Stimulation of the adenosine A3 receptor reverses vascular hyporeactivity after hemorrhagic shock in rats.

Aim: To investigate whether adenosine A(3) receptors (A(3)AR) stimulation restore vascular reactivity after hemorrhagic shock through a ryanodine receptor (RyR)-mediated and large conductance calcium-activated potassium (BK(Ca)) channel-dependent pathway.

Methods: Rat hemorrhagic shock model (40 mmHg) and vascular smooth muscle cell (VSMC) hypoxic model were used. The expression of A(3)AR was determined by Western blot and RT-PCR.

[The role of interferon-gamma in prevention of hydrogen peroxide-induced oxidative injury to vascular endothelium].

Objective: To observe the protective effects of interferon-gamma (IFN-gamma) on hydrogen peroxide (H(2)O(2))-induced oxidative injury to vascular endothelial cell (VEC), and to explore the role of 26S proteasome protection against IFN-gamma-induced endothelial oxidative injury.

Methods: A H(2)O(2)-induced VEC oxidative injury to cell and isolated organ models were reproduced in the current study. The VEC oxidative damage in cellular level was evaluated by the contents of lactate dehydrogenase (LDH) and malondialdehyde (MDA) in culture medium, and the degree of oxidative injury of VEC in isolated organ level was evaluated by acetylcholine (Ach)-induced endothelium- dependent vascular relaxation.

HSD is a better resuscitation fluid for hemorrhagic shock with pulmonary edema at high altitude.

To investigate the fluid tolerance of hemorrhagic shock with pulmonary edema (HSPE) at high altitude in unacclimated rats and the beneficial effect of 7.5% hypertonic saline/6% dextran (HSD). One hundred seventy-six Sprague-Dawley rats, transported to LaSa, Tibet, 3,760 m above the sea level, were anesthetized with sodium pentobarbital (30 mg/kg, i.

Subclass opioid receptors associated with the cardiovascular depression after traumatic shock and the antishock effects of its specific receptor antagonists.

The present available opioid receptor antagonists such as naloxone and naltrexone are not highly receptor selective. They may antagonize mu opioid receptors to affect the pain threshold of the patients with traumatic shock while they exert antishock effects. Therefore, they are not suitable for traumatic shock.

Effect of nitric oxide-induced tyrosine phosphorylation of calcium-activated potassium channel alpha subunit on vascular hyporesponsiveness in rats.

Objective: To study the effect of nitric oxide-induced tyrosine phosphorylation of large-conductance calcium-activated potassium (BK(Ca)) channel alpha subunit on vascular hyporesponsiveness in rats.

Methods: A total of 46 Wistar rats of either sex, weighing 250 g +/- 20 g, were used in this study. Models of vascular hyporesponsiveness induced by hemorrhagic shock (30 mm Hg for 2 hours) in vivo and by L-arginine in vitro were established respectively.

Opioid receptor antagonists increase [Ca2+]i in rat arterial smooth muscle cells in hemorrhagic shock.

Aim: To examine the effects of opioid receptor antagonists and norepinephrine on intracellular free Ca2+ concentration ([Ca2+]i) in mesenteric arterial (MA) smooth muscle cells (SMC) isolated from normal and hemorrhagic shocked rats in the vascular hyporesponse stage.

Methods: The rat model of hemorrhagic shock was made by withdrawing blood to decrease the artery mean blood pressure to 3.73-4.

The effect of different volumes of fluid resuscitation on traumatic-hemorrhagic shock at high altitude in the unacclimated rat.

The effects of different volumes of fluid resuscitation on traumatic hemorrhagic shock in unacclimated rats to high altitude were investigated. Seventy-eight Wistar rats were transported to LaSa, Tibet, 3760 meters above sea level, and traumatic hemorrhagic shock was induced by right-femur fracture plus bleeding to 45 mmHg of mean arterial pressure (MAP) for 1 h under the anesthesia of sodium pentobarbital (40 mg/kg, i.p.

[Effect of different volumes of fluid resuscitation on hemorrhagic shock with pulmonary edema at high altitude in the unacclimated rat].

Objective: To study the effects of different volumes of fluid resuscitation on hemorrhagic shock with pulmonary edema at high altitude in the unacclimated rat.

Methods: One hundred and twenty-six SD rats transported to Lasa, Tibet, 3 760 meters above the sea level, were anesthetized one week later with sodium pentobarbital (30 mg/kg, intraperitoneal). Hemorrhagic shock with pulmonary edema model was induced by hemorrhage (50 mm Hg for 1 hour, 1 mmHg=0.

[Beneficial effect of thyrotropin-releasing hormone in combination with HSD on hemorrhagic shock with pulmonary edema at high altitude in the rat].

Objective: To study the effects of thyrotropin-releasing hormone (TRH) in combination with hypertonic saline/dextran (7.5% NaCl + 6% Dextran 40, HSD ) on hemorrhagic shock with pulmonary edema in the rats which were recently brought to high altitude.

Methods: Forty-nine SD rats, transported to Lasa, Tibet, which was 3,760 meters above the sea level, were anesthetized one week later with sodium pentobarbital (30 mg/kg, intraperitoneal).

Opioid receptor antagonists modulate Ca2+-activated K+ channels in mesenteric arterial smooth muscle cells of rats in hemorrhagic shock.

Previous study has indicated a significant enhancement of activity of large-conductance Ca2+-activated K+ channel (BKCa) in mesenteric arterial vascular smooth muscle cells isolated from rats in vascular hyporesponsive stage of hemorrhagic shock. In the present study, the effect of opioid receptor antagonism on BKCa activity in the vascular smooth muscle cells of rats in the hyporesponse stage of hemorrhagic shock was investigated by using inside-out configuration of the patch-clamp technique. The results showed that naloxone (10 microM) down-regulated the activity of BKCa by reducing open probability (Po) and open frequency of the channels.

Protective effects of apocynin on "two-hit" injury induced by hemorrhagic shock and lipopolysaccharide.

Aim: To evaluate the protective effects of apocynin on "two-hit" injury in rats.

Methods: "Two-hit" injury model of rat was induced by hemorrhagic shock (40 mmHg for 45 min) followed by iv administration of lipopolysaccharide (LPS, 150 microg/kg). Rats were randomized into seven groups: Sham, LPS, hemorrhage, hemorrhage/LPS, and hemorrhage/LPS+apocynin (2.

Modulation of Ca2+ channels by opioid receptor antagonists in mesenteric arterial smooth muscle cells of rats in hemorrhagic shock.

The effects of hemorrhagic shock on Ba currents ( ) via Ca channels and the regulation of the channels in the vascular hyporesponse stage of hemorrhagic shock by opioid receptor antagonists were examined by using the whole-cell recording of patch-clamp technique in mesenteric arterial smooth muscle cells of rats. The results showed that hemorrhagic shock induced an inhibition of Ca channels in the cells; 10 micro M of naloxone and 100 n of naltrindole, nor-binaltorphimine, and beta-funaltrexamine increased the in the cells of rats in shock. After inhibition of protein kinase C by using 1-(5-isoquindinesulfonyl)-2-methylpiperazine via electrodes, the enhancement of by the antagonists was not observed.