The Different Responses of the Hepatic Arterial Bed to Hypovolaemia and to Halothane Anaesthesia

Ten dogs were subjected to a period of hypovolaemia (bleeding volume: 2% of body weight) and to a period of halothane anaesthesia (end-tidal halothane concentration: 1%). Mean arterial blood pressure decreased to 79% of control value during hypovolaemia and to 58% of control value during halothane anaesthesia. Mean total peripheral and preportal vascular resistances increased during hypovolaemia and were unchanged during halothane. Mean hepatic arterial and portal venous blood flows decreased to 82% and 55% of control values, respectively, during hypovolaemia, and to 41% and 56% of control value, respectively, during exposure to halothane. Mean hepatic arterial resistance was unchanged during hypovolaemia, but increased during halothane. Mean hepatic oxygen consumption did not change significantly during hypovolaemia, but decreased during halothane anaesthesia, in spite of an increased extraction of oxygen from both the hepatic arterial and the portal venous blood. Possible mechanisms which may maintain oxygen supply to the liver by increasing the hepatic arterial fraction of total liver blood flow when portal venous blood flow is reduced are discussed. It is concluded that this mechanism is upset or inhibited during halothane anaesthesia.     

EFFECT OF ISOFLURANE ON THE CANINE HEPATIC CIRCULATION AND HEPATIC OXYGEN BALANCE

We have studied the effects of increasing concentrations ofisoflurane (1%, 1.5% and 2%) on the hepatic circulation andthe oxygen supply and demand of the liver in six barbiturate-anaesthetizedgreyhounds. Following laparotomy, the hepatic arterial and portalvenous blood flows were measured continuously using electromagneticflow probes, and mean arterial pressure and cardiac output weremeasured as appropriate. Cardiac output was maintained whilemean arterial pressure and systemic vascular resistance decreasedin a dose dependent manner. Hepatic arterial and total liverblood flows and oxygen supplies decreased significantly at allisoflurane concentrations. Portal venous blood flow and portalvenous oxygen supply did not decrease significantly untill theconcentration of isoflurane was increased to 2% and 1.5%, respectively.Hepatic oxygen consumption was reduced with 2% isoflurane (P< 0.05), but this was insufficient to offset the reductionin hepatic oxygen supply and resulted in an increased extractionof oxygen by the liver. ^*Department of Anaesthesia, Stobhill General Hospital, 133 BalornockRoad, Glasgow G21 3UW. Medical Department, Lilly Industries Ltd, Dextra Court, Chapelhill,Basingstoke, Hampshire RG21 2SY.     

Hepatic oxygen supply and consumption in rats exposed to thiopental, halothane, enflurane, and isoflurane in the presence of hypoxia

Hepatic oxygen supply and uptake were assessed in phenobarbital-pretreated male Sprague-Dawley rats receiving subanesthetic doses of thiopental, halothane, enflurane, or isoflurane combined with hypoxia (approximately 0.5 MAC and 12% oxygen) for the purpose of evaluating the role of these combinations in hepatic blood flow alterations and the concomitant hepatic oxygen supply and uptake. Hepatic blood flow was measured using microspheres; hepatic oxygen supply and consumption was calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous, and hepatic venous blood. In all anesthetic groups, total hepatic blood flow did not change from the control value. Oxygen supply to the liver was decreased from air control values in all anesthetic groups, but there were no significant differences among anesthetic groups. Hepatic oxygen consumption was significantly lower in animals exposed to halothane and isoflurane versus air controls, whereas it was not significantly decreased in animals receiving thiopental or enflurane. The hepatic oxygen supply/consumption ratio was higher in the air control and the isoflurane groups than in other groups; however, no significant differences in this ratio were observed among the thiopental, halothane, and enflurane groups. Oxygen content in hepatic venous blood correlated well with hepatic oxygen supply/consumption ratio in all five groups. These results show that, during exposure to mild hypoxia, a sub-MAC dose of isoflurane maintains the relationship of hepatic oxygen supply to uptake better than thiopental, halothane, or enflurane. However, a subanesthetic dose of halothane did not aggravate liver hypoxia specifically, compared with thiopental or enflurane.     

EFFECT OF HYPERCARBIA ON HEPATIC BLOOD FLOW AND OXYGEN CONSUMPTION IN THE GREYHOUND

The stability of a technique for measuring hepatic blood flowand oxygen consumption was established in six greyhounds anaesthetizedwith pentobarbitone (group A). Subsequently, the effects ofincreased Pa_CO2 were studied in another six animals (group B).With one exception (splenic blood flow) no significant changeswere observed in any of the indices measured in group A. Ingroup B, although hepatic arterial blood flow (HABF) decreasedwhen Pa_CO2 increased, both portal venous blood flow (PVBF) andtotal liver blood flow (HABF + PVBF) increased. However, thesechanges were much less marked after 20 min. Hepatic oxygen consumptionand splenic venous blood flow were unchanged with an increasein Pa_CO2     

Effects of halothane and hypoxia on hepatic oxygen metabolism in the dog

Hepatic oxygen delivery and consumption were assessed in mongrel dogs receiving 2MAC of halothane combined with graded hypoxic hypoxemia (21–8% oxygen). Hepatic blood flow was measured using electromagnetic flowmetry; hepatic oxygen delivery and consumption were calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous and hepatic venous blood. In hypoxia-halothane group, total hepatic blood flow decreased at mild hypoxia (15% O₂) from control value, but recovered to control level at moderate hypoxia (10% O₂), then again decreased at 8% O₂. Oxygen supply to the liver was decreased with the augmentation of hypoxia in hypoxia-halothane and hypoxia-alone groups, and it was significantly lower in the hypoxia-halothane group at 15 and 12% O₂. Hepatic oxygen consumption also decreased from air control values with the increment of hypoxia, but there was no significant difference between the groups. Arterial ketone body ratio, which indicates mitochondrial energy charge level, decreased with the development of hypoxia but there was no significant difference in this ratio between the groups. These results show that halothane aggravated oxygen supply to the liver at mild to moderate hypoxia (15–12% O₂), but did not worsen it specifically at more serious hypoxia (10–8% O₂) compared with hypoxia alone. Hepatic hypoxia itself could not thus be a main cause of halothane hepatotoxicity.(Matsumoto N, Hori T, Miyazaki T et al.: Effects of halothane and hypoxia on hepatic oxygen metabolism in the dog. J Anesth 3: 27–34, 1989)     

Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs

We investigated the relative effects of 0.5, 1.0, 1.5, 2.0 MAC halothane and enflurane, and concurrent noxious stimulus on hepatic blood flow and oxygen consumption in 14 mongrel dogs randomly divided into groups of seven each. Hepatic arterial and portal venous blood flow (HABF and PVBF, respectively) were measured continuously using ultrasonic transit time flow meter. Mean arterial blood pressure (MAP), cardiac index (CI), hepatic oxygen supply, and hepatic oxygen consumption (H _{O 2}) were measured. Halothane significantly deceased HABF, but not PVBF in a dose dependent manner. Enflurane did not affect HABF and PVBF significantly. MAP and CI decreased in both groups, with halothane producing more marked decreases than enflurane. H _{O 2} did not change with enflurane, but did with halothane, producing significant differences, with halothane being greater at 1.5, 2.0 MAC. A noxious stimulus only caused minor change in blood flow. The results suggest that liver blood flow and oxygen consumption are affected differently by halothane and enflurane and that halothane has a stronger tendency to cause an imbalance between liver oxygen supply and consumption than dose enflurane.(Masaki E, Yasuda N, Tanifuji Y et al.: Effect of halothane and enflurane on hepatic blood flow and oxygen consumption in dogs. J Anesth 3: 118–122, 1989)     

EFFECT OF VERAPAMIL ON CANINE LEFT VENTRICULAR FUNCTION IN THE PRESENCE OF FENTANYL WHEN APICAL BLOOD FLOW IS CRITICALLY LIMITED

Instruments were inserted to seven dogs under halothane anaesthesia,to measure global and regional left ventricular function. Anaesthesiawas continued with fentanyl (100 µg kg^–1 bolus,then 1.5 µg kg^–1 min^–1). Critical constrictionwas applied to the left anterior descending coronary artery.Control recordings were made, followed by bolus administrationof verapamil 0.08, 0.16 and 0.32 mg kg^–1, with recordings10 min after each bolus. At the highest dose, verapamil decreasedsystemic arterial pressure, left ventricular dP/dt, stroke volumeand systemic vascular resistance, and increased heart rate significantly.Coronary perfusion pressure decreased and, in the presence ofcritical constriction, coronary flow per beat decreased significantly.In the region with constriction, systolic shortening of myocardiumdecreased and post-systolic shortening increased significantlywith addition of verapamil. The addition of a high dose of verapamilto fentanyl anaesthesia caused reduction in systolic functionand development of early diastolic dysfunction in myocardiumwith critically limited blood supply.     

Hepatic oxygen supply during halothane or isoflurane anesthesia in guinea pigs

The present study was designed to determine changes in hepatic oxygen supply in guinea pigs during halothane or isoflurane anesthesia. Twenty-seven guinea pigs were randomly divided into three equal groups: control (no anesthesia) group, and animals anesthetized with halothane or isoflurane to decrease mean arterial pressure (MAP) by 50%. Hepatic arterial blood flow (HABF) and portal blood flow (PBF), as well as arterial and portal venous blood oxygen content, were determined in awake animals (stage I, baseline values), and during anesthesia (stage II). HABF was found to be extremely low (0.04 ml.min-1.g-1) during both stages of observation in the control (no anesthesia) group, as well as during stage I (awake) in animals treated with halothane or isoflurane. Equal degrees of arterial hypotension during halothane and isoflurane anesthesia were accompanied by decreased HABF during halothane (37%), but no significant change in HABF during isoflurane anesthesia. PBF decreased significantly in both experimental groups; however, the decrease was more prominent during halothane than during isoflurane anesthesia (57% vs. 23%). The observed hepatic circulatory changes led to a 65% decrease in hepatic oxygen delivery during halothane, but only a 34% decrease during isoflurane anesthesia. The present study does not exclude the possibility that liver damage in the guinea pig model is related to the reductive metabolism of halothane or any other mechanism. However, the extremely low HABF and a prominent reduction in both HABF and PBF during halothane anesthesia may be responsible for hepatic damage observed in the guinea pig model.     

Hepatic circulation during surgical stress and anesthesia with halothane, isoflurane, or fentanyl

Hepatic blood flow and the oxygen supply/uptake relation were studied in 19 miniature pigs using labeled microspheres. Changes in hepatic arterial blood flow and portal blood flow, as well as total hepatic blood flow during halothane anesthesia were more closely associated with changes in mean arterial pressure (MAP) and cardiac output than during anesthesia with isoflurane or fentanyl. Halothane or isoflurane administered in concentrations that decreased MAP by approximately 30% were accompanied by decreases in hepatic oxygen delivery (DO2th) averaging 46% during halothane and 31% during isoflurane anesthesia and parallel decreases in hepatic blood flow. In concentrations that decreased MAP by 50%, halothane and isoflurane decreased DO2th 61 and 37%, respectively. DO2th was maintained (statistically insignificant, 23% increase) during both doses of fentanyl administered (20 micrograms/kg followed by 0.17 microgram . kg-1 . min-1, and 50 micrograms/kg followed by 0.42 microgram . kg-1 . min-1). Hepatic oxygen uptake increased 50% during fentanyl and was maintained at baseline levels during both doses of halothane and isoflurane anesthesia. Oxygen content in hepatic venous blood was maintained at baseline levels during fentanyl and isoflurane administration and was decreased by both concentrations of halothane anesthesia. The hepatic oxygen supply demand ratio was maintained at baseline levels after both doses of fentanyl and during isoflurane administered in a concentration that decreased blood pressure 30%; the ratio decreased during isoflurane administered in a concentration decreasing blood pressure by 50% and during both doses of halothane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of propofol on hepatic blood flow and oxygen balance in rabbits

PURPOSE: Propofol has been reported to alter hepatic blood flow and to increase hepatic oxygen consumption. This study was designed to determine the effect of propofol on hepatic blood flow and oxygenation in rabbits, in order to establish its net effect on hepatic oxygen balance. METHODS: Twenty, adult male, New Zealand white rabbits were randomly divided into two groups: Group P (propofol, 0.6 mg.kg(-1).min(-1)) or Group C (10% intralipid, 0.6 mg.kg(-1).min(-1)). An electromagnetic flowmeter was used to measure hepatic blood flow, and blood, from the carotid artery, the portal vein, and the hepatic vein, was used to determine hepatic oxygenation. After we obtained baseline values, we repeated measurements ten, 30, and 60 min after initiating the infusion. RESULTS: Intralipid did not affect systemic hemodynamics, hepatic blood flow, or oxygenation during the 60 min infusion; however, propofol caused a time-dependent decrease in mean arterial blood pressures and an increase in portal venous flow and total hepatic blood flow. In contrast, hepatic arterial blood flow remained unchanged during the propofol infusion. Hepatic oxygen delivery and consumption increased in a time-dependent manner to maximums of 25% and 21.4% (both, P < 0.05) above baseline, respectively. Hepatic venous oxygen saturation and extraction was unchanged throughout the study period. CONCLUSION: Propofol increases total hepatic blood flow, primarily by increasing hepatic portal venous flow. The increase in liver oxygen consumption was fully compensated by an increase in oxygen supply to the liver, resulting in a preserved, hepatic oxygen balance.     

Comparative effects of halothane, isoflurane, and sevoflurane on the liver with hepatic artery ligation in the beagle.

Recently, there has been increasing interest in the alterations in splanchnic and hepatic circulation and preservation of hepatic oxygenation and function during anesthesia and surgery. However, the effects of volatile anesthetics under a condition of marginal hepatic oxygen supply are not well understood. Using a crossover design, we therefore studied the effects of equianesthetic concentrations (1.5 MAC) of halothane, isoflurane, and sevoflurane on hepatic oxygenation and function in nine beagles in which the hepatic artery had been ligated. Portal blood flow was measured by an electro-magnetic flow meter. Hepatic function was assessed by indocyanine green elimination kinetics. While cardiac output and mean arterial pressure were greater during halothane anesthesia than during isoflurane and sevoflurane anesthesia, portal blood flow and hepatic oxygen supply were significantly less during halothane and sevoflurane anesthesia than during isoflurane anesthesia. With regard to hepatic oxygen uptake, there was a significant difference between halothane (2.7 +/- 1.2 ml.min-1 x 100 g-1) and sevoflurane (3.7 +/- 2.0 ml.min-1 x 100 g-1; P less than 0.05). Consequently, the hepatic oxygen supply/uptake ratio and the hemoglobin oxygen saturation and oxygen partial pressure in hepatic venous blood during sevoflurane anesthesia were significantly less than they were with the other anesthetics. Indocyanine green clearance was better preserved during sevoflurane anesthesia (39.7 +/- 12.0 ml.min-1) than during halothane anesthesia (30.9 +/- 8.4 ml.min-1; P less than 0.05). We conclude that sevoflurane is accompanied by a smaller oxygen supply/uptake ratio than is halothane and isoflurane, while it preserves hepatic function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of PEEP on splanchnic hemodynamics and blood volume

The effects of intermittent positive pressure ventilation with PEEP on splanchnic circulation and hepatic oxygen supply were studied in six beagles. PEEP of 0, 0.5 and 1.0 kPa (0, 5, 10 cmH₂O, PEEP₀, PEEP₅ and PEEP₁₀, respectively) of 30 min duration was applied in a random sequence. Hepatic arterial blood flow and portal venous blood flow were measured by electromagnetic flow meters. Blood volume changes in the splanchnic area were assessed from hepatic and splenic dimensions determined by sonomicrometry. PEEP₅ and PEEP₁₀ were associated with proportional decreases in both hepatic blood flow and cardiac output, while mean arterial pressure remained unchanged. Reflecting the decrease in hepatic blood flow, the hepatic oxygen supply decreased with the level of PEEP, and hepatic venous hemoglobin oxygen saturation was significantly less during PEEP₁₀ (55.1 ± 14.3%) than during PEEP₅ (62.6 ± 17.4%) and PEEP₀ (62.3 ± 11.9%). Hepatic venous and portal venous pressure increased with the level of PEEP. Hepatic dimensions increased by 7–8% and 16–19% during PEEP₅ and PEEP₁₀, respectively, but no significant changes in splenic dimension were observed. We conclude that PEEP₅ and PEEP₁₀ are accompanied by a decrease in hepatic blood flow and oxygen supply along with hepatic congestion.     

Acidaemia is less severe following reperfusion via the hepatic artery compared with the portal vein during liver transplantation

Reperfusion of the liver during transplantation can cause cardiovascularchanges such as systemic vasodilatation, pulmonary hypertensionand cardiac dysfunction. We have previously demonstrated a slowerincrease in oxygen consumption when the hepatic artery was usedfor reperfusion rather than the portal vein, and had the clinicalimpression that overall patient stability was greater with theformer technique.¹ We therefore compared the acid–basechanges which occur following reperfusion with each of thesetechniques. Twenty patients undergoing liver transplantation were studied.In all cases the piggyback technique was used, and anaestheticmanagement was similar. In 10 patients liver reperfusion wasfirst via the portal vein followed by the hepatic artery; inthe other 10 patients the hepatic artery was anastomosed firstfollowed by the portal vein. Ventilation remained constant duringthe study period. Arterial blood was drawn for acid–baseand whole blood lactate measurement at three time points: (1)immediately prior to reperfusion, (2) 30 min after reperfusion,(3) 60 min after reperfusion. Changes in variables were comparedbetween the groups by Mann–Whitney U test corrected formultiple tests using the Bonferroni method. Data are shown in Table 18. All acid–base variables weresimilar between the groups prior to reperfusion. Following reperfusionacidaemia (H⁺ concentration) was more marked in the portal veingroup and was accompanied by a larger increase in Pa_CO2. Changesin blood lactate and acidosis (Standard Bicarbonate Concentration)were similar between the groups. Our data indicate that a smaller acid load is released intothe systemic circulation immediately after reperfusion whenthe hepatic artery is anastomosed first rather than the portalvein, as is conventional. This may be because the release ofischaemic metabolites from the splanchnic circulation is delayed,or because the rate of flushing of acid from the donor liveris slower via the hepatic artery which has a lower overall flowand is a higher resistance circulation. Less marked acidosisand hypercapnia are potentially beneficial particularly in highrisk patients, such as those with fulminant hepatic failurewho are at risk of intracranial hypertension following reperfusion.     

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)     

EFFECTS OF ENFLURANE AND HALOTHANE ON LIVER BLOOD FLOW AND OXYGEN CONSUMPTION IN THE GREYHOUND

The effect of increasing inspired concentrations of halothane0.5, 1.0, 1.5, 2.0% and cdurane 1.0, 1.5, 2.0, 3.0% on the hepaticcirculation, were investigated in two groups of anasthetizedgreyhounds. Hepatic arterial a d portal venous blood flow weremeasured continuously using electromagnetic flow probes. Meanarterial pressure and cardiac output were monitored throughouteach investigation. At equiptent anaesthetic concentrationsthere were similar and dose-dependcnt decreases in hepatic arterial,portal venous and total liver blood flows in b t h groups. Enfluraneproduced a more marked decrease in mean arterial pressure thanhalothane because of a significant decrease in systemic vascularresistance. Hepatic arterial resistance decreased significantlywith enflurane but was unchanged in the group receiving halothane.Nather drug affected hepatic oxygen consumption significandy.     

SURVIVAL OF BLED DOGS AFTER HALOTHANE AND ETHER ANAESTHESIA

Sixty spontaneously-breathing atropinized dogs anaesthetizedwith 79 per cent ethylene/21 per cent oxygen were bled to amean aortic blood pressure of 40 mm Hg for 90 minutes, and theirsurvival observed during and after an additional 30 minutesof halothane or di-ethyl ether anaesthesia followed by bloodreplacement. Blood volumes were reduced approximately 40 percent by an average haemorrhage of 46.3 ml/kg. It is concludedthat: (a) Survival experiments did not demonstrate a deleteriouseffect of 1.5 per cent halothane due to its hypotensive actionin oligaemia when compared with lighter planes of ether anaesthesia,(b) Maintenance of a normal minute volume will not suffice foradequate oxygenation of the arterial blood during anaesthesiawith either agent after haemorrhage with air as carrier gas.(c) Enrichment of the inspired oxygen to 30 per cent ensuresadequate arterial oxygenation when pulmonary ventilation isreduced by 1.5 per cent halothane after haemorrhage of thisseverity, and a survival rate insignificantly different fromthat resulting when 100 per cent oxygen is used as carrier gas. ^*Present address: University College Hospital, London.     

The postoperative effects of halothane versus isoflurane on hepatic artery and portal vein blood flow in humans

Animal studies have shown that halothane decreases total hepatic blood flow (THBF) by reducing both arterial (HABF) and portal (PVBF) inflow, whereas isoflurane appears to preserve them. In this study we assessed the effect of halothane and isoflurane on HABF and PVBF in surgical patients by using the pulsed Doppler technique. A validation study was conducted in six cynomolgus monkeys to compare the values of THBF obtained by the pulsed Doppler and indocyanine green clearance methods. Subsequently, six patients (ASA status I and II) undergoing elective open cholecystectomy were studied after surgery by using implanted pulsed Doppler probes. THBF and liver flow partition were compared during 1% halothane and 1.5% isoflurane (end-tidal concentrations). In the animal study, there was good agreement between the techniques (Bland and Altmann representation). In flunitrazepam-anesthetized patients, THBF was 1120 +/- 284 mL/min. Compared with this baseline and for a similar mean arterial blood pressure decrease (10%), THBF was maintained with isoflurane, whereas it decreased by 36% (P < 0.05) under halothane. With isoflurane, PVBF increased (25%; P = 0.067) with a maintained HABF. With halothane, both PVBF (-44%; P < 0.05) and HABF (-20%; P < 0.05) were reduced. Halothane acted mainly as a vasoconstrictor of the hepatic circulation, whereas isoflurane was a vasodilator, confirming the beneficial effect of isoflurane on hepatic oxygen supply. IMPLICATIONS: Volatile anesthetics may alter liver circulation with serious adverse effects. Using implanted pulsed Doppler probes in six anesthetized patients, we showed that halothane acted mainly as a vasoconstrictor of the liver vascular bed, whereas isoflurane was a vasodilator, confirming the beneficial effect of isoflurane on liver oxygen supply.     

The effect of halothane, isoflurane, and blood loss on hepatotoxicity and hepatic oxygen availability in phenobarbital-pretreated hypoxic rats

This study evaluated the role of ventilatory and circulatory depression in anesthesia-induced hepatotoxicity in rats. Male Sprague-Dawley rats (181 animals) were pretreated with phenobarbital and exposed to hypoxia (FIO2 = 0.14) for 2 hr. The animals were divided into four groups: group 1 received 1% inspired halothane in the hypoxic gas mixture; group 2 received 1.4% inspired isoflurane and hypoxia; group 3 had 25-30% of their blood volume removed 2 hr before exposure to hypoxia; and group 4 served as a control with no treatment other than hypoxia. Hepatic blood flow was studied using microspheres; oxygen availability to the liver was calculated using values of hepatic blood flow and oxygen content of arterial and portal venous blood; and liver injury was quantitatively evaluated. Ventilation was depressed in rats that received halothane and, to a lesser extent, isoflurane. The lowest portal blood flow was observed in groups 1 and 3. Hepatic arterial blood flow was lowest in group 1 and highest in group 3. There was an inverse relationship between hepatic oxygen availability and severity of histologic lesions. The most severe lesions and lowest oxygen availability was associated with halothane. Hemorrhage and isoflurane were associated with less diminution of oxygen availability and less severe hepatic lesions. The least decrease in oxygen availability and the least severe histologic changes occurred in control rats subjected to hypoxia only.     

EFFECTS OF METOPROLOL ON SYSTEMIC HAEMODYNAMICS, MYOCARDIAL PERFORMANCE AND THE CORONARY CIRCULATION DURING HALOTHANE ANAESTHESIA

The effects of metoprolol 1 mg kg^–1 i.v. on the systemicand coronary circulations and on myo-cardial performance werestudied in nine open-chested dogs ventilated with halothane0.8% in oxygen at normocarbia. In terms of the chronotropiceffect, this dose of metoprolol produced a substantial shiftto the right of the dose-response curve to isoprenaline: substantialreductions of arterial pressure (10%), cardiac output (21%),aortic blood acceleration (13%), left ventricular dP/dt max(13%) and left ventricular power (25%) were observed. Both preload,represented by left ventricular end diastolic pressure, andafterload, represented by systemic vascular resistance, increased.Left circumflex coronary blood flow and myocardial oxygen consumptiondecreased by approximately the same amount as peak ventricularpower.     

Effects of sevoflurane and halothane anesthesia on liver circulation and oxygen metabolism in the dog during hepatolobectomy

Purpose Effects of sevoflurane and halothane anesthesia on liver circulation and oxygen metabolism during hepatolobectomy were investigated in the dog, with the aim of choosing a better anesthetic for hepatic resection. Methods Sixteen mongrel dogs were randomly divided into two groups with eight in each. Electromagnetic flowmeters were used to measure hepatic arterial and portal venous blood flows (1) before the inhalation of each anesthetic (base line); (2) 1 h after the start of inhalation of 1.5 minimum alveolar concentration (MAC) anesthetic; (3) 1 h after hepatolobectomy with the same MAC of anesthesia; and (4) 2 h after the discontinuation of anesthesia. Measurements of systemic hemodynamics, blood gas tensions, plasma enzyme leaks and arterial ketone body ratio were made at the same time. Results Sevoflurane maintained hepatic arterial blood flow better than halothane anesthesia, both before and after hepatolobectomy. Hepatic arterial vascular resistance increased in the halothane group but did not change in the sevoflurane group after hepatolobectomy. No significant difference was found in oxygen metabolism and arterial ketone body ratio between two groups. Serum enzyme leakage was less in the sevoflurane group. Conclusion Sevoflurane has less adverse effects on liver circulation, especially hepatic arterial blood flow, and hepatic function than halothane in the case of hepatolobectomy.