Yulong Cui, Mengqi Shen, Jia Qi, Junmei Xu, Lijun Cao
{"title":"降低肺血管阻力改善猪lps诱导休克模型的血流动力学和液体反应性。","authors":"Yulong Cui, Mengqi Shen, Jia Qi, Junmei Xu, Lijun Cao","doi":"10.1097/SHK.0000000000002629","DOIUrl":null,"url":null,"abstract":"<p><strong>Abstract: </strong>Background: Septic pulmonary hypertension disrupts the homeostasis between the left- and right-sided heart and is associated with poor prognosis. This study assessed whether lowering the pulmonary vascular resistance (PVR) by administering the prostacyclin analog treprostinil would improve hemodynamics, short - term survival, and fluid resuscitation in endotoxic shock. Methods: A preclinical randomized controlled study was conducted. Bama miniature pigs (n = 24; 12 male and 12 female) with LPS-induced endotoxic shock were randomized into four groups in two parts (n = 6 per group): part 1 (control group and treprostinil treatment group) and part 2 (fluid resuscitation group and treprostinil treatment + fluid resuscitation group). The primary outcome measures were cardiac performance and short - term survival, and the secondary outcome measures were mean urine volume, fluid balance volume, and norepinephrine consumption. Results: Compared with the control group, the treprostinil treatment group showed significantly reduced PVR, increased cardiac output, right ventricular stroke volume, right ventricular ejection fraction (RVEF), short-term survival, and mean urine volume. Compared with the fluid resuscitation group, the treprostinil treatment + fluid resuscitation group exhibited notably reduced PVR, increased cardiac output, right ventricular stroke volume, right ventricular ejection fraction, and decreased fluid balance volume, with no statistically significant difference in norepinephrine consumption. Conclusion: The high-resistance pulmonary circulation in endotoxic shock acted as an \"obstruction\" impeding the blood flow from the right to the left side of the heart. Weakening this \"obstruction\" improved cardiac performance and fluid responsiveness in an experimental endotoxic shock model, suggesting that targeting PVR could be a potential adjunctive strategy for managing shock in critically ill patients.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"363-369"},"PeriodicalIF":2.9000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LOWERING PULMONARY VASCULAR RESISTANCE IMPROVES HEMODYNAMICS AND FLUID RESPONSIVENESS IN A PORCINE MODEL OF LPS-INDUCED SHOCK.\",\"authors\":\"Yulong Cui, Mengqi Shen, Jia Qi, Junmei Xu, Lijun Cao\",\"doi\":\"10.1097/SHK.0000000000002629\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Abstract: </strong>Background: Septic pulmonary hypertension disrupts the homeostasis between the left- and right-sided heart and is associated with poor prognosis. This study assessed whether lowering the pulmonary vascular resistance (PVR) by administering the prostacyclin analog treprostinil would improve hemodynamics, short - term survival, and fluid resuscitation in endotoxic shock. Methods: A preclinical randomized controlled study was conducted. Bama miniature pigs (n = 24; 12 male and 12 female) with LPS-induced endotoxic shock were randomized into four groups in two parts (n = 6 per group): part 1 (control group and treprostinil treatment group) and part 2 (fluid resuscitation group and treprostinil treatment + fluid resuscitation group). The primary outcome measures were cardiac performance and short - term survival, and the secondary outcome measures were mean urine volume, fluid balance volume, and norepinephrine consumption. Results: Compared with the control group, the treprostinil treatment group showed significantly reduced PVR, increased cardiac output, right ventricular stroke volume, right ventricular ejection fraction (RVEF), short-term survival, and mean urine volume. Compared with the fluid resuscitation group, the treprostinil treatment + fluid resuscitation group exhibited notably reduced PVR, increased cardiac output, right ventricular stroke volume, right ventricular ejection fraction, and decreased fluid balance volume, with no statistically significant difference in norepinephrine consumption. Conclusion: The high-resistance pulmonary circulation in endotoxic shock acted as an \\\"obstruction\\\" impeding the blood flow from the right to the left side of the heart. Weakening this \\\"obstruction\\\" improved cardiac performance and fluid responsiveness in an experimental endotoxic shock model, suggesting that targeting PVR could be a potential adjunctive strategy for managing shock in critically ill patients.</p>\",\"PeriodicalId\":21667,\"journal\":{\"name\":\"SHOCK\",\"volume\":\" \",\"pages\":\"363-369\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"SHOCK\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1097/SHK.0000000000002629\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/5/12 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"CRITICAL CARE MEDICINE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"SHOCK","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/SHK.0000000000002629","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/5/12 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"CRITICAL CARE MEDICINE","Score":null,"Total":0}
LOWERING PULMONARY VASCULAR RESISTANCE IMPROVES HEMODYNAMICS AND FLUID RESPONSIVENESS IN A PORCINE MODEL OF LPS-INDUCED SHOCK.
Abstract: Background: Septic pulmonary hypertension disrupts the homeostasis between the left- and right-sided heart and is associated with poor prognosis. This study assessed whether lowering the pulmonary vascular resistance (PVR) by administering the prostacyclin analog treprostinil would improve hemodynamics, short - term survival, and fluid resuscitation in endotoxic shock. Methods: A preclinical randomized controlled study was conducted. Bama miniature pigs (n = 24; 12 male and 12 female) with LPS-induced endotoxic shock were randomized into four groups in two parts (n = 6 per group): part 1 (control group and treprostinil treatment group) and part 2 (fluid resuscitation group and treprostinil treatment + fluid resuscitation group). The primary outcome measures were cardiac performance and short - term survival, and the secondary outcome measures were mean urine volume, fluid balance volume, and norepinephrine consumption. Results: Compared with the control group, the treprostinil treatment group showed significantly reduced PVR, increased cardiac output, right ventricular stroke volume, right ventricular ejection fraction (RVEF), short-term survival, and mean urine volume. Compared with the fluid resuscitation group, the treprostinil treatment + fluid resuscitation group exhibited notably reduced PVR, increased cardiac output, right ventricular stroke volume, right ventricular ejection fraction, and decreased fluid balance volume, with no statistically significant difference in norepinephrine consumption. Conclusion: The high-resistance pulmonary circulation in endotoxic shock acted as an "obstruction" impeding the blood flow from the right to the left side of the heart. Weakening this "obstruction" improved cardiac performance and fluid responsiveness in an experimental endotoxic shock model, suggesting that targeting PVR could be a potential adjunctive strategy for managing shock in critically ill patients.
期刊介绍：
SHOCK®: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches includes studies of novel therapeutic approaches, such as immunomodulation, gene therapy, nutrition, and others. The mission of the Journal is to foster and promote multidisciplinary studies, both experimental and clinical in nature, that critically examine the etiology, mechanisms and novel therapeutics of shock-related pathophysiological conditions. Its purpose is to excel as a vehicle for timely publication in the areas of basic and clinical studies of shock, trauma, sepsis, inflammation, ischemia, and related pathobiological states, with particular emphasis on the biologic mechanisms that determine the response to such injury. Making such information available will ultimately facilitate improved care of the traumatized or septic individual.
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