Chronic Disease ; Humans ; Rhinitis

Animals ; Blood Pressure ; Heat-Shock Proteins ; metabolism ; Heat-Shock Response ; Hypotension ; metabolism ; Male ; Myocardium ; metabolism ; Nitric Oxide ; metabolism ; Rats ; Rats, Sprague-Dawley

Endoscopy ; methods ; Frontal Sinus ; surgery ; Humans

Humans ; Sinusitis ; classification ; Terminology as Topic

Objective To study the effects of nitric oxide on Ca2+-activated K+ (KCa) channels in the hypothalamus neurons of newborn SD rats. Methods The data were recorded using inside-out or cell-attached configuration of patch-clamp technique and the kinetic changes of KCa channels are compared before and after 100 μmol/L sodium nitroprusside (SNP) was added into the bathing solution. Results When 100 μmol/L SNP was added to the bathing solution in cell-attached configuration, the open probability of the KCa channels increased from (7.3±1.5)% to (40.2±6.5)%, open time from (7.12±1.41) ms to (15.34±3.45) ms, frequency from (11.3±3.5) Hz to (26.6±4.2) Hz. Conclusion NO-cGMP signal pathway could greatly increase the open probability of the channels as a result of both the prolongation of open period and increase of open frequency, but the pathological or physiological roles it may play require further study.

Objective To study the effects of nitric oxide on Ca2+-activated K+ (KCa) channels in the hypothalamus neurons of newborn SD rats. Methods The data were recorded using inside-out or cell-attached configuration of patch-clamp technique and the kinetic changes of KCa channels are compared before and after 100 μmol/L sodium nitroprusside (SNP) was added into the bathing solution. Results When 100 μmol/L SNP was added to the bathing solution in cell-attached configuration, the open probability of the KCa channels increased from (7.3±1.5)% to (40.2±6.5)%, open time from (7.12±1.41) ms to (15.34±3.45) ms, frequency from (11.3±3.5) Hz to (26.6±4.2) Hz. Conclusion NO-cGMP signal pathway could greatly increase the open probability of the channels as a result of both the prolongation of open period and increase of open frequency, but the pathological or physiological roles it may play require further study.

OBJECTIVETo evaluate the change of blood pressure, ECG and nitric oxide (NO) in rat heat stroke and effects of aminoguanidine (AG) against heatstroke.

METHODSThe male SD rats were randomly assigned into 1 of the following 2 groups: control group or AG group. The rats of control group (n = 10) and AG group (n = 10) were exposed to high ambient temperature (41 degrees C, relative humidity 65%) to induce heatstroke, arterial blood pressures, colonic temperature (T(co)), electrocardiograph (ECG) were monitored. The other rats of both groups (both n = 10) were exposed to high ambient temperature (41 degrees C, relative humidity 65%), and the blood samples were taken at 0, 60 min after the start of heat exposure for determination of the plasma NO concentrations.

RESULTS(1) From 0 min to 50 min after heat exposure, MAPs of two groups were not significantly different, but at about 55 approximately 60 min after the start of heat exposure, MAPs of control group were decreased significantly differently from that of AG group, K value and dicrotic pulse relative height (h(D)/H) were gradually decreased, especially at 40 min after the start of heat exposure, K value of control group decreased significantly comparison with that of AG group; (2) Heart rate (HR) and QT interval of both groups were increased, while PR interval were decreased after the start of heat exposure; (3) T(co) of both groups were increased after the start of heat exposure until T(co) increased to 42 degrees C (the onset of heatstroke), but there was not significantly difference between the two groups; (4) The time of the onset of heatstroke (TOHS) and survival time (ST) of AG group were significantly longer than those of control group; (5) The plasma NO concentrations of the two groups were significantly higher at 60 min than at 0 min after the start of heat exposure, and the plasma NO concentrations of control group were significantly higher than that of AG group at 60 min after the start of heat exposure.

CONCLUSIONiNOS may contribute to heatstroke, and aminoguanidine can provide protective effects on heatstroke as a selective iNOS inhibitor.

Animals ; Blood Pressure ; drug effects ; Electrocardiography ; drug effects ; Guanidines ; pharmacology ; Heat Stroke ; drug therapy ; physiopathology ; Male ; Nitric Oxide ; blood ; Nitric Oxide Synthase ; antagonists & inhibitors ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Objective To evaluate the safety and efficiency of domestic snare applied during retrograde percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) lesions.Methods A total of 27 patients who underwent retrograde PCI for CTO and used domestic snare during the procedure were enrolled in our study from March 2012 to November 2016.Clinical data, angiographic characteristics and PCI details were collected.Clinical data, characteristics of CTO lesion, effect of the domestic snare and snaring time were retrospectively analyzed.Special complications related to the domestic snare and major adverse cardiovascular events (MACE) were also documented.Results Domestic snare was used in all the procedures, which included facillitating the micro-catheter to pass through the CTO lesions in 6 patients and assisting the RG3/rotational guide-wire externalization in all the 27 patients.Mean snaring time was 3.5±5.4 minutes.Stents were successfully implanted in 26 patients except in 1 patient who failed to receive stent implantation for severe coronary calcification.No complications including coronary dissection, fracture of guide-wire and unreleased snare happened during the procedures and no MACE occurred during hospitalization.Conclusions Domestic snare facilitates retrograde micro-catheter crossing CTO lesions and retrograde guide-wire entering the guiding catheter and externalization.It is a simple, safe and efficient method.

OBJECTIVETo observe the change in vital signs and arterial blood gas in Lipopolysaccharide (LPS)-injected heat exposed rats.

METHODSMale pathogen-free Wistar rats were randomly assigned to the following groups: saline-injected normothermic control (C-Group), saline-injected heat exposed (H-Group), LPS-injected normothermic control (L-Group), LPS-injected heat exposed (HL-Group). Rectal temperature (Tr), heart rate (HR), mean arterial pressure (MAP), arterial blood gas were continually monitored.

RESULTS(1) The rats in HL-Group displayed significantly high values of Tr (43.04 degrees C +/- 0.11 degrees C) and HR [(660 +/- 42) beats/min] and low values of MAP [(49.0 +/- 3.5) mm Hg] compared with C-Group. There was a significant difference in the values of Tr, HR, and MAP between HL-Group and L-Group and in the values of HR and MAP between HL-Group and H-Group. (2) The values of PaO(2), HCO(3)(-), PaCO(2) were significantly lower than those in C-Group at 40 min after LPS-injected heat stress. At 120 min, the PaO(2) [(11.59 +/- 1.11) kPa], HCO(3)(-) [(10.42 +/- 1.06) mmol/L], PaCO(2) [(2.82 +/- 0.81) kPa] in HL-Group were significantly lower than those in L-Group. A significant difference in the values of HCO(3)(-) and PaCO(2) between HL-Group and H-Group was also observed.

CONCLUSIONLPS-injected heat stress primes the rat to advance and augment the change in vital signs, arterial blood gas, and systemic inflammatory response syndrome.

Animals ; Blood Gas Analysis ; Blood Pressure ; physiology ; Body Temperature ; physiology ; Heart Rate ; physiology ; Heat Stress Disorders ; blood ; physiopathology ; Lipopolysaccharides ; toxicity ; Male ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo study the mechanism of Ca(2+) on the apoptosis induced by hyperthermia in neonate rat hippocampal neurons to provide the applicative evidence of dantrolene for preventing brain injuries.

METHODSDantrolene, Ca(2+) specific blocking agent, was used in the hyperthermia-induced apoptosis of primary hippocampal neurons in vitro to observe its effect on the apoptosis, fluorescent intensity, and dynamic change of Ca(2+) by flowcytometry and laser confocal microscopy.

RESULTSThe rate of apoptosis was decreased significantly after hyperthermia treatment by dantrolene sodium. The intracellular Ca(2+) fluorescent intensity in 42 degrees C treatment group (107.35 +/- 6.0) was significantly lower than that in control group (159.12 +/- 33.8). The concentration of Ca(2+) began to decrease 20 approximately 25 s after adding dantrolene sodium, and reached the lowest level about 50 s later, and then kept lower than the basal level.

CONCLUSIONDantrolene sodium has an important protective effect on hippocampal neurons apoptosis induced by hyperthermia and may have some applicative value of preventing heat-induced brain injury.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Calcium ; metabolism ; Calcium Channel Blockers ; pharmacology ; Cells, Cultured ; Dantrolene ; pharmacology ; Female ; Hippocampus ; cytology ; drug effects ; Male ; Neurons ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley ; Temperature