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

Humans ; Sinusitis ; classification ; Terminology as Topic

Endoscopy ; methods ; Frontal Sinus ; surgery ; Humans

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 investigate the protective effects and mechanism of heat shock response (HSR) on circulatory collapse induced by hyperthermia.

METHODSTwo experiments were carried out: (1) Protective effects of HSR. Rats were divided into 2 groups: heat shock (HS) group, sham control (SC) group. After HS group was pretreated with heat shock and recovered for 20 h at room temperature, both groups were exposed to heat till death, and blood pressure, electrocardiogram were measured continuously during exposure. Mean arterial pressure (MAP), survival time etc were acquired through Chart software. (2) Mechanism of effects. Rats were divided into 3 groups: HS group, SC group and normal control (NC) group. The treatment in HS and SC groups was identical with that in the first experiment, but it would be terminated at 73 min after heat exposure. Systolic pressure (Ps), diastolic pressure (Pd) etc were recorded and content of NO and HSP70 in myocardium were measured.

RESULTS(1) The survival time in HS group [(102.3 +/- 11.4) min] was longer than that in SC group [(87.9 +/- 7.7) min] and shock revealed later (P < 0.01); (2) During early heat exposure MAP in HS group was not different from that in SC group, but after 60 min MAP in HS group were higher than that in SC group; (3) MAP, Ps, Pd, HR and HSP70 in HS group were significantly higher but content of NO was lower than those in SC group (P < 0.01, P < 0.05).

CONCLUSIONHSR may induce upregulation of HSP70 and inhibit excessive production of NO in myocardium, thus result in relief of circulatory collapse induced by hyperthermia.

Animals ; Heat-Shock Proteins ; analysis ; Heat-Shock Response ; physiology ; Hot Temperature ; Male ; Nitric Oxide ; analysis ; Rats ; Rats, Sprague-Dawley ; Shock ; metabolism ; physiopathology ; Time Factors

OBJECTIVETo study the early change of serum nitric oxide (NO) after acute heat exposure with trauma and the effect of NO on mean arterial pressure (MAP), thus to provide theoretical basis for studying the mechanism of NO effect in acute stress.

METHODSThe rabbit model of acute heat exposure combined with trauma was established. The animals were divided into four groups, including control, trauma, hyperthermia and hyperthermia combined with trauma. The levels of NO were measured at different time points: 0 h, 1 h, 2 h and MAP was monitored throughout the whole experiment.

RESULTSThe concentration of NO declined at first and then increased at 1 h or so after acute heat exposure and trauma. The levels of NO in hyperthermia with trauma group at 1 h, 2 h were (42.75 +/- 8.24), (59.54 +/- 9.05) micro mol/L respectively (P < 0.05), while those in control group were (56.63 +/- 3.79) and (55.22 +/- 7.15) micro mol/L, the difference at 1h between two groups was significant (P < 0.05). Under the circumstance of hyperthermia and trauma, the level of MAP declined to the lowest point at 60 - 70 min and then showed a transient rise, after that, the level declined rapidly.

CONCLUSIONSAt the early stage of acute heat exposure and trauma, the concentration of serum NO declined at first and then increased, and had certain relationship with the change of MAP.

Animals ; Blood Pressure ; Cytokines ; biosynthesis ; Hot Temperature ; Male ; Nitric Oxide ; blood ; Rabbits ; Wounds and Injuries ; blood ; physiopathology

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

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