Hepatic Oxygen Tension Research Articles

Кровоток и напряжение кислорода в печени при различных способах ее повреждения и гипероксии

The aim of study was to investigate hepatic blood flow and oxygen tension in mechanical, chemical, and combined injury of the liver and during a course of hyperbaric oxygenation (HBO). Methods. Experiments were performed on 143 white female rats weighing 180-220 g. Mechanical injury of the liver was modeled with partial hepatectomy (PHE) by removing a part of the left hepatic lobe (HL) (15-20% of liver weight). Chemical injury was modeled by subcutaneous injection of 50% ССl4 in olive oil (0.1 ml/100 g). Injections were performed every second day for 65 days. For the combined injury, PHE followed by HBO (3 ATA, 50 min) was performed on day 65 (last day) of ССl4 administration. HBO was applied three times, at 4-8, 24, and 48 hours after PHE. Hepatic blood flow was studied using hydrogen clearance in the operated, left HL (LHL) and in one of unoperated, middle HL (MHL). Hepatic oxygen tension (рО2) was evaluated by polarography with a platinum electrode; data were corrected for the temperature coefficient. Studies were performed on postoperative days 3, 7 and 14 (posthyperoxia days 1, 4, and 11). Results. In normal animals, PHE stimulated blood flow in both studied hepatic lobes and decreased рО2 only in the remaining LHL on postoperative days 3 and 7. On day 65 of ССl4 administration, blood flow was reduced by 42% and 39%, respectively, in remaining LHL and MHL while рО2 was reduced by 50%. These changes were not reversed by day 14 following the toxin withdrawal. PHE performed on day 65 of ССl4 administration caused an increase in blood flow on postoperative days 3 and 7 only in MHL; however, on day 14, the blood flow decreased to the level of the end of toxin administration. This was associated with a brief normalization of the reduced рО2 on postoperative day 7. In the remaining LHL of animals with chronic ССl4-induced hepatitis and PHE, values of blood flow and рО2 did not change and remained below the normal level at 14 days after PHE. The HBO exposure of healthy rats with PHE abolished the stimulating effect of surgery on blood flow in both studied hepatic lobes, thereby normalizing pO2 in the remaining LHL and decreasing pO2 in MHL on days 3 and 7. This was reversed by postoperative day 14 due to the stimulating effect of hyperoxia on blood flow in this HL. In animals with combined injury of the liver, HBO stimulated blood flow in both studied HLs, thereby increasing рО2 above the preoperative level; however, a complete recovery did not occur. The stimulating effect of HBO on blood flow in animals with combined injury remained by day 11 of the posthyperoxic period. Conclusion. A prolonged exposure to ССl4 reduced the sensitivity of hepatic blood flow to the stimulating effect of PHE, which facilitated development of persistent hypoxia in both injured and uninjured HLs. Responses to HBO of blood flow and tissue рО2 in operated liver directly depend on the state of liver at the moment of hyperoxia exposure.

Consequences of Pneumoperitoneum on Liver Ischemia During Laparoscopic Portal Triad Clamping in a Swine Model

Portal triad clamping (PTC) may be required during laparoscopic liver resection to limit blood loss. The aim of this study was to test in a swine model the hypothesis that during laparoscopic PTC, increased intraperitoneal pressure may alter hepatic vein reverse circulation, inducing a more severe hepatic ischemia compared with PTC performed in laparotomy. Fifteen pigs were randomized into three groups: laparoscopy (1 h of pneumoperitoneum at 15 mmHg and 3 h of surveillance), open PTC (1 h PTC through laparotomy and 3 h of reperfusion), and laparoscopic PTC (1 h PTC with 15 mmHg pneumoperitoneum and 3 h of reperfusion). PTC was performed under mesenteric decompression using a veno-venous splenofemoral bypass. Hepatic partial oxygen tension and microcirculatory flow were continuously measured using a Clarke-type electrode and a laser Doppler flow probe, respectively. Liver consequences of PTC was assessed by right atrium serum determination of transaminases, creatinine, bilirubin, INR, and several ischemia/reperfusion parameters, drawn before PTC (T0), before unclamping (T60), and 1 (T120) and 3 h after reperfusion (T240). Histology was performed on T240 liver biopsies. Compared with open PTC, laparoscopic PTC produced a more rapid and more severe decrease in hepatic oxygen tension, indicating a more severe tissular hypoxia, and a more severe decrease in hepatic microcirculatory flow, indicating a decrease in hepatic backflow. At T240, the laparoscopic PTC livers suffered from a higher degree of hepatocellular damage, shown by higher transaminases and increased necrotic index at pathology. These results indicate that in this pig model, laparoscopic PTC induces a more severe liver ischemia, related to decreased hepatic oxygen content and decreased hepatic backflow. If confirmed by clinical studies, these results may indicate that caution is necessary when performing prolonged PTC during laparoscopic hepatic resection, particularly in cirrhotic or steatotic livers.

Effect of acute and chronic ethanol consumption on hepatic tissue oxygen tension in rats

In vivo hepatic tissue oxygenation was investigated in chronically ethanol-treated rats using micro oxygen electrode and reflectance spectrophotometry. Effect of acute ethanol administration was also studied. Hepatic oxygen tension of rats treated with ethanol chronically (daily ethanol intake, 9∼12 g/kg for 9 months) was very low as compared with that of normal rats, the decrease being comparable to that of rats treated with carbon tetrachloride. The hepatic oxygen tension in normal controls shortly after ethanol ingestion increased from basal level (median, 23 mmHg) to 40∼70 mmHg, while in chronically ethanol-treated rats, the hepatic oxygen tension decreased transiently, followed by a gradual increase, but it still remained low. In CCl 4-treated rats, the hepatic oxygen tension decreased further after the ethanol ingestion. It is concluded that chronic ethanol consumption in rats resulted in hepatic hypoxia with decreased liver blood flow and volume. Also acute ethanol administration does not induce hepatic hypoxia in normal rats, while in rats with injured liver it induces hypoxia.

Inefficacy of oxygenated drinking water in accelerating ethanol elimination in humans

In our earlier report it was found that after intravenous infusion of ethanol into monkeys the drinking of oxygenated water accelerated their elimination rate of ethanol 60% on the average. The acceleration was assumed to be due to increased hepatic oxygen tension through the portal blood flow. Now we have repeated similar experiments using humans as subjects. In humans the elimination rate of ethanol was not changed by oxygenated drinks. We are not able to explain the species difference, because the mechanism by which oxygenated water increased ethanol elimination in monkeys is unsettled.

THE EFFECT OF ENTERAL OXYGEN ADMINISTRATION ON THE HEPATIC CIRCULATION DURING HALOTHANE ANAESTHESIA: EXPERIMENTAL INVESTIGATIONS

An investigation of the hepatic microcirculation and oxygen tension in 20 white rats showed that halothane anaesthesia was associated with a reduction in the diameter of the terminal portal venous branches, sinusoids and central veins, and with a decrease in the hepatic oxygen tension from 28.8+/-4.8 to 22.4+/-3.9 mmHg (mean +/-SEM). Enteral oxygen administration was followed by an increased blood flow in all the observed vessels, by an increase in the number of simultaneously filled sinusoids and also by an increase in the hepatic oxygen tension to 35.2+/-10.1 mm Hg. Subsequently, changes in blood flow in the hepatic artery and portal vein were investigated in 10 cats by cineangiography. During inhalation of halothane the hepatic artery blood flow was observed to increase by 30%, while portal vein blood flow was found to decrease by 57% of the initial value. Thus total hepatic blood flow was reduced by 40%, with the ratio of hepatic artery blood flow to total hepatic blood flow increasing from 19% to 43%. When enteral oxygen was administered, the total hepatic blood flow was restored to 92% of the value before anaesthesia. This resulted from an increase in the portal blood flow fraction only. It is concluded that disturbances in the liver circulation in cats and rats produced by halothane anaesthesia can be modified by the simultaneous administration of enteral oxygen.