ABSTRACT
OBJECTIVE: This study was designed to evaluate the effects of terlipressin versus fluid resuscitation with normal saline, hypertonic saline or hypertonic-hyperoncotic hydroxyethyl starch, on hemodynamics, metabolics, blood loss and short-term survival in hemorrhagic shock. METHOD: Twenty-nine pigs were subjected to severe liver injury and treated 30 min later with either: (1) 2 mg terlipressin in a bolus, (2) placebo-treated controls, (3) 4 mL/kg 7.5% hypertonic NaCl, (4) 4 mL/kg 7.2% hypertonic-hyperoncotic hydroxyethyl starch 200/0.5, or (5) normal saline at three times lost blood volume. RESULTS: The overall mortality rate was 69%. Blood loss was significantly higher in the hypertonic-hyperoncotic hydroxyethyl starch and normal saline groups than in the terlipressin, hypertonic NaCl and placebo-treated controls groups (p<0.005). Hyperkalemia (K>5 mmol/L) before any treatment occurred in 66% of the patients (80% among non-survivors vs. 22% among survivors, p=0.019). Post-resuscitation hyperkalemia occurred in 86.66% of non-survivors vs. 0% of survivors (p<0.001). Hyperkalemia was the first sign of an unsuccessful outcome for the usual resuscitative procedure and was not related to arterial acidemia. Successfully resuscitated animals showed a significant decrease in serum potassium levels relative to the baseline value. CONCLUSION: Hyperkalemia accompanies hemorrhagic shock and, in addition to providing an early sign of the acute ischemic insult severity, may be responsible for cardiac arrest related to hemorrhagic shock.
Subject(s)
Animals , Male , Heart Arrest/therapy , Hemostatics/therapeutic use , Hyperkalemia/therapy , Lypressin/analogs & derivatives , Resuscitation/methods , Shock, Hemorrhagic/therapy , Disease Models, Animal , Fluid Therapy/methods , Hyperkalemia/mortality , Lypressin/therapeutic use , Survival Rate , Swine , Shock, Hemorrhagic/mortalityABSTRACT
Experimental studies have demonstrated a decrease in hepatocyte transmembrane potential (HTP) during ischemia, whereas HTP is improved in livers with greater glycogen reserves. The present study was undertaken to assess blood glucose. pH, K+ and hepatic glycogen levels during determined periods of warm liver ischemia and after reperfusion. The study was conducted on 15 mongrel dogs (9-17 kg) submitted to warm liver ischemia by clamping of the portal vein and hepatic artery (90 ñ 20 min) with blood flow of the infradiaphragmatic region shunted into left external jugular vein through a venovenous bypass draining the portal vein and the inferior vena cava. Blood samples and hepatic tissue biopsies were obtained before ischemia (control), after 15 and 45 min of ischemia, and 15 min after liver reperfusion. A significant increase in blood glucose was observed during reperfusion of the liver (p < O.05 vs control, 15 and 45 min of ischemia). The period of ischemia had a progressive glycogenolysis which became more marked after reperfusion, possibly explaining the increase in blood glucose levels observed during this period.
Subject(s)
Animals , Dogs , Blood Glucose/analysis , Liver/metabolism , Liver Glycogen/analysis , Hyperglycemia/chemically induced , Ischemia/metabolism , Potassium/analysis , Reperfusion/adverse effects , Blood Glucose/metabolism , Liver/blood supply , Liver/chemistry , Liver Glycogen/metabolism , Hepatic Artery , Hydrogen-Ion Concentration , Membrane Potentials , Portal Vein , Potassium/metabolism , Reperfusion Injury , Time FactorsABSTRACT
A perda progressiva do parênquima hepático, que é substituído por tecido fibroso e nódulos de regeneraçäo, determina a destruiçäo da arquitetura normal que modifica as características da irrigaçäo sanguínea e entäo ocorre a rápida deterioraçäo do estado geral do paciente que passa a apresentar distúrbios de vários órgäos e sistemas, que säo extremamente graves e que compöem o estágio terminal do acometimento hepático - cirrose. Existem várias situaçöes nas quais pacientes portadores de cirrose hepática säo submetidos a intervençöes cirúrgicas e, para tanto é necessário o conhecimento e rápida atuaçäo da equipe médica pois o sofrimento hepático resultante da combinaçäo do binômio cirurgia-anestesia tem várias razöes e graus e é dever do médico que assiste o paciente na qualidade de anestesiologista näo somente administrar drogas capazes de abolir a consciência, drogas que promovam analgesia e relaxamento muscular como também propiciar condiçöes hemodinâmicas, ventilatórias e renais suficientes para a manutençäo da homeostase interna bem como corrigir os distúrbios da coagulaçäo de modo a diminuir as perdas sanguíneas, baseando-se em profundos conhecimentos da farmacocinética e farmacodinâmica dos anestésicos na vigência de distúrbios hepáticos e, com único objetivo em mente que é prevenir prejuízo adicional da funçäo hepática ainda remanescente nesses pacientes