Hemodynamic changes and cytokine trends during abdominal stop-flow
© Current Science Ltd 1999
Published: 16 March 2000
The stop-flow is a therapeutic technique to treat local splanchnic malignant neoplasm, especially of the liver. The rational of this technique is to reach and maintain high concentration of antiblastic drugs in the site of the tumor. This is made positioning two intravascular devices to stop both the arterial in-flow and the venous out-flow of the site where the tumor is localized. In this way a decreased vascular flow with consequent hypoxia is created to increase the efficacy of some antiblastic drugs. The aim of this work is to verify the hemodynamic changes due to the splanchnic hypoxia and the trend of TNFa, interleukin 1B, 6 and 8.
Material and methods
We have examined three patients: two with metastasis from carcinoma of colon-rectum and another with not operable carcinoma of pancreas. Before the stop-flow a pulmonary catheter to measure the cardiac output on-line (Vigilance, Baxter), a gastric tonometer and a radial artery were positioned. After the induction of anesthesia (fentanyl, thiopental, vecuronium) a venous device in vein cava and an arterial device in aorta artery, both with a balloon in the top, were positioned just under diaphragma muscle and inflated. In this way the aortic and caval flows were interrupted for 20 min and in this time antiblastic drugs were administred in the hypoxic and isolated splanchnich area. After 20 min the baloons were deflated, splanchnic area was revasculated and a dyalisis started to eliminate as soon as possible the drugs. At 5 times (after the induction of anesthesia, after 10', 20' of stop flow and after 15' and 40' of the end of stop-flow) all hemodynamic and oxyphoretic parameters, pHi and blood lactate were measured and sierum to detect cytokine TNFa, Il-1B, Il-6, Il-8, was stored at -60°C.
In all three patients there was an increase of more 100% and a decrease of systemic vascular resistance after the stop flow and these changes were still present after 40 min from the revascularisation. At the same time blood lactate increased and pHi decreases below 7.32. Among the cytokines only Il-6 showed an increase of more 100% after the stop-flow, while the others had no significant movements.
Decreasing tissue perfusion causes hypoxia and then acidosis that provokes a cellular damn, increasing of cellular permeability with loss of barrier function of gut mucosa. This induces the liberation of some substances, such as endotoxins, which start the inflammatory cascade of TNFa, Il-1, Il-6, Il-8. Moreover, another way to induce the formation of toxic substances, in the presence of ischemia followed by riperfusion, is the activation of purine metabolism with activation of xantine-oxydase (XO) and consequent production of the anion superoxydodismutasis, that, in the presence of iron (Fenton reaction) causes the formation of ossidryl ion, very dangerous for the organism. The hemodynamic response of these two cases (high CO, low SVR, pHa, pHi and increased blood lactate) and the increasing of I1-6 are not explanable only in terms of hypoxia and it could be supposed that these changes probably are due to a septic state, caused by the substances liberated from the hypoxic splanchnic tissue. This experimental model could be useful in the comprehension of physiopathology of hypoxia and perhaps of septic shock and, in some way in the experimentation of new drugs against the effects of hypoxia.
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