The purpose of our study was to test the hypothesis that the quotient between plasma glucose and whole body oxygen consumption (VO2) as a 'metabolic index' is a sensitive indicator of early graft function. Arterial levels of glucose and oxygen consumption were determined in 100 consecutive patients during orthotopic liver transplantation performed without anhepatic veno-venous bypass. Patients were divided into survivors with no obvious problems related to graft function and those with primary nonfunction of the graft. The neohepatic increase in VO2 was significantly higher in survivors (112 +/- 4 vs 88 +/- 11 ml.min-1.m-2; p < 0.05), whereas blood glucose levels after reperfusion were higher (352 +/- 18 vs. 287 +/- 36 mg dl-1) in those with primary non-function of the graft. The calculated metabolic index was also higher (4.02 +/- 0.93 vs 2.67 +/- 0.45, p < 0.05) in patients with primary nonfunction of the graft. Our principal conclusion was that 92% of normal functioning liver grafts could be classified correctly by the metabolic index immediately after reperfusion, whereas glucose levels and VO2 alone classified only 67% and 70% of normal functioning liver grafts correctly.

Anesthesia, General↗

PubMed1992

[Anesthesia-relevant changes in metabolic parameters with different circulatory and liver functions].

The relationship between oxygen consumption (VO2) and oxygen delivery (DO2) is of interest in critically ill patients. Various studies of these parameters have resulted in different concepts for optimizing DO2 and VO2. During liver transplantation without anhepatic veno-venous bypass, caval cross-clamping initiates a series of haemodynamic and metabolic alterations including the rapid change from hyperdynamic to hypodynamic conditions. In addition, simultaneous changes in DO2 and VO2 occur in these patients. The goal of our present study was to test the clinical relevance of therapeutic interventions based on metabolic monitoring in patients with terminal liver disease undergoing orthotopic liver transplantation. PATIENTS AND METHODS. One hundred sixty-two consecutive patients were evaluated. According to outcome, patients were divided into survivors (n = 115, group A), nonsurvivors (n = 30, group B), and patients with primary nonfunction of the liver graft (n = 17, group C). One hundred twenty patients were cirrhotics due to either alcohol (n = 36), aggressive hepatitis (n = 30), or biliary cirrhosis (n = 54); 42 had a neoplastic disease. Haemodynamic measurements, data for calculations of DO2 and VO2, and blood samples for arterial and mixed-venous blood gases and subsequent laboratory analysis were taken during the surgical procedure at six timepoints: after induction of anaesthesia (I); during preparation of the recipient liver, before cross-clamping (II); 10 min after clamping of the inferior vena cava (III); 10 min before unclamping (IV); with all vessels open, 10 min after declamping during reperfusion (V); and 60 min after declamping (VI). Anaesthesia was induced with thiopentone (3-5 mg/kg i.v.) and fentanyl (15 micrograms/kg min i.v.). Muscle relaxation was achieved with pancuronium (0.1 mg/kg i.v.). Anaesthesia was maintained with i.v. supplements of fentanyl (5-10 micrograms/kg) and pancuronium (4 mg) as required. Volume-cycled ventilation was established with a mixture of O2 in air with a positive end-expiratory pressure of 5 mm H2O to keep the PaO2 above 100 mm Hg and the PaCO2 around 35 mm Hg (Servo 900 C-Ventilator, Siemens). To maintain body temperature, all patients were positioned on a heating blanket set at 38 degrees C. The inspired gases were warmed and humidified using a dual servo-heated humidifier. Mannitol (20-40 g i.v.) or sorbitol (16-24 g i.v.) was given to prevent renal dysfunction during the cross-clamping procedure. Lactated Ringer's solution and fresh frozen plasma administration was guided by cardiovascular performance and requirements for clotting factors, respectively. Cardiac output was measured by the thermodilution method using a pulmonary artery catheter. Blood lactate, haemoglobin concentration, arterial and mixed-venous oxygen content, and oxygen saturation were measured (Hemoxymeter OSM3). VO2 and DO2 were calculated according to standard formulas. STATISTICAL ANALYSIS. The data from groups A, B, and C were compared using a multivariate analysis of variance with Tukey's method for multiple comparisons. A least-square regression was used to correlate metabolic data. RESULTS. The perioperative course of the determinants of oxygen transport is shown in Table 1. After cross-clamping, the cardiac index (CI) decreased in groups A (47%), B (53%), and C (51%) and increased to pre-anhepatic levels after reperfusion of the new liver. This was associated with distinct decreases in DO2 (A: 42%, B: 47%, and C: 45%) and VO2 (A: 8%, B: 19%, C: 25%). After reperfusion of the new allograft (V), VO2 increased in groups A (24%) and B (18%) as compared to controls (I). By contrast, in group C, a distinct further decrease in VO2 (13%) was detected. In these patients, there was a significantly greater increase in mixed-venous saturation accompanied by a further decrease in body temperature. As shown in Figures 1 and 2, no significant relationship was found between O2 transport, VO2, and blood lactate. DISC

Adult↗

PubMed1991

Isoflurane impairs the function of ischemic myocardium in acutely but not in chronically instrumented dogs.

To compare the effects of isoflurane on ischemic myocardium in acutely and chronically instrumented animals, 12 mongrel dogs were monitored with electromagnetic or Doppler ultrasonic flow transducers and hydraulic occluders around the left circumflex coronary artery, pressure transducers in the left ventricle, and heparin-filled catheters in the descending aorta. Regional function of normal and ischemic myocardium was assessed by sonomicrometry. The hemodynamic effects of isoflurane (2% inspired concentration) were more pronounced in the acutely than in the chronically instrumented dogs. Decreases in mean arterial pressure (-47% +/- 5% in the acute and -22% +/- 4% in the chronic preparation, P less than 0.01), left ventricular contractility (-51% +/- 6% and -33% +/- 4%, P less than 0.01), and coronary perfusion pressure (-59% +/- 6% and -12% +/- 9%, P less than 0.01) were more distinct in the acutely instrumented animals. Although the reduction of regional function during isoflurane anesthesia was similar in normal myocardium in both preparations (-33% +/- 4% acute and -34% +/- 6% chronic preparation, not a significant difference), an exaggerated dysfunction was observed in the ischemic myocardium of the acutely instrumented dogs (-66% +/- 2% and -30% +/- 4%, P less than 0.01). It is concluded that acutely instrumented dogs respond to the hemodynamic effects of isoflurane, resulting in ischemic myocardial dysfunction, significantly more than do chronically instrumented dogs.

Animals↗

PubMed1991

Two-dimensional transesophageal echocardiography in early diagnosis and treatment of hemodynamic disturbances during liver transplantation.

Explore the source record for details and available documents.

Cardiac Output↗

PubMed1991

Kinetics of oxygen during orthotopic liver transplantation.

Explore the source record for details and available documents.

Cardiac Output↗

PubMed1991

Heparin and prostacyclin in hemofiltration after orthotopic liver transplantation.

Explore the source record for details and available documents.

Acute Kidney Injury↗

PubMed1990

Enflurane alters compensatory hemodynamic and humoral responses to hemorrhage.

This study examined the impact of enflurane (3%) on the hemodynamic and humoral defense mechanisms in a canine model of hemorrhagic shock. In order to obtain reasonable reference values with confounding influences of anesthesia and recent surgical preparation, the dogs were chronically instrumented 8-10 days prior to the experiments enabling measurements in the conscious state. While arterial pressure, cardiac output, and the corresponding derivatives were recorded continuously, plasma catecholamines and plasma renin activity were determined intermittently. As anticipated, the conscious dogs were able to tolerate considerable more severe levels of hemorrhage than the dogs anesthetized with enflurane. This finding is associated with reciprocal responses of both the renin-angiotensin system and the sympathoadrenal system in the conscious and anesthetized states. While the sympathoadrenal system prevailed in the conscious dogs, the renin-angiotensin system predominated during enflurane anesthesia. Despite the augmented response of the renin-angiotensin system, the activation of this defense mechanism was not sufficiently powerful enough to prevent overall hemodynamic deterioration with hemorrhage in the animals anesthetized with enflurane.

Anesthesia, Inhalation↗

PubMed1990

[The intraoperative use of falipamil (AQ-A39), a new calcium antagonist with specific bradytropic properties].

Tachycardia caused by surgical stimulation can compromise the myocardial oxygen balance and may also lead to a reduction of cardiac output. Conventional drugs with negative chronotropic effects also cause reduction of inotropy. Recent so-called specific bradytropic agents are expected to act merely upon chronotropy without affecting pressure of the systemic or coronary circulation. The goal of this study was to investigate the effects of a calcium channel blocker. Falipamil, on the circulation controlling excessive intraoperative tachycardia. PATIENTS AND METHODS. In this study 15 patients, aged 32 to 73 years, mean 55 +/- 12 were investigated. The cardiac risk classes included classification I-III, according to Goldman. The patients underwent major abdominal or thoracoabdominal operations. Monitoring consisted of a radial arterial cannula, as well as a 7 French Swan-Ganz catheter, which was introduced via the internal jugular vein. Determination of cardiac output was done using the thermodilution technique with a Kimray Medical Association Oklahoma City model 3500; related indexes were calculated. Electrophysiological data were read from the ECG. The recorded QT interval was corrected for heart rate according to the formula of Hegglin and Holzmann. Anesthesia consisted of premedication with diazepam, 0.1 mg/kg, 1 h preoperatively. Anesthesia was induced with thiopentone, 5 mg/kg, and fentanyl, 1.5 micrograms/kg. After giving 1 mg alcuronium, succinylcholine, 1 mg/kg, was used for intubation. Anesthesia was continued using ventilation with O2: N2O 1:2 and intermittent doses of fentanyl and alcuronium. When tachycardia occurred at a rate higher than 100 beats per minute, a dose of 2 micrograms/kg fentanyl was administered to deepen the anesthesia. If this had no influence, control readings were taken and subsequently falipamil 2 mg/kg was injected. After that the hemodynamic parameters were monitored for 1, 2, 3, 5, 10, and 20 min. Statistical analysis was performed using the analyses of variance, followed by the Newman-Keuls test. The level of significance was p less than 0.05. RESULTS. The means and standard deviations of the hemodynamic parameters following induction of anesthesia (0) and at the peak rate are shown in Table 1. The mean increase in heart rate at that time was 38 +/- 18% and the QT and RR interval were reduced concomitantly. Both times the QT measured and the QT corrected for rate did not significantly differ from each other. (ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1989

Fentanyl inhibits the canine carotid chemoreceptor reflex.

To investigate the impact of fentanyl on the carotid chemoreceptor reflex, nine mongrel dogs were permanently monitored with electromagnetic flow transducers around the right common iliac artery and with heparin-filled catheters in the descending aorta and in one of the main carotid arteries with the tip just proximal to the carotid sinus. Carotid chemoreceptor activation (CCRA) produced by consecutive injections of nicotine (0.2-0.4 micrograms/kg) through the carotid catheter elicited bradycardia, expressed as an increase in cardiac cycle length by 140% +/- 18%, and a 252% +/- 16% increase in mean iliac arterial vascular resistance. These responses were markedly attenuated by fentanyl in a dose-dependent fashion: cardiac cycle length increased only by 50% +/- 7% (P less than 0.01) with 4 micrograms/kg and by 19% +/- 6% (P less than 0.01) with 8 micrograms/kg of intravenous fentanyl. These changes were paralleled by significantly (P less than 0.01) lesser increases in mean iliac arterial resistance (122% +/- 9% and 50% +/- 5%). It is concluded that fentanyl impairs the integrity of the carotid chemoreceptor reflex.

Animals↗

PubMed1988

Chronic instrumentation techniques for haemodynamic measurements.

Research in chronically instrumented experimental animals has shown basal anaesthesia may cause a considerable disruption of the autonomic control of the cardiovascular system, and a profound change in basal haemodynamics, myocardial function and coronary haemodynamics--variables which are of fundamental importance in studying the impact of various anaesthetics on the cardiovascular system. It is, therefore, important to make sequential haemodynamic measurements which enable comparisons to be made of the conscious v. the anaesthetized state. The present article describes some of the chronic instrumentation techniques used to study the effects of anaesthetic agents on overall haemodynamics, coronary blood flow and regional myocardial function in comparison with the conscious state. It is suggested that the effects of anaesthesia on the integrative control of the circulation are not sufficiently recognized.

Anesthetics↗

PubMed1988

[Falipamil for decreasing intraoperative heart rate in pheochromocytoma].

In 4 patients (2 males, 2 females), aged between 16 and 62 years, who had surgery for pheochromocytoma, the effects of Falipamil, a compound with selective negative chronotropic action, was tested. This drug, which is a slow calcium channel blocking agent, was administered during the period of massive endogenous catecholamine output caused by tumor mobilisation; the influence on mean arterial pressure, pulmonary artery pressure, central venous pressure and cardiac index as well as catecholamines was investigated. When the pulse rate exceeded 100 beats per minute in the course of surgical preparation, 2 mg/kg BW Falipamil were administered as in i.v. bolus dose. Epinephrine and norepinephrine were determined before and 5 minutes after Falipamil administration in one patient. The effect of this bolus dose was a significant decrease in heart rate. There was also a moderate decrease in mean arterial pressure and cardiac index, with was probably caused by pretreatment with alpha- and beta-blockers prior to surgery, whereas central venous pressure and pulmonary artery pressure remained unchanged. Norepinephrine increased, epinephrine decreased. These findings lead us to conclude that Falipamil is a valuable adjunct to control circulation in patients with high catecholamines.

Adolescent↗

PubMed1987

[Hemodynamic effects of an osmotic bolus for the reversible opening of the blood-brain barrier].

Reversible opening of the blood-brain barrier before administration of watersoluble cytoreductive agents constitutes a new tool in the treatment of central nervous malignancies. In this study a volume of 172 ml mannitol 25% has been injected into one of the cerebral arteries within 30 seconds. 5 minutes later the osmolality had augmented from 286 to 303 mosmol/kg and the plasma volume by 15%. The hemodynamic measurements--cardiac index (+47%), heart rate (+7%), LVSWI (+50%), systemic vascular resistance (-20%) and blood volume (+15%)--indicate a biphasic response with early fall in SVR followed by a rise in cardiac performance which is independent of the preload.

Adult↗

PubMed1987

Effects of ischemia on the canine myocardial beta-adrenoceptor-linked adenylate cyclase system.

Several studies indicate that myocardial ischemia causes a redistribution of beta-adrenergic receptors from a presumably intracellular compartment to the cell surface. However, a decreased adenylate cyclase and contractile responsiveness to beta-adrenergic stimuli has also been reported. The aim of the present study was to investigate possible ischemia-induced changes in myocardial beta-adrenoceptor coupling to adenylate cyclase. Myocardial ischemia was induced by hydraulic occlusion of the LAD in mongrel dogs anesthetized with isoflurane. After 90 min of ischemia, tissue samples were removed from the ischemic and nonischemic regions for tissue catecholamine determinations and for the preparation of particulate fractions from tissue homogenates. Saturation experiments on microsomal fractions obtained from the ischemic and control areas did not reveal any significant changes in the calculated dissociation constant for (-)[125I]iodocyanopindolol binding nor in the calculated receptor density. Likewise, the relative numbers of beta 2-adrenergic receptors were comparable in both preparations (approximately 20%). On the other hand, the proportion of beta-adrenoceptors stabilized in the high-affinity state by (-)isoproterenol was significantly reduced in the ischemic region when compared with the control myocardium (17 +/- 5 vs. 41 +/- 4%). This change was accompanied by a significant decrease in the intrinsic activity of (-)isoproterenol in stimulating adenylate cyclase activity. We propose that the initial uncoupling of the beta-adrenoceptor from its effector is a physiologically important, protective mechanism which guards the ischemic myocardium against the deleterious effect of excessive sympathetic stimulation.

Adenylyl Cyclases↗