Effects of halothane,isoflurane and sevoflurane on ischemiareperfusion injury in the perfused liver of fasted rats

Background : Although intraoperative ischemia-reperfusion of the liver generally occurs under general anesthesia, little is known about the direct effect of anesthetic agents on hepatic injury due to this phenomenon. The effect of volatile anesthetics on ischemia-reperfusion injury was studied using isolated liver perfusion. Methods : The liver was isolated from 24-h-fasted male Sprague-Dawley rats and perfused through the portal vein with a modified Krebs-Ringer bicarbonate solution in a recirculating perfusion-aeration system. Ischemia was induced by reducing the baseline perfusion pressure from 1.2 to 0.2 kPa followed by reperfusion to baseline level. The ischemia-reperfusion injury was assessed by LDH release from the perfused liver. We studied the effect of halothane, isoflurane and sevoflurane on the ischemia-reperfusion injury during 20 min of control conditions, exposure of the liver to 60 min of ischemia and reperfusion for 90 min. Results : Ischemia was evident by reduced portal vein flow and oxygen consumption, and caused an increase in lactate production. Reperfusion caused a transient reduction in lactate production and a significant increase in LDH release. All anesthetics reduced hepatic oxygen consumption and increased the net lactate production during control conditions. Volatile anesthetics also significantly attenuated LDH release during reperfusion. The suppression of LDH release was observed even when isoflurane was administered during the reperfusion period, but not when it was administered only during ischemia. Conclusion : These results indicate that volatile anesthetics may protect the fasted liver from early, neutrophil-independent, ischemia-reperfusion injury by acting during the reperfusion phase.     

Effects of halothane, isoflurane and sevoflurane on calcium-related contraction in porcine coronary arteries

Background: Volatile anaesthetics have a direct inhibitory effect upon epicardial coronary arterial smooth muscles (1–4). The site and mode of their action at the cellular level need to be clarified, which was the purpose of our study. The present investigation attempted to answer the question in what way volatile anaesthetics influence Ca²⁺-related contraction in isolated porcine epicardial coronary to understand their intracellular mechanism. Methods: Isolated helical strips of porcine epicardial coronary artery without endothelium were suspended for isotonic contraction recordings in Krebs-Ringer's solution. 9.4×10^-2 MK+, 2.5×10^-1 M Ca²⁺-induced shortening of the strips was regarded as the reference value (100%). After incubation in Ca²⁺-free solution with 10^-3 M ethlene glycol bis (β-aminoethyl ether)-N, N-tetraacetic acid (EGTA) for 60 minutes, the muscle strips were exposed to increasing Ca²⁺ concentrations (10^-4-10^-2) either in the presence or absence of 1.5 or 2.5 minimum alveolar concentration (MAC) halothane, isoflurane or sevoflurane, with 9.4×10^-2 M K⁺ bath solution. Results: All three drug groups produced apparent biphasic effects with a cumulative increase of Ca²⁺ concentration compared with control groups. An initial increase at low Ca²⁺ concentration was followed by a decrease of Ca²⁺-activated contractions. Isoflurane affected Ca²⁺-induced contraction significantly more than halothane and sevoflurane. Conclusions: The results imply that volatile anaesthetics influence Ca²⁺-dependent activity of coronary smooth muscle by complex mechanisms, which involve promotion of intracellular Ca²⁺ release and other mechanisms that alter sensitivity to calcium.     

Hepatic energy charge and adenine nucleotide status in rats anesthetized with halothane, isoflurane or enflurane

Background: Volatile anesthetics are known to have varying effects on hepatic oxygen supply in vivo and have been shown to depress hepatic mitochondrial respiration and so energy charge in vitro. However, the effect of halothane, isoflurane and enflurane on hepatic adenine nucleotide status in viuo has not been evaluated.
Methods: Ninety male rats were exposed to 40% oxygen (n=22) or 40% oxygen in equipotent (1 MAC) concentrations of halothane (1%) (n=23), isoflurane (1.4%) (n=22) or enflurane (2%) (n=23) for 2 hours. All animals were then administered intraperitoneal pentobarbital and anesthesia continued and laparotomy was performed. A liver biopsy was taken for determination of hepatocellular adenosine-5-triphosphate (ATP), adenosine-5-diphosphate (ADP) and adenosine-5-monophosphate (AMP) and computation of energy charge (EC) from ((ATP+1/2 ADP)+(ATP+ADP+AMP)) and total ade nine nucleotides (TAN) from (ATP+ADP+AMP). After the biopsy the aorta was cannulated for blood sampling.
Results: Rats in each group were similar in weight, as well as acid base and blood gas status just after liver biopsy. Hepatic energy charge, ATP, ADP, AMP, and TAN levels were not different in animals receiving either halothane, isoflurane or enflurane when compared with those receiving only oxygen.
Conclusions: One MAC of anesthesia for a period of 2 hours with the described volatile anesthetic agents did not affect adenine nucleotide status in viuo in rats.     

应用钙离子载体A23187及6-甲基嘌呤对人卵母细胞进行孤雌激活

目的 :观察钙离子载体 A2 3 1 87( Ca-A2 3 1 87)及 6-甲基嘌呤 ( 6-DMAP)对人类卵母细胞的孤雌激活作用。方法 :收集体外受精周期中不适于进行卵胞浆内单精子注射的生发泡期或第一次减数分裂中期的不成熟卵母细胞 2 44个在体外培养成熟 ,其中 1 55个体外成熟卵母细胞按不同激活方案分组 :5μmol/ L Ca-A2 3 1 87组、1 0 μmol/ L Ca-A2 3 1 87组、对照组、6-DMAP组及 Ca-A2 3 1 87+6-DMAP组。激活处理后 1 2～ 1 8h观察第二极体排出及原核形成情况。结果 :5及 1 0 μmol/ L Ca-A2 3 1 87组卵母细胞激活率分别为 40 .7% ( 1 1 / 2 7)和 3 7.1 % ( 1 3 / 3 5) ,较对照组的 9.5% ( 2 / 2 1 )明显增加 ( P<0 .0 1 ) ;6-DMAP组的激活率 ,1 1 .5% ( 3 / 2 6)较 Ca-A2 3 1 87+6-DMAP组 ,58.7% ( 2 7/ 46)明显下降。 Ca-A2 3 1 87激活后卵母细胞主要表现为一原核二极体 ,而 Ca-A2 3 1 87+6-DMAP激活的卵母细胞以一原核一极体占多数 ( 1 9/ 2 7,70 .4% )。结论 :卵母细胞孤雌激活的发生及原核形成类型与激活方案有关 ,单独 Ca-A2 3 1 87或与蛋白激酶抑制剂 6-DMAP联合应用都能使人类卵母细胞发生孤雌激活 ,二者联合应用更易于诱导卵母细胞发生孤雌激活     

Different effects of halothane, isoflurane and sevoflurane on sarcoplasmic reticulum of vascular smooth muscle in dog mesenteric artery

Background: The direct effect of halothane on vascular smooth muscle is mediated in part via its effects on the sarcoplasmic reticulum (SR). Little information is available concerning the effects of other volatile anesthetics including isoflurane and sevoflurane, whose vascular effects differ from those of halothane. The aim of the present study was to compare the effects of halothane, isoflurane and sevoflurane on the SR by testing the contraction induced by caffeine in vascular smooth muscle. Methods: Rings without endothelium from isolated canine mesenteric artery were mounted in physiological saline solution (PSS) for isometric tension recording. After complete depletion of Ca²⁺ from the SR by adding 35 mM caffeine, the rings were exposed to normal Ca²⁺ containing PSS (Ca²⁺ loading), to Ca²⁺-free PSS for 10 min, and then to 15 mM caffeine to induce contraction. Anesthetics were administered during Ca²⁺ loading, the Ca²⁺-free phase and simultaneously with caffeine administration. Results: Halothane (0.5-2%) attenuated the caffeine-induced contraction of canine mesenteric artery when administered during Ca²⁺ loading in the SR (P<0.001), whereas isoflurane and sevoflurane (1–4%) failed to affect the contraction. When given simultaneously with caffeine, halothane (1–2%) potentiated the caffeine-induced contraction (P<0.05), but isoflurane and sevoflurane had no effect. When given before caffeine administration, halothane (0.5-2%), isoflurane (24%) and sevoflurane (4%) all potentiated the caffeine-induced contraction (P<0.05). Conclusion: It has been shown that halothane not only potentiates caffeine- induced Ca²⁺ release from the SR, but also induces contraction by releasing Ca²⁺ from the SR. We conclude that halothane decreases Ca²⁺ accumulation in the SR while exerting facilitative and additive effects on caffeine-induced Ca²⁺ release from the SR when applied before caffeine administration and simultaneously with caffeine, respectively, whereas isoflurane and sevoflurane lack both the ability to decrease Ca²⁺ accumulation and an additive effect on caffeine-induced Ca²⁺ release from the SR, but are able to facilitate Ca²⁺ release by caffeine.     

In vivo effects of halothane, enflurane, and isoflurane on hepatic sinusoidal microcirculation

Background: It has been proposed that halogenated anaesthetics interfere with the endothelium-dependent circulatory control by attenuating the effects of endothelium-derived relaxing factor (EDRF/NO). This study was designed to determine whether or not volatile anaesthetics in vivo influence the microvascular tone in hepatic sinusoids. Methods: Using epifluorescence videomicroscopy, we compared the effects of the volatile anaesthetics halothane, enflurane, and isoflurane on hepatic microcirculation in ventilated Lewis rats. Animals were initially anaesthetized with pentobarbitone (50 mg-kg^-1 i.p.) to allow instrumentation and laparotomy and were randomly allocated to one of 4 groups (n=5–6 each) to receive either a supplementary dose of i.v. pentobarbitone (25 mg kg^-1; control group) or 0.75 MAC halothane, enflurane or isoflurane (1.5 MAC h). Results: Halothane decreased significantly the volumetric blood flow as compared with isoflurane (P < 0.05) or pentobarbitone controls (P < 0.05). The decrease in sinusoidal blood flow caused by halothane was largely attributable to a decrease in sinusoidal diameter (P < 0.05), while red blood cell velocity remained unchanged. Isoflurane led to a significant decrease in sinusoidal width compared with controls (P < 0.05) but an increase in red cell velocity offset the effect of sinusoidal narrowing on volumetric blood flow, while enflurane had no significant effect on any of the measured parameters. Conclusion: This study provides the first direct evidence that the volatile anaesthetics halothane and isoflurane in vivo shift the hepatic microvascular tone toward a more constricted state; however, flow velocity is enhanced with isoflurane, offsetting this effect. As a result the volumetric flow is at least affected by isoflurane, then enflurane and most significantly by halothane. Furthermore, our data are consistent with the concept that volatile anaesthetics in clinically relevant concentrations may influence the balance between endothelium-derived vasoactive factors which control microvascular tone.     

Protective effects of halothane but not isoflurane against global ischaemic injury in the isolated working rat heart

The effects of equi-anaesthetic concentrations of halothane (HAL) and isoflurane (ISO) on myocardial performance, perfusion, oxygenation and lactate release were studied before, during and after a low-flow, global ischaemic insult in isolated, paced rat left heart preparations. An antegrade perfusion technique was used, where left atrial pressure (LAP) and mean aortic pressure (MAP) could be altered independently of each other. Aortic flow, coronary flow (CF) and PO₂ in venous coronary effluent were continuously recorded and stroke volume, myocardial oxygen consumption (MVO₂) and myocardial oxygen extraction as well as lactate release were calculated. The hearts were exposed for at least ten minutes to the perfusate without (control, n=10) or with HAL (n=10) or ISO (n= 10) at a MAP of 80 mmHg (10.4 kPa) and a LAP of 7.5 mmHg (1.0 kPa). After baseline measurements, MAP was reduced to 25 mmHg (3,2 kPa) for a total of nine minutes. Thereafter MAP was increased to 80 mmHg (10.4 kPa) for another nine minute period. During the whole experimental procedure, LAP was maintained at 7.5 mmHg (1.0 kPa) and heart rate at 325 beats per minute. In the pre-ischaemic control period, MVO₂ was lower with HAL compared to ISO (P<0.05) and control (P<0.05). Stroke volume was also lower with HAL compared to control (P<0.05). During hypoperfusion, lactate release was twice as high in the control group (P<0.0I) and with ISO (P<0.01) compared to HAL. This was accompanied by a lower oxygen extraction with HAL compared to control (P<0.05) and ISO (P<0.05). In the post-ischaemic periods, MVO₂ and stroke volume were lower with HAL compared to ISO and control. There were no significant differences in CF between the groups. We conclude that HAL, but not ISO, exerts a direct protective effect against a glycon'c anaerobic metabolism during low-flow global myocardial ischaemia.     

Effects of desflurane, sevoflurane and halothane on postinfarction spontaneous dysrhythmias in dogs

Background: Although desflurane (DES) and sevoflurane (SEV) have desirable features for use in patients with coronary artery disease, their effects on ventricular dysrhythmias following infarction are less known. We therefore examined the effects of DES and SEV upon spontaneous postinfarction ventricular dysrhythmias in dogs, and compared those effects to the well-established antidysrhythmic effects of halothane (HAL) in this model.
Methods : After institutional approval, the left anterior descending coronary artery was ligated in 16 adult mongrel dogs during isoflurane anesthesia. All dogs developed acute myocardial infarction and severe ventricular tachydysrhythmias. Twenty-two hours after infarction, dogs were anesthetized at 1.5 MAC with desflurane (10.8%) followed by sevoflurane (3.5%) in the treatment group (n=10), or halothane (1.3%) in the other group (n=6). Anesthetic gases were allowed to equilibrate for at least 20 min at each end-tidal concentration. At this time, the ECG was recorded for 9 min and evaluated for the number of ventricular ectopic and sinoatrial beats and summed duration of ventricular tachycardia.
Results: DES and SEV reduced the average rate of total ventricular ectopic beats by 40 ±4% and 42 ±4%, respectively. HAL decreased total ventricular ectopic rate by 59 ±6% and 62 ±5% after durations of anesthesia comparable to DES and SEV, respectively. Decreases in dysrhythmia in the presence of DES and SEV were significantly smaller than those produced by HAL after a comparable total duration of anesthesia.
Conclusions: DES and SEV inhibit spontaneous postinfarction ventricular dysrhythmias, although attenuation of dysrhythmias was smaller than the inhibition during comparable doses of HAL.     

Effects of halothane, isoflurane, and sevoflurane on lipid peroxidation following experimental closed head trauma in rats

Background: In a rat closed head trauma model we examined both the time course of lipid peroxidation and the effects of halothane, isoflurane, and sevoflurane on it by analysis of malondialdehyde (MDA) formation.
Methods: Animals were divided randomly into five groups: sham-operated (SO), n =18; control-closed head trauma to left frontal pole, n =18; closed head trauma model+halothane, n =18; closed head trauma model+isoflurane, n =18; and closed head trauma model+sevoflurane, n =18. Halothane, isoflurane, or sevoflurane were applied 15 min after trauma for 30 min. Rats were euthanized 1,3, and 5 h after the inhalation agents. Brain tissue samples were taken 5 mm from the left and right frontal poles. MDA was considered to reflect the degree of lipid peroxidation.
Results: MDA concentrations were greater in the control, halothane, sevoflurane, and isoflurane groups than in SO animals ( P <0.001). No statistical difference between the hemispheres was found between the halothane, isoflurane, or sevoflurane groups, but MDA levels were lower with isoflurane than in the halothane, sevoflurane, and control groups at 1, 3, and 5 h ( P <0.001). MDA levels were higher as compared with the halothane and sevoflurane groups at 1 h but not at 3 or 5 h ( P <0.001).
Conclusion: MDA levels with the isoflurane group were lower than in the other trauma groups, which suggest that isoflurane, given after closed head trauma, might be protective against lipid peroxidation of cerebral injury.     

The influence of halothane, isoflurane and sevoflurane on rocuronium infusion in children

BACKGROUND: Rocuronium is a non-depolarizing neuromuscular blocking agent with intermediate duration of action and without significant cumulative properties, suitable for continuous infusion. This study was designed to determine the infusion requirements in children under nitrous oxide and fentanyl, halothane, isoflurane or sevoflurane anaesthesia. METHODS: Forty children, 3-11 years old, ASA physical status group I or II were studied. They were randomly allocated to receive fentanyl-nitrous oxide, 1 MAC halothane-nitrous oxide, 1 MAC isoflurane-nitrous oxide or 1 MAC sevoflurane-nitrous oxide anaesthesia. Rocuronium, 0.6 mg(-1) was used to facilitate endotracheal intubation. Electromyographic response of adductor pollicis to train-of-four (TOF) stimulation, 2 Hz for 2 s, applied to the ulnar nerve at 10-s intervals was recorded using Relaxograph (Datex, Helsinki, Finland). Once the first twitch response (T1) returned to 5%, muscle relaxation was maintained by continuous infusion of rocuronium, adjusted automatically in a closed-loop system to maintain a stable 90-99% T1 depression. The block was considered stable if it changed by no more than 2% over a 10-min observation period. RESULTS: Halothane, isoflurane and sevoflurane groups had ower infusion requirements than the fentanyl-nitrous oxide group (P<0.00075). Rocuronium requirement (mean +/- SD) at one hour from the commencement of anaesthesia was 16.7+/-2.3, 13.6+/-3.7, 13.1+/-5.1 and 8.4+/-1.6 microg x kg(-1) x min(-1) for children receiving fentanyl-nitrous oxide, halothane, isoflurane and sevoflurane anaesthesia, respectively. CONCLUSIONS: The rocuronium infusion rate required to maintain stable 90-99% T1 depression was reduced by approximately 20% with halothane and isoflurane anaesthesia, and by 50% with evoflurane anaesthesia when compared to fentanyl-nitrous oxide anaesthesia. Significant patient-to-patient variability of infusion rate makes monitoring of neuromuscular transmission necessary.     

Effects of sevoflurane and isoflurane anesthesia on arterial ketone body ratio and liver function

BACKGROUND: The purpose of this study was to compare the effect on arterial ketone body ratio (AKBR), which indicates hepatic mitochondrial energy charge in relation to hepatic blood flow, and liver function test (serum levels of liver enzymes) between sevoflurane and isoflurane anesthesia. METHODS: Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (TBil), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GTP), and lactate dehydrogenase (LDH) were measured before and 1,2,3,7, and 14 days after anesthesia in each of 60 patients receiving either sevoflurane or isoflurane anesthesia for neurosurgery (tumor resection). In 13 patients of both groups, arterial concentrations of acetoacetate and 3-hydroxybutyrate were also measured before, during and after (up to 12 h) anesthesia and the AKBR was calculated. RESULTS: AST, ALT and GTP increased, peaking 7 days after anesthesia, especially in the isoflurane group. There was a significantly greater number of patients with abnormal AST and ALT values in the isoflurane group than in the sevoflurane group. The increase of TBil had its peak 1 day after anesthesia in both groups. AKBR decreased after anesthesia induction and recovered to the control value 12 h after anesthesia in both groups. There was no difference between the two anesthetic groups in AKBR. CONCLUSION: Isoflurane induced an elevation of serum levels of liver enzymes more frequently than did sevoflurane 3 to 14 days after anesthesia, while AKBR until 12 h after anesthesia did not show any significant difference between sevoflurane and isoflurane anesthesia.     

Comparison of isoflurane and halothane on recovery from neuromuscular blockade using atracurium in infants with hepatic dysfunction undergoing major abdominal surgery

The effects of either isoflurane or halothane on recovery from neuromuscular blockade with atracurium in infants with hepatic dysfunction undergoing major abdominal surgery were studied. Neuromuscular blockade was assessed visually at minute intervals by 'train-of-four' using supra-maximal stimuli. The times to first and second increment and total requirement of atracurium in two groups of infants randomly allocated to receive either isoflurane or halothane for induction and supplementation were recorded. Fourteen patients completed the study, seven with isoflurane and seven with halothane. No evidence was found that recovery from neuromuscular blockade with atracurium was prolonged by isoflurane as compared to halothane.     

Effects of volatile anesthetics on cardiac metabolism in the low-pressure perfused rat heart

Effects of halothane, enflurane and isoflurane on the myocardial metabolism were studied in the rat heart-lung preparation. Hearts were perfused at a low perfusion pressure (SBP 50mmHg, DBP 30mmHg) with succinate or glutamate as substrates. Thirty minutes after the perfusion, intramyocardial ATP, pyruvate, lactate and glycogen were measured enzymatically. Although there was no significant difference in ATP levels of hearts with either substrate, and whether or not volatile anesthetics were present, 1% halothane and 1.5% isoflurane reduced the L/P ratio when succinate was substrate (24.46 ± 4.81, 17.68 ± 9.10 vs 39.82 ± 10.83), and 2% enflurane decreased it when glutamate was substrate (22.25 ± 10.99 vs 38.44 ± 6.55). The glycogen levels in volatile anesthetics groups were lower than control when succinate was substrate. The improvement of energy demand-supply balance by inhalation anesthetics may be stronger than their inhibition of electron transport in mitochondria under certain ischemic conditions.(Kashimoto S, Hinohara S, Kumazawa T: Effects of volatile anesthetics on cardiac metabolism in the low-pressure perfused rat heart. J Anesth 2: 12–16, 1988)     

Dose effect of sevoflurane and isoflurane anesthetics on cortical blood flow during controlled hypotension in the pig

BACKGROUND: The ability of the brain to preserve adequate cerebral blood flow (CBF) during alterations in systemic perfusion pressure is of fundamental importance. At increasing concentrations, isoflurane and sevoflurane have been known to alter CBF, which may be disadvantageous for patients with increased intracranial pressure. The aim was to examine the effects of isoflurane and sevoflurane at increasing minimum alveolar concentrations (MAC) on CBF, during controlled hypotension. METHODS: We studied eight pigs during variations in perfusion pressure induced by caval block (100, 60, 50, and 40 mmHg) under normocapnia. CBF was measured locally in a defined area (4 x 5 measurement points covering 1 cm(2)) of the motor cortex using laser Doppler perfusion imaging. Physiological variables, assessed by analysis of arterial O(2) and CO(2), hemoglobin and hematocrit, were controlled. CBF was measured during propofol (10 mg x kg(-1)x h(-1)) and fentanyl (0.002 mg x kg(-1)x h(-1)) anesthesia, and then during anesthesia with either isoflurane or sevoflurane (given in random order) at increasing MAC (0.3-1.2). After a washout period, the measurements were repeated with the other gas. RESULTS: CBF was significantly higher in the cortex during normotensive (control) settings, MAP approximately 100 mmHg, compared with during hypotension (MAP 40-60 mmHg). Neither different anesthetic nor MAC or local measurement sites were found to influence CBF at any perfusion pressure. CONCLUSION: In this experimental model, the effect of hypotension on CBF was not altered by the anesthetics used [isoflurane, sevoflurane (MAC 0.3-1.2) or propofol (10 mg x kg(-1)x h(-1))]. In this aspect (cortical tissue perspective), these volatile agents appear as suitable as propofol for neurosurgical anesthesia for patients at risk.     

The effects of prolonged isoflurane anaesthesia on cerebral blood flow and metabolism in the dog

To determine whether cerebral blood flow (CBF) changed with time under isoflurane anaesthesia, as has been reported for halothane, CBF and cerebral metabolic rate for oxygen (CMRO2) were studied in five dogs under prolonged isoflurane anaesthesia. CBF was measured with a modified sagittal sinus technique and CMRO2 was calculated as the product of CBF and the arteriovenous O2 difference. Maintaining this experimental dog model with 1% isoflurane in oxygen and nitrogen for 3 h in five dogs and for 4 h in three dogs did not cause any significant changes in CMRO2 or CBF. Cerebral metabolite levels were consistent with earlier reports from short-time studies and the EEG recordings showed a continuous sleep pattern with no pathological changes. It is concluded that there is no change in CBF or CMRO2 in our modified sagittal outflow model during 3-4 h of 1% isoflurane anaesthesia.     

Effects of hypoxia and isoflurane on liver blood flow: the role of adenosine

We investigated the role of endogenous adenosine in mediatingthe effects of hypoxia and isoflurane on portal tributary bloodflow (PTBF) and hepatic arterial blood flow (HABF) in rats.Liver blood flows were determined using radiolabelled microspheres.Hypoxia resulting from the exposure of rats to an atmospherecontaining 15% oxygen for 30 min decreased PTBF (23%) (P<0.05)and cardiac index (15%) (P<0.05), and increased HABF (78%)(P<0.05). Isoflurane (1.4 vol%) increased HABF in both normoxicand hypoxic conditions but did not affect PTBF. The adenosinereceptor antagonist 8-phenyltheophylline attenuated the hypoxia-inducedincrease in HABF but did not affect that resulting from theadministration of isoflurane. In conclusion, in contrast tothe increase in HABF induced by hypoxia, that induced by isofluraneappears to be independent of endogenous adenosine. Br J Anaesth 2000; 86: 425–7     

Effects of ketamine on liver blood flow and hepatic oxygen consumption. Studies in the anaesthetised greyhound

The effects of three increasing doses of ketamine on the blood flow to, and oxygen consumption of, the liver, were studied in seven anaesthetised greyhounds. Hepatic arterial and portal venous blood flows were measured continuously using electromagnetic flow probes, and mean arterial pressure and cardiac output monitored as appropriate. Ketamine, even at the highest dose, had little effect on the blood flow to the liver: hepatic arterial blood flow and portal venous blood flow did not differ significantly from their baseline values. However, the oxygen delivery to the liver decreased due, probably, to an increase in oxygen consumption by the pre-portal organs.     

The effects of halothane and isoflurane on hand blood flow in children. (As determined by venous occlusion plethysmography)

The effects of increasing concentrations of halothane and isoflurane were studied in two groups of twenty children aged from 2.9 to 9.8 years using the technique of water filled venous occlusion plethysmography. Halothane significantly increased hand blood flow and reduced vascular resistance only at a concentration of 0.5 MAC. However, isoflurane caused significant dose related increases in hand blood flow and reductions in hand vascular resistance at 0.5, 1.0 and 1.5 MAC. These findings suggest that in children isoflurane has a more potent vasodilator effect on the skin circulation than halothane.     

Effects of cholecalciferol and calcium on experimental hepatic osteodystrophy in rats

To investigate cholecalciferol (vitamin D) metabolism disorders in hepatic osteodystrophy (HOD) and the effects of vitamin D, its metabolites, and calcium (Ca) on HOD, an experimental HOD model in rats was developed using carbon tetrachloride. In the serum level of 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, and 24R,25-dihydroxycholecalciferol, there were no significant differences between normal and control cirrhotic rats. Vitamin D supplementation significantly inhibited the atrophy of intestinal villi, reduction of bone calcium content, elevation of bone resorption, reduction of osteoid volume, and reduction of bone volume. Ca supplementation significantly increased the serum free Ca index and inhibited the elevation of bone resorption, the reduction of bone ash and Ca content, and the reduction of bone volume. This experimental study demonstrates that: (1) no marked vitamin D hydroxylation disorder was found in HOD; (2) vitamin D supplementation was effective in inhibiting HOD; and (3) sufficient Ca supplementation was also effective in inhibiting HOD.A portion of this work was presented at the 13th Annual Meeting of the Japanese Society for Bone and Mineral Research, July 1995, Fukuoka, Japan.     

Effects of halothane and isoflurane on left ventricular diastolic function during surgical stress in patients with coronary artery disease

Background: The effects of inhalation anesthetics on left ventricular (LV) systolic function are well documented, while the effects of these agents on LV diastolic function have mainly been evaluated in animal studies, with conflicting results.
Methods: We investigated the effects of halothane and isoflurane, when used to control the stress response to sternotomy in 33 patients with coronary artery disease (CAD). LV early diastolic relaxation and end-diastolic stiffness were evaluated from mitral Doppler flow profiles, transesophageal two-dimensional echocardiography, and central hemodynamic measurements. Measurements were performed a) after induction of anesthesia, b) after volume loading, c) prior to surgery and d) during surgery, 10 min after introduction of the inhalation anesthetic. The effects of the anesthetics on Doppler indices reflecting early diastolic relaxation, and on the left ventricular end-diastolic pressure-area (LVED P/A) relationship, were studied.
Results: When data obtained during surgical stress were compared to the control situation, we found an increase in the LV filling pressures in both groups, while only the isoflurane group showed an increase in heart rate. An increase in end-systolic LV area and decreased fractional area change was present in the halothane group, while an increase in LV end-diastolic area, and similar changes in the mitral Doppler indices (decreases of deceleration rate and time of early diastolic filling), indicating an impairment of early diastolic relaxation, was present in both groups. Isoflurane induced a displacement of the LVED P/A relationship leftwards from the baseline LVED P/A curve.
Conclusion: Both halothane and isoflurane impair early diastolic relaxation in patients with CAD, when used to control intraoperative surgical stress. In contrast to halothane, isoflurane induced a change in the LVED P/A relationship, suggestive of an increased LVED stiffness.