Effects of enflurane, isoflurane, sevoflurane and desflurane on reperfusion injury after regional myocardial ischaemia in the rabbit heart in vivo

It is known that volatile anaesthetics protect myocardial tissue against ischaemic and reperfusion injury in vitro. In this investigation, we have determined the effects of the inhalation anaesthetics, enflurane, isoflurane, sevoflurane and desflurane, administered only during early reperfusion, on myocardial reperfusion injury in vivo. Fifty chloralose-anaesthetized rabbits were subjected to 30 min of occlusion of a major coronary artery followed by 120 min of reperfusion. Left ventricular pressure (LVP, tip-manometer), cardiac output (CO, ultrasonic flow probe) and infarct size (triphenyltetrazolium staining) were determined. During the first 15 min of reperfusion, five groups of 10 rabbits each received 1 MAC of enflurane (enflurane group), isoflurane (isoflurane group), sevoflurane (sevoflurane group) or desflurane (desflurane group), and 10 rabbits served as untreated controls (control group). Haemodynamic baseline values were similar between groups (mean LVP 106 (SEM 2) mm Hg; CO 281(7) ml min-1). During coronary occlusion, LVP and CO were reduced to the same extent in all groups (LVP 89% of baseline; CO 89%). Administration of inhalation anaesthetics during early reperfusion further reduced both variables, but they recovered after discontinuation of the anaesthetics to values not different from control animals. Infarct size was reduced from 49 (5)% of the area at risk in the control group to 32 (3)% in the desflurane group (P = 0.021), and to 36 (2)% in the sevoflurane group (P = 0.097). In the enflurane group, infarct size was 39 (5)% (P = 0.272). Isoflurane had no effect on infarct size (48 (5)%, P = 1.000). The results show that desflurane and sevoflurane markedly reduced infarct size and therefore can protect myocardium against reperfusion injury in vivo. Enflurane had only a marginal effect and isoflurane offered no protection against reperfusion injury in vivo. These different effects suggest different protective mechanisms at the cellular level.      

Effects of ischaemia and reperfusion on vasoactive neuropeptide levels in the canine infrarenal aortic revascularization model

Infrarenal aortic cross-clamping is associated with remote vascular events, including myocardial infarction and renal insufficiency. The purpose of this study was to determine whether hindlimb ischaemia and reperfusion associated with infrarenal aortic cross-clamping results in the production of vasoactive regulatory neuropeptides. A canine model of infrarenal aortic cross-clamping was used for the study. Serial blood samples were drawn, prior to, at the time of, and serially following placement of the clamp and subsequent release of the clamp and reperfusion. Ischaemia resulted in increased mean (s.e.m.) plasma levels of neuropeptide Y (NPY) (initial 10.0(1.8) pmol/l versus ischaemia 24.7(2.3) pmol/l, P<0.001) and vasoactive intestinal polypeptide (VIP) (initial 2.53(0.5) pmol/l versus ischaemia, 7.3(1.3) pmol/l, P<0.05). Reperfusion produced three-fold elevation of VIP (initial 2.5(0.5) pmol/l versus reperfusion 9.6(1.5) pmol/l, P<0.001), two-fold elevation in the plasma levels of endothelin-1 (initial 1.3(0.1) pmol/l versus reperfusion maximum 2.5(0.3) pmol/l, P<0.01) and NPY (initial 10.0(0.8) pmol/l versus reperfusion maximum 23.9(2.3) pmol/l, P<0.001). Ischaemia and reperfusion did not alter calcitonin gene-related peptide (CGRP) (a potent vasodilator) levels. Endothelin-1 (ET-1) plasma levels were also increased following haemorrhagic shock (initial 1.3(0.1) pmol/l versus exsanguination 3.4(0.4) pmol/l, P<0.001), but not during ischaemia (initial 1.3(0.1) pmol/l versus ischaemia maximum 1.7(0.2) pmol/l, P=0.7). It was concluded that vasoactive regulatory peptides are released following ischaemia, reperfusion and shock in the canine infrarenal aortic revascularization model and, therefore could contribute to remote vascular events observed with infrarenal aortic cross-clamping. Copyright © 1996 The International Society for Cardiovascular Surgery.     

Effects of isoflurane on myocardial metabolism during postischaemic reperfusion in the rat

In experiments on isolated rat heart lung preparation, the effects of isoflurane on myocardial metabolism during postischaemic reperfusion were evaluated with intramyocardial high energy phosphates, lactate and glycogen. Hearts were perfused for 10 min initially and made globally ischaemic for 8 min in ischaemic groups. Afterwards, they were reperfused for 12 min. Isoflurane was administered from 5 min after the start of perfusion to the end of reperfusion. There was no significant difference in myocardial lactate levels between ischaemic isoflurane and control groups. However, the ATP level in the hearts in the ischaemic isoflurane group was significantly higher than that in the ischaemic control group (17.96 +/- 1.31 vs 15.50 +/- 0.87; P less than 0.005). The administration of isoflurane to the isolated rat heart during pre- and post-ischaemia enhanced metabolic recovery in the postischaemic state.     

Halothane reduces reperfusion injury after regional ischaemia in the rabbit heart in vivo

In addition to having anti-ischaemic effects, halothane can protect isolated rat hearts and isolated cardiomyocytes against reperfusion injury of the "oxygen paradox" type. The aim of this study was to investigate if halothane can also protect against myocardial reperfusion injury in vivo. Twenty-two rabbits anaesthetized with alpha- chloralose underwent 30 min of occlusion of a major coronary artery and 2 h of subsequent reperfusion. Seven animals received 1 MAC of halothane for the first 15 min of reperfusion (halothane group), and eight animals served as untreated controls (controls group). In seven additional animals, the haemodynamic effects of halothane were antagonized by an i.v. infusion of noradrenaline (halothane- noradrenaline group). We measured cardiac output (CO) by an ultrasonic flow probe around the ascending aorta, left ventricular pressure (LVP) by a tip manometer and infarct size by triphenyltetrazolium staining. Baseline LVP was mean 92 (SEM 4) mm Hg and CO was 289 (16) ml min-1. During coronary occlusion, LVP was reduced to 86 (4)% of baseline and CO to 84 (4)% (similar in all groups). During halothane administration at reperfusion, LVP declined further to 55 (6)% of baseline and CO to 66 (9)% (P < 0.05 halothane group vs control group). Noradrenaline prevented the reduction in LVP (halothane-noradrenaline group 87 (5)% of baseline, control group 84 (6)% and reduction in CO (halothane- noradrenaline group 89 (5)%, control group 83 (6)%. Infarct size was 49 (6)% of the area at risk in controls and was reduced markedly by administration of halothane to 32 (3)% in the halothane group (P < 0.05) and to 30 (3)% in the halothane-noradrenaline group (P < 0.05). Treatment with halothane during the early reperfusion period after myocardial ischaemia protected the myocardium against infarction in vivo, independent of the haemodynamic effect of halothane.      

Xenon and isoflurane improved biventricular function during right ventricular ischemia and reperfusion

Background: Although anesthetics have some cardioprotective properties, these benefits are often counterbalanced by their negative inotropic effects. Xenon, on the other hand, does not influence myocardial contractility. Thus, xenon may be a superior treatment for the maintenance of global hemodynamics, especially during right ventricular ischemia, which is generally characterized by a high acute complication rate. Methods: The effects of 70 vol% xenon and 0.9 vol% isoflurane on biventricular function were assessed in a porcine model (n=36) using the conductance catheter technique, and the expression of the type B natriuretic peptide (BNP) gene was measured. The animals underwent 90 min of right ventricular ischemia followed by 120 min of reperfusion. A barbiturate‐anesthetized group was included as a control. Results: Cardiac output was compromised in unprotected animals during ischemia by 33±18% and during reperfusion by 53±17%. This was mainly due to impaired contractility in the left ventricle (LV) and increased stiffness. Isoflurane attenuated the increase in stiffness and resulted in a higher preload. In contrast, xenon increased the right ventricular afterload, which was compensated by an increase in contractility. Its effects on diastolic function were less pronounced. Upregulation of BNP mRNA expression was impeded in the remote area of the LV by both isoflurane and xenon. Conclusions: Xenon and isoflurane demonstrated equipotent effects in preventing the hemodynamic compromise that is induced by right ventricular ischemia and reperfusion, although they acted through somewhat differential inotropic and vasodilatory effects.     

Effect of propofol on reperfusion injury after regional ischaemia in the isolated rat heart

Free oxygen radicals and intracellular calcium homeostasis play important roles in the development of myocardial reperfusion injury. Propofol is a radical scavenger with calcium channel blocking properties. We have investigated the effects of propofol on myocardial reperfusion injury. We used an isolated rat heart model where heart rate, ventricular volume and perfusion pressure were constant. The left anterior descending coronary artery (LAD) was occluded for 30 min and reperfused for 2 h. We studied an untreated control group, an Intralipid group (1 microliter ml-1) and a propofol group (Intralipid 1 microliter ml-1 and propofol 1 microgram ml-1) (n = 12 each). Drugs were infused for 20 min starting 5 min before reperfusion. We measured left ventricular developed pressure (LVDP), coronary flow and infarct size. LAD occlusion reduced mean LVDP from 129 (SEM 4) to 36 (3) mm Hg and mean coronary flow from 12.2 (0.3) to 5.2 (0.2) ml min-1. During reperfusion, LVDP recovered to 98 (4) mm Hg and coronary flow to 11.9 (0.4) ml min-1. Haemodynamic variables were similar in all groups. Propofol had no effect on infarct size compared with the Intralipid group (25.0 (3.7) vs 26.9 (3.3)% of the area at risk; P = 0.89). Infarct size in the Intralipid group tended to be smaller compared with the control group (34.8 (3.2)%; P = 0.19). We conclude that propofol, at a clinically relevant concentration, provided no protective effect against myocardial reperfusion injury in the rat heart in vitro.      

Haemodynamic instability and myocardial ischaemia during carotid endarterectomy: A comparison of propofol and isoflurane

The purpose of this study was to compare two anaesthetic protocols for haemodynamic instability (heart rate (HR) or mean arterial pressure (MAP) <80 or > 120% of ward baseline values) measured at one-minute intervals during carotid endarterectomy (CEA). One group received propofol/alfentanil (Group Prop; n = 14) and the other isoflurane I alfentanil (Group Iso; n = 13). Periods of haemodynamic instability were correlated to episodes of myocardial ischaemia as assessed by Holler monitoring (begun the evening before surgery and ceasing the morning of the first postoperative day). In Group Prop, anaesthesia was induced with alfentanil 30 μg · kg^?1 rv, propofol up to 1.5 mg · kg^?1 and vecuronium 0.15 mg · kg^?1, and maintained with infusions of propofol at 3–12 mg · kg^?1· hr^?1 and alfentanil at 30 μg · kg^?1 · hr^?1. In Group Iso, anaesthesia was induced with alfentanil and vecuronium as above, thiopentone up to 4 mg · kg^?1 and maintained with isoflurane and alfentanil infusion. Phenylephrine was infused to support MAP at 110 ± 10% of ward values during cross-clamp of the internal carotid artery (ICA) in both groups. Emergence hypertension and/or tachycardia was treated with labetalol, diazoxide or propranolol. Myocardial ischaemia was defined as ST-segment depression of >-1 mm (60 msec past the J-point) persisting for >-one minute. For the entire anaesthetic course (induction to post-emergence), there was no difference between groups for either duration or magnitude outside the <80 or >120% range for HR or MAP. However, when the period of emergence from anaesthesia (reversal of neuromuscular blockade to post-extubation) was assessed, more patients were hypertensive (P = 0.004) and required vasodilator therapy in Group Iso (10/ 13 vs 5/14; P = 0.038 Fisher’s Exact Test). The mean dose of labetalol was greater in Group Iso (P = 0.035). No patient demonstrated myocardial ischaemia during ICA cross-clamp. On emergence, 6/13 patients in Group Iso demonstrated myocardial ischaemia compared with 1/14 in Group Prop (P = 0.029). Therefore, supporting the blood pressure with phenylephrine, during the period of ICA cross-clamping, appears to be safe as we did not observe any myocardial ischaemia at this time. During emergence from anaesthesia, haemodynamic instability was associated with myocardial ischaemia. Under these specific experimental conditions, with emergence, hypertension and myocardial ischaemia were more prevalent with more frequent pharmacological interventions in patients receiving isoflurane.     

Repeated episodes of myocardial ischaemia during combined thoracic epidural – isoflurane anaesthesia

A patient with a history of coronary artery disease developed new ST segment depressions in the ECG registration during a low dose (0.7%) isoflurane anaesthesia that was combined with a continuous thoracic epidural analgesia. Simultaneously a small decrease in mean arterial blood pressure (MAP) was noted. During the next 5 min these changes were followed by a severe drop in MAP (from 88 to 60 mmHg) and in cardiac output from 5.5 to 3.2 L/min. When isoflurane was discontinued both the ECG and the cardiovascular changes returned to the previous condition. Later, when 0.5% isoflurane was restarted, the ECG changes reappeared within ten min, but disappeared once again when isoflurane administration was discontinued. Thus, this patient had repeated episodes of myocardial ischaemia which were associated with the use of low dose isoflurane. Although isoflurane–induced "coronary steal" may appear as a likely cause of these ischaemic episodes, it is possible that the thoracic epidural had synergistic action and rendered the patient exceptionally sensitive to minor changes in perfusion pressure.     

Modulation of the NO pathway during short or prolonged blood reperfusion following ischaemia in a heterotopic rat heart transplantation model

Ischemia-reperfusion injury plays a major role in graft dysfunction following transplantation. Extensive research has demonstrated that nitric oxide (NO) plays a fundamental role to protect the heart against this injury. Consequently, we quantified NO synthase (NOS) isoform protein levels in a rat heart transplant model during short and prolonged reperfusion following ischemia. Experiments were performed using a modified Lewis to Lewis heterotopic abdominal heart transplantation with a total ischemic time of 3 hours followed by 1 or 24 hours of blood reperfusion (n = 12). Heart function, as represented by the rate pressure product, increased from 7912 +/- 489 to 27067 +/- 9982 mm Hg/min (mean +/- SEM, short vs prolonged reperfusion, P = .0027). NOS isoform protein levels determined using Western blotting of freeze-clamped hearts were compared to baseline values. eNOS protein levels were significantly lower during short reperfusion compared to the basal value (P = .0077) or to prolonged reperfusion (P = .004), returning to the basal value after 24 hours of reflow. iNOS protein was not detected in the basal condition or after 1 hour of reflow, but was present after 24 hours of reflow (P = .0001 vs basal value and 1-hour reflow). nNOS protein was 69% lower after 1 hour of reflow compared with the baseline value (P = .0001), it was not restored after 24 hours of reflow (P = .002). These results suggest involvement of the NO pathway in ischemia-reperfusion injury with distinctive roles of NOS isoforms during short and prolonged reperfusion following ischemia.     

Isoprostanes--markers of ischaemia reperfusion injury

Ischaemia reperfusion injury is a common and important phenomenon that occurs predictably in patients undergoing such procedures as cardiopulmonary bypass, thrombolysis, surgery under tourniquet, organ transplantation or embolectomy. Oxidative stress and the resulting lipid peroxidation play a major role in reperfusion injury. Membrane and cellular dysfunction result and, subsequently, organ injury or failure may ensue. Traditional methods of quantifying ischaemia reperfusion injury, including measurement of malondialdehyde, lack specificity and sensitivity. It was reported in 1990 that isoprostanes, a series of prostaglandin-like compounds, are produced by the free radical-catalyzed peroxidation of arachidonic acid. Measurement of the isoprostane concentration in urine or plasma provides the most reliable, non-invasive method currently available to assess oxidative stress in vivo. Serial measurement of isoprostanes in biological fluids has enhanced our understanding of the mechanisms underlying ischaemia reperfusion injury itself and its role in certain diseases. Furthermore, measurement of the isoprostane concentration provides a means to assess the effects of prophylactic and therapeutic interventions. In the future, the development of rapid, simple assays for isoprostanes offers the potential to assess prognosis during and after ischaemia reperfusion events.     

Protective effect of liraglutide on experimental testicular ischaemia reperfusion in rats

This study was performed to evaluate the effect of liraglutide on experimental testicular ischaemia reperfusion in rats in terms of biochemistry, histopathology and immunohistochemistry. A total of 28 male Wistar-Albino rats were divided randomly into 4 groups: control (7), sham (7), ischaemia-reperfusion (7) and ischaemia-reperfusion + liraglutide (7). Biochemically, Nitric Oxide, Malondialdehyde, Superoxide dismutase, Glutathione peroxidase and Catalase levels were measured in the testis. Apoptosis protease activating factor-1 and inducible nitric oxide synthase activity were evaluated immunohistochemically as well. Statistical analyses were made via the Kruskal–Wallis and Mann–Whitney U tests. In the reperfusion group, CAT and SOD values were increased (p > .05), NO and MDA values were decreased (p < .05) after administration of liraglutide. In addition, GPx values were significantly increased in ischaemia reperfusion + liraglutide administered group compared to reperfusion group (p < .05). Apaf-1 and iNOS activity were significantly decreased with the addition of liraglutide treatment to the ischaemia-reperfusion group (p < .05). First of all, we would like to say that liraglutide treatment is moderately preventive against I/R injury in testicular torsion. The anti-inflammatory, antioxidant and antiapoptotic properties of liraglutide are create a moderately protective effect as we show in this study.     

The effect of ketamine on acute muscular ischaemia reperfusion in rats

BACKGROUND AND OBJECTIVE: The aim of this study was to investigate any possible protective effect of ketamine in acute muscular ischaemia and reperfusion injury by measuring malondialdehyde using thiobarbituric acid assay in rats. METHODS: Twelve female Wistar albino rats were anaesthetized with chloral hydrate and randomly assigned into two groups to receive ketamine 1 mg kg(-1) min(-1) or saline infusion. Blood and gastrocnemius muscle samples were obtained 10 min after onset of infusion, before ischaemia. Then, femoral arteries were clamped for 30 min. Blood and muscle samples were obtained at the 30th minute of ischaemia and 10 min after reperfusion. RESULTS: Muscle malondialdehyde concentrations were 27.88 +/- 2.45, 27.62 +/- 3.98 before ischaemia, 32.10 +/- 4.19, 30.77 +/- 2.73 in the 30th minute of ischaemia and 44.34 +/- 2.45, 34.83 +/- 2.78 after reperfusion in saline and ketamine-treated rats, respectively (nmol g(-1), mean +/- SD). The muscle malondialdehyde level after reperfusion was lower in ketamine-treated rats compared to saline group (P < 0.002). Plasma malondialdehyde levels were 3.77 +/- 0.16, 3.78 +/- 0.18 before ischaemia, 3.81 +/- 0.25, 4.00 +/- 0.86 at the 30th minute of ischaemia and 4.00 +/- 0.53, 3.94 +/- 0.95 after reperfusion, respectively, in saline and ketamine-treated rats (micromol L(-1), mean +/- SD). The effect of ketamine on muscular malondialdehyde was not observed in concurrent plasma malondialdehyde levels. CONCLUSION: Ketamine was found to attenuate acute ischaemia-reperfusion injury in muscle tissue in rats (muscular protective). Ketamine may attenuate lipid peroxidation in muscle tissue in tourniquet-requiring manoeuvres.     

Experimental study of the effect of intraportal prostaglandin E1 on hepatic blood flow during reperfusion after ischaemia and hepatectomy.

BACKGROUND: Prostaglandin E1 (PGE1) has protective effects experimentally and clinically in individual models of hepatic ischaemia-reperfusion injury and of partial hepatectomy. The present study investigated the effects of intraportal administration of PGE1 on hepatic blood flow, systemic arterial pressure and long-term animal survival after 60 min of total liver ischaemia followed by 70 per cent partial hepatectomy in rats. METHODS: Total liver ischaemia was induced by occluding the hepatoduodenal ligament for 60 min. PGE1 0.5 microg per kg per min was infused intraportally for 15 min before inducing ischaemia and for 120 min after ischaemia in the treatment group. Normal saline was infused in the control group. During ischaemia 70 per cent partial hepatectomy was performed. Portal venous flow (PVF), peripheral tissue blood flow (PTBF) and hepatic artery flow were measured before and after ischaemia. Serum biochemical analysis was carried out at 1, 3 and 24 h, and 7 and 14 days; and liver histology at 1 and 24 h, and 7 days after reperfusion. Survival was followed for 1 year. RESULTS: Intraportal infusion of PGE1 significantly improved PVF and PTBF without affecting the systemic arterial pressure. Long-term survival was significantly higher in the PGE1 group. Serum aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase levels decreased significantly, and 2-h bile flow was significantly improved, in the PGE1 group. Histological examination revealed significant portal venous congestion, sinusoidal congestion, fatty degeneration and tissue necrosis 24 h and 7 days after reperfusion in the control group. CONCLUSION: PGE1 has a protective effect against liver damage when the liver is injured by warm ischaemia and reperfusion followed by partial resection.     

Large concentrations of nitrous oxide decrease the isoflurane minimum alveolar concentration sparing effect of morphine in the rat

Many adjuvant drugs have demonstrated anesthetic-sparing properties when combined with volatile anesthetics. Nitrous oxide is combined with volatile anesthetics to reduce the concentrations of volatile anesthetics required to produce anesthesia. Analgesic doses of opioids clearly reduce the requirement for inhaled anesthetics in both human patients and experimental animals. We performed this study to determine whether the combination of nitrous oxide and morphine decreased isoflurane minimum alveolar anesthetic concentration (MAC) even further in the rat. Fifty-eight female rats were used. The rats were divided into 8 groups: isoflurane in 4 possible nitrous oxide concentrations (0%, 30%, 50%, or 70%) with saline or morphine (1 mg/kg). Then the MAC of isoflurane (MAC(ISO))was determined from alveolar gas samples at the time of tail clamp. The MAC of isoflurane was significantly different at each nitrous oxide concentration, and increasing nitrous oxide concentrations reduced anesthetic requirements for isoflurane. The administration of morphine reduced the MAC(ISO) when used with 0% or 30% nitrous oxide. This MAC(ISO) by morphine reduction was less with 50% nitrous oxide and nonexistent at 70% nitrous oxide. However, with morphine present the MAC(ISO) was independent of the nitrous oxide concentration in the 30%-70% range.     

Combined negative inotropic effects of calcium entry blockers and isoflurane on canine isolated heart muscles

The combined negative inotropic effects of isoflurane and calcium entry blockers (verapamil, diltiazem, nifedipine, nicardipine) were studied utilizing isolated heart preparations of ventricular muscles from dogs. All of these calcium entry blockers exerted dose-dependent decreases in maximal velocity of shortening (Vmax), maximal developed isometric force (Fm), and the maximal first derivative of Fm (maximal dF/dt). Dose-dependent decreases of these variables of muscle mechanics were augmented in isoflurane-depressed myocardium. At equimolar concentrations, direct myocardial depression was demonstrated in the following order of severity: nifedipine > diltiazem = verapamil > nicardipine. Percent depressions of Vmax, Fm and maximal dF/dt were significantly greater in muscles when calcium entry blockers were combined with 1MAC isoflurane than in muscles of calcium entry blockers alone. These data suggest that the negative inotropic effects of verapamil, diltiazem, nifedipine, and nicardipine were potentiated by isoflurane.(Nakata F, Kemmotsu O: Combined negative inotropic effects of calcium entry blockers and isoflurane on canine isolated heart muscles. J Anesth 5: 48–55, 1991)     

L-Arginine-enriched preservation solution decreases ischaemia/reperfusion injury in canine kidneys after long-term cold storage.

BACKGROUND: Kidneys stored hypothermically for transplantation show varying degrees of tissue injury, depending on the duration of preservation. The causes of injury are not entirely clear. We investigated the quality of renal functional recovery in canine kidneys after 72 h hypothermic preservation in custodiol solution or custodiol solution plus L-arginine. METHODS: Kidneys obtained from mongrel dogs, weighing 18-25 kg, were subjected to 72-h cold ischaemia after flushing. Animals were divided into two groups (n=18/group). A flush solution of either custodiol solution or custodiol solution plus L-arginine 1 mmol/l was used for each group. After 72-h cold storage all animals had a contralateral nephrectomy, and autotransplantation was performed to external iliac artery and vein. Survivals were evaluated at 3 days. RESULTS: Renal damage was assessed by kidney function tests, serum creatinine (SCr), blood urea nitrogen (BUN) and light histology. Malondialdehyde (MDA) was measured as an index of lipid peroxidation. SCr and BUN (24, 48 and 72 h) were significantly different from the control and L-arginine groups. Histological damage was less in the L-arginine group. MDA levels were significantly different with the lower levels in the L-arginine group. CONCLUSIONS:On the basis of these data, we concluded that exogenous L-arginine (a substrate for NO synthesis) has a beneficial and protective effect on long-term (72 h) hypothermic ischaemical damage in canine kidneys.     

Intestinal pHi studied with continuous saline tonometry during ischaemia and reperfusion in the pig.

OBJECTIVE: To evaluate continuous saline tonometry for detection of progressive intestinal ischaemia and reperfusion in a porcine model. DESIGN: In eight anaesthetised pigs, small bowel mucosal pCO2 was recorded by means of two identical equipments for continuous saline tonometry and a standard tonometry balloon during ischaemia and reperfusion. RESULTS: Both systems of saline tonometry functioned stably during the four hour protocol ischaemia, although not significant until after 45 min for one of the tonometers. CONCLUSION: The equipment for continuous saline tonometry has a good reactivity, an accuracy comparable with standard tonometry.