AIM: To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in lipopolysaccharide (LPS)-induced endotoxic shock (ES) rats. METHODS: The changes of blood pressure wer...AIM: To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in lipopolysaccharide (LPS)-induced endotoxic shock (ES) rats. METHODS: The changes of blood pressure were observed using physiological record instrument in four groups of rats: LPS (8mg.kg(-1),iv) induced ES; CCK-8 (40 microg.kg(-1), iv) pretreatment 10 min before LPS (8mg.kg(-1)); CCK-8 (40 micro.kg(-1), iv) or normal saline (control) groups. Differences in tissue and circulating specificity of the proinflammatory cytokines (TNF-alpha, IL-1beta and IL-6) were assayed with ELISA kits. RESULTS: CCK-8 reversed LPS-induced decrease of mean artery blood pressure (MABP) in rats. Compared with control, LPS elevated the serum level of IL-6 significantly (3567 +/- 687 ng.L(-1) vs 128 +/- 22 ng.L(-1), P【0.01), while contents of TNF-alpha and IL-1beta elevated significantly (277 +/- 86 ng.L(-1) vs not detectable and 43 +/- 9 ng.L(-1) vsnot detectable, P【0.01) but less extent than IL-6. CCK-8 significantly inhibited the LPS-induced increase in serum TNF-alpha IL-1beta and IL-6. LPS elevated spleen and lung content of IL-1beta significantly (5184 +/- 85 ng.L(-1) vs 1047 +/- 21 ng.L(-1) and 4050 +/- 614 ng.L(-1) vs not detectable, P【0.01), while levels of TNF-alpha and IL-6 also rose significantly but in less extent than IL-1beta. CCK-8 inhibited the LPS-induced increase of the cytokines in spleen and lung. In the heart, CCK-8 significantly inhibited LPS-induced increase of TNF-alpha (864 +/- 123 ng.L(-1) in CCK-8+LPS group vs 1599 +/- 227 ng.L(-1) in LPS group, P 【 0.01), and IL-1beta (282 +/- 93 ng.L(-1) in CCK-8+LPS group vs 621 +/- 145ng.L(-1) in LPS group, P 【 0.01). CONCLUSION: CCK-8 reverses ES, which may be related to its inhibitory effect on the overproduction of cytokines.展开更多
Background Central venous pressure （CVP） and intrathoracic blood volume index （ITBVI） were used to assess the fluid status. It has previously been shown that CVP is not as accurate as ITBVI for all the shock patie...Background Central venous pressure （CVP） and intrathoracic blood volume index （ITBVI） were used to assess the fluid status. It has previously been shown that CVP is not as accurate as ITBVI for all the shock patients. We therefore hypothesized that the change of CVP has the ability to predict fluid responsiveness in some clinical cases of shock. Methods From September 1st 2009 to September 1st 2011, sixty-three patients with shock from different Intensive Care Unit （ICU） were collected into this retrospective study. All the patients received fluid challenge strategy （infusing 300 ml hydroxyethyl starch in 20 minutes）, were monitored with CVP and pulse-indicated continuous cardiac output （PICCO）. The correlation between changes in cardiac index （ACI）, CVP （ACVP） and ITBVI （AITBVI） were analyzed. Fluid responsiveness was defined as an increase in CI 〉10%. Receiver operating characteristic （ROC） curves were generated for ACVP and AITBVI. Results For all the patients, there was no correlation between ACI and ACVP （P=0.073）, but in the subgroup analysis, the correlation between ACI and ACVP was significant in those younger than 60 years old （P=0.018） and those with hypovolemic shock （P=0.001）. The difference of areas under the ROC curves of ACVP and AITBVI were not statistically significant in the group younger than 60 years old or hypovolemic shock group （P 〉0.05, respectively）. However, no similar results can be found in the group older than 60 years old and the other two shock type groups from ROC curves of ACVP and AITBVI. Conclusions ACVP is not suitable for evaluating the volume status of the shock patients with fluid resuscitation regardless of their condition. However, in some ways, ACVP have the ability to predict fluid responsiveness in the younger shock patients or in the hypovolemic shock patients.展开更多
文摘AIM: To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in lipopolysaccharide (LPS)-induced endotoxic shock (ES) rats. METHODS: The changes of blood pressure were observed using physiological record instrument in four groups of rats: LPS (8mg.kg(-1),iv) induced ES; CCK-8 (40 microg.kg(-1), iv) pretreatment 10 min before LPS (8mg.kg(-1)); CCK-8 (40 micro.kg(-1), iv) or normal saline (control) groups. Differences in tissue and circulating specificity of the proinflammatory cytokines (TNF-alpha, IL-1beta and IL-6) were assayed with ELISA kits. RESULTS: CCK-8 reversed LPS-induced decrease of mean artery blood pressure (MABP) in rats. Compared with control, LPS elevated the serum level of IL-6 significantly (3567 +/- 687 ng.L(-1) vs 128 +/- 22 ng.L(-1), P【0.01), while contents of TNF-alpha and IL-1beta elevated significantly (277 +/- 86 ng.L(-1) vs not detectable and 43 +/- 9 ng.L(-1) vsnot detectable, P【0.01) but less extent than IL-6. CCK-8 significantly inhibited the LPS-induced increase in serum TNF-alpha IL-1beta and IL-6. LPS elevated spleen and lung content of IL-1beta significantly (5184 +/- 85 ng.L(-1) vs 1047 +/- 21 ng.L(-1) and 4050 +/- 614 ng.L(-1) vs not detectable, P【0.01), while levels of TNF-alpha and IL-6 also rose significantly but in less extent than IL-1beta. CCK-8 inhibited the LPS-induced increase of the cytokines in spleen and lung. In the heart, CCK-8 significantly inhibited LPS-induced increase of TNF-alpha (864 +/- 123 ng.L(-1) in CCK-8+LPS group vs 1599 +/- 227 ng.L(-1) in LPS group, P 【 0.01), and IL-1beta (282 +/- 93 ng.L(-1) in CCK-8+LPS group vs 621 +/- 145ng.L(-1) in LPS group, P 【 0.01). CONCLUSION: CCK-8 reverses ES, which may be related to its inhibitory effect on the overproduction of cytokines.
文摘Background Central venous pressure （CVP） and intrathoracic blood volume index （ITBVI） were used to assess the fluid status. It has previously been shown that CVP is not as accurate as ITBVI for all the shock patients. We therefore hypothesized that the change of CVP has the ability to predict fluid responsiveness in some clinical cases of shock. Methods From September 1st 2009 to September 1st 2011, sixty-three patients with shock from different Intensive Care Unit （ICU） were collected into this retrospective study. All the patients received fluid challenge strategy （infusing 300 ml hydroxyethyl starch in 20 minutes）, were monitored with CVP and pulse-indicated continuous cardiac output （PICCO）. The correlation between changes in cardiac index （ACI）, CVP （ACVP） and ITBVI （AITBVI） were analyzed. Fluid responsiveness was defined as an increase in CI 〉10%. Receiver operating characteristic （ROC） curves were generated for ACVP and AITBVI. Results For all the patients, there was no correlation between ACI and ACVP （P=0.073）, but in the subgroup analysis, the correlation between ACI and ACVP was significant in those younger than 60 years old （P=0.018） and those with hypovolemic shock （P=0.001）. The difference of areas under the ROC curves of ACVP and AITBVI were not statistically significant in the group younger than 60 years old or hypovolemic shock group （P 〉0.05, respectively）. However, no similar results can be found in the group older than 60 years old and the other two shock type groups from ROC curves of ACVP and AITBVI. Conclusions ACVP is not suitable for evaluating the volume status of the shock patients with fluid resuscitation regardless of their condition. However, in some ways, ACVP have the ability to predict fluid responsiveness in the younger shock patients or in the hypovolemic shock patients.
