response. The results suggest that ACh-evoked membrane hyperpolarization in rat vas deferens SMCs is mediated by M(3) receptor followed with activation of K(ATP) channels, K(ir) channels, and NO release.

[Effects of chloride channel blockers on excitatory junction potentials in smooth muscle cells of cochlear spiral modiolar artery in guinea pigs].

Chloride channels have been identified in vascular smooth muscle cells (SMCs). It has been shown that these channels are involved in myogenic tone regulation and neuromuscular transmission in various vascular beds. However, whether the chloride channels are responsible for the formation of excitatory junction potentials (EJPs) of SMCs in the spiral modiolar artery (SMA) remains unelucidated. In the present study, the effects of chloride channel blockers (niflumic acid, NFA; indanyloxyacetic acid 94, IAA-94; disodium 4, 4'-diisothiocyanatostilbene-2, 2'-disulfonate, DIDS) on EJP were explored in guinea pigs, using intracellular recording techniques on acutely isolated SMA. It was found that EJP was evoked in the majority of the SMCs (75%, n=49) with an adequate electronic stimulation. The amplitude of the EJP was partially blocked (30% approximately 80%) by combined application of alpha(1) receptor antagonist (prazosin) and alpha(2) receptor antagonist (idazoxan) at concentration of up to 1 micromol/L, and P(2x) receptor antagonist (PPADS, 10 approximately 100 micromol/L). NFA (100 micromol/L) could further inhibit the residual EJP in the presence of alpha(1), alpha(2)-adrenergic and P(2x) receptor antagonists. IAA-94 or DIDS not only inhibited the amplitude but also shortened the duration of EJP. Decrease of extracellular chloride concentration from 135.6 mmol/L to 60 mmol/L would enhance EJP. Moreover, IAA-94 (100 micromol/L) and DIDS (200 mumol/L) could reverse the enhancement of EJP by low extracellular Cl(-). NFA (100 micromol/L) could also block the residual depolarizations evoked by norepinephrine (NE, 1 approximately 50 micromol/L). Based on these results, it is inferred that NE could activate a novel adrenoceptor to open the chloride channel on the membrane of the SMCs, leading to a transmembrane Cl(-) current. This current is involved, at least partially, in the formation of EJP.