ABSTRACT
Irreversible shock is one of the major target in shock research. The dysfunction of mitochondria involves in the pathogenesis of shock and MODS. Capillary no-reflow post-treatment leads to decrease of functional capillary density (FCD), which is a predictor of bad prognosis. Refractory hypotension after treatment results in low perfusion of vital organ, which is also one of the causes for death. Hypovisosaemia is a problem in shock treatment with massive fluid infusion leading to the decrease of FCD and survival rate. The mechanisms of the issues mentioned above are discussed in the text.
ABSTRACT
AIM: To investigate the role of nitric oxide (NO) in vascular hyporeactivity during prolonged hemorrhagic shock (HS). METHODS: Anesthetized Sprague-Dawley rats (180-220 g) were subjected to HS insult in which they were bled to a mean arterial pressure (MAP) of 40 mmHg (5.33 kPa) and arteriolar reactivity to norepinephrine in spinotrapezius was detected. The constant MAP of 40 mmHg was maintained until vascular hyporeactivity had occurred and then were resuscitated or sacrificed for further analysis. NO synthase (NOS) activity was measured ex vivo by the conversion of [3H]-arginine to [3H]-citrulline in homogenates from heart, lung, liver, spleen, duodunum, skeletal muscle. 24 h survival rates of resuscitated rats were observed with and without administration of aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor. Mesenteric arteriolar smooth muscle cells (ASMC) were isolated, and the effects of L-arginine (L-Arg) on membrane potential (MP) of ASMC were determined by fluorescent probe and confocal microscopy in the absence and presence of AG. RESULTS: When vascular hyporeactivity occurred, an increase of NOS activity was observed in liver and heart. Resuscitated rats with AG had a higher survival rate compared with that of control. The MP of ASMC was decreased (more negative) immediately following the addition of L-Arg, and the hyperpolarization effects of L-Arg were partially blocked in the presence of AG. CONCLUSION: These results suggest that excessive NO produced in HS is responsible for the occurrence of vascular hyporeactivity in prolonged hemorrhagic shock, and one of the mechanisms of which may be hyperpolarization of ASMC caused by NO.
ABSTRACT
An irreversible hemorrhagic shock model was produced on dog. The effect of external counterpulsation on systemic circulation and microcireulation was observed by using a model CN-1821 colour microscopic TV set (Hitachi Denshia Ltd.) and a YKMICAS multiple parameters computer analysis system of microcirculation image. It was shown that 10 min after external counterpulsation treatment the decreased central venous pressure and mean arterial pressure during hemorrhagic shock rose and 120 min after treatment the microcirculatory disorder of conjunctiva in shock state, including vessel diameter, blood velocity, and blood flow, nearly returned to normal. Half of the animals survived more than 3 days. These results indicated that the application of external counterpulsation could improve the circulatory disturbance markedly in hemorrhagic shock, which led to increased survival rate.
ABSTRACT
The rats of left ventrcular pressure change was significantly decreased in rabbits 1 hr after hemorrhage (P