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We addressed the question to which extent cerebral blood flow (CBF) is maintained when, in addition to a high blood viscosity ([B.sub.vis]) arterial oxygen content ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]) is gradually decreased. [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] was decreased by hemodilution to hematocrits (Hct) of 30, 22, 19, and 15% in two groups. One group received blood replacement (BR) only and served as the control. The second group received an additional high viscosity solution of polyvinylpyrrolidone (BR/PVP). [B.sub.vis] was reduced in the BR group and was doubled in the BR/PVP. Despite different [B.sub.vis], CBF did not differ between BR and BR/PVP rats at Hct values of 30 and 22%, indicating a complete vascular compensation of the increased [B.sub.vis] at decreased [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]. At an Hct of 19%, local cerebral blood flow (LCBF) in some brain structures was lower in BR/PVP rats than in BR rats. At the lowest Hct of 15%, LCBF of 15 brain structures and mean CBF were reduced in BR/PVP. The resulting decrease in cerebral oxygen delivery in the BR/PVP group indicates a global loss of vascular compensation. We concluded that vasodilating mechanisms compensated for [B.sub.vis] increases thereby maintaining constant cerebral oxygen delivery. Compensatory mechanisms were exhausted at a Hct of 19% and lower as indicated by the reduction of CBF and cerebral oxygen delivery. anemia; cerebral blood flow; autoradiography blood replacement; microcirculation

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Intestinal ischaemia is a major complication of shock syndromes causing translocation of bacteria and endotoxins and multiple organ failure in intensive care patients. The present study was designed to use microdialysis as a tool to monitor intestinal ischaemia after cardiac arrest and resuscitation in pigs. For this purpose, microdialysis probes were implanted in pig jejunal wall, peritoneum, skeletal muscle and brain, and interstitial fluid was obtained during circulatory arrest (induced by ventricular fibrillation) and after return of spontaneous circulation (ROSC). Cardiac arrest for 4 min caused a prolonged (60 min) reduction of blood flow in jejunal wall, muscle and brain as determined by the ethanol technique. This was accompanied by cellular damage in heart muscle and brain as indicated by increased levels of troponin-I and protein S-100, respectively. Plasma levels of glucose, lactate and choline were increased at 15-60 min following cardiac arrest. In contrast, cardiac arrest induced a rapid but variable decrease of interstitial glucose levels in all monitored organs; this decrease was followed by an increase over baseline during reperfusion. In the intestine, lactate, glutamate and choline levels were increased during ischaemia and reperfusion for 60-120 min; intestinal and peritoneal samples yielded parallel changes of lactate levels. Brain and muscle samples showed similar changes as in intestinum and peritoneum except for glutamate, which was increased in brain but not in muscle. We conclude that intestinal ischaemia occurs as a consequence of cardiac arrest and resuscitation and can be monitored by in vivo microdialysis. Comparative analysis by multi-site microdialysis reveals that the intestine is equally or even more sensitive to ischaemia than brain or muscle.

Unlabelled: In some patients, cardiopulmonary resuscitation (CPR) can revive spontaneous circulation (ROSC). However, neurological outcome often remains poor. Hypertonic-hyperoncotic solutions (HHS) have been shown to improve microvascular conductivity after regional and global ischemia. We investigated the effect of infusion of HHS in a porcine CPR model. Cardiac arrest was induced by ventricular fibrillation. Advanced cardiac life support was begun after 4 min of nonintervention and 1 min of basic life support. Upon ROSC, the animals randomly received 125 mL of either normal saline (placebo, n = 8) or 7.2% NaCl and 10% hydroxyethyl starch 200,000/0.5 (HHS, n = 7). Myocardial and cerebral damage were assessed by serum concentrations of cardiac troponin I and astroglial protein S-100, respectively, up to 240 min after ROSC. In all animals, the levels of cardiac troponin I and S-100 increased after ROSC (P < 0.01). This increase was significantly blunted in animals that received HHS instead of placebo. The use of HHS in the setting of CPR may provide a new option in reducing cell damage in postischemic myocardial and cerebral tissues., Implications: Infusion of hypertonic-hyperoncotic solutions (HHS) after successful cardiopulmonary resuscitation in pigs significantly reduced the release of cardiac troponin I and cerebral protein S-100, which are sensitive and specific markers of cell damage. Treatment with HHS may provide a new option to improve the outcome of cardiopulmonary resuscitation.

Unlabelled: For quantification of hepatic [(18)F]FDG uptake, the dual blood supply to the liver must be considered. In contrast to the arterial input, however, the portal venous blood supply to the liver cannot be monitored directly by PET because of the inaccessibility of the portal vein on PET scans. In this study, we investigated whether the dual hepatic input can be predicted from the measurable arterial input. Moreover, we assessed the effect of different input models on the rate constants of the standard 3-compartment model describing regional uptake of FDG., Methods: Dynamic FDG PET scanning was performed on 5 foxhounds. Activity concentrations in blood from the aorta and the portal vein were measured simultaneously using external circuits. After image reconstruction, time--activity courses were determined from the aorta and the liver. The venous input was approximated by convolving the arterial input with a notional system function describing the dispersion of the arterial input on its way through the gastrointestinal tract. On the basis of these data, 5 different hepatic input models, which pertain to a single-input as well as a dual-input scenario, were statistically compared with regard to the adequacy of the model fits to liver data and to differences in the estimated rate constants., Results: Portal venous input to the liver could be approximated by convolving the arterial input function with a system function. From this function, a mean transit time of 25 s was computed for FDG to pass through the gastrointestinal tract. According to the statistical analysis, dual-input models were superior to their single-input counterparts. However, differences in the rate constants estimated for the 5 input models were in the same order as interindividual variations within the different model groups. For the dephosphorylation rate constant, a consistent value of 0.05 +/- 0.01 min(-1) was found., Conclusion: Dual-input models proved to be superior to single-input models with respect to the adequacy of FDG model fits to normal liver data. However, the hepatic blood supply may be approximated by the arterial input function as well, especially for the evaluation of liver lesions mainly fed by the hepatic artery.

To date no satisfactory method has been available for the quantitative in vivo measurement of the complex hepatic blood flow. In this study two modelling approaches are proposed for the analysis of liver blood flow using positron emission tomography (PET). Five experiments were performed on three foxhounds. The anaesthetised dogs were each given an intravenous bolus injection of oxygen-15 labelled water, and their livers were then scanned using PET. Radioactivity in the blood from the aorta and portal vein was measured directly and simultaneously using closed external circuits. Time-activity curves were constructed from sequential PET data. Data analysis was performed by assuming that water behaves as a freely diffusible tracer and adapting the standard one-compartment blood flow model to describe the dual blood supply of the liver. Two particular modelling approaches were investigated: the dual-input model used both directly measured input functions (i.e. using the hepatic artery and the portal vein input, determined from the radioactivity detected in the aorta and portal vein respectively) whereas the single-input model used only the measured arterial curve and predicted the corresponding portal input function. Hepatic arterial flow, portal flow and blood volume were fitted from the PET data in several regions of the liver. The resulting estimates were then compared with reference blood flow measurements, obtained using a standard microsphere technique. The microspheres were injected in a separate experiment on the same dogs immediately prior to PET scanning. Whilst neither the single- nor the dual-input models accurately reproduced the arterial reference flow values, the flow values from the single-input model were closer to the microsphere flow values. The proposed single-input model would be a good approximation for liver blood flow measurements in man. The observed discrepancies between the PET and microsphere flow values may be due to the inherent temporal and spatial heterogeneity of liver blood flow. The results presented suggest that adaptation of the standard one-compartment blood flow model to describe the dual blood supply of the liver is limited and other flow tracers have to be considered for quantitative PET measurements in the liver.

Oxidized glutathione (GSSG) but not its reduced form (GSH) is taken up by intact myocardial cells, and is rapidly converted into GSH. Reduced glutathione is an important intracellular defense against oxygen-derived free radicals and has been found to enhance calcium sensitivity in skinned cardiac fibers. We have investigated the effects of intravenous GSSG on left ventricular systolic pressure, maximal rate of rise of pressure and regional segment-shortening in dogs subjected to occlusion of the left anterior descending artery for 30 minutes, followed by 45 minutes reperfusion. Starting 10 minutes before reperfusion, the dogs were randomly treated with either GSSG (100 mM, 5 ml/min, n = 5) or Ringer's solution (5 ml/min, n = 5) until 30 minutes of reperfusion. Myocardial blood flow was measured by radioactive microspheres. Infusion of GSSG increased total glutathione content in both ischemic (47 +/- 16 mumol/g protein) and nonischemic myocardium (71 +/- 17 mumol/g protein) as compared to controls (23 +/- 2 mumol/g protein, p < 0.05). In both groups paradoxical wall motion occurred in the ischemic region during occlusion. On reperfusion, regional dyskinesia persisted in controls; while, in glutathione-treated dogs, systolic segment-shortening reached half the baseline values (p < 0.05, treated vs controls, at 15, 30, 45 minutes reperfusion). During ischemia the area of pressure-length loops, obtained from simultaneous recordings of left ventricular pressure and regional segment length, decreased to 30 +/- 7% of baseline in controls and to 40 +/- 18% of baseline in GSSG-treated animals. After 45 minutes reperfusion it was restored to 78 +/- 22% baseline in treated hearts but was still 36 +/- 16 of baseline in controls (p < 0.05). We conclude that infusion of GSSG increases the intracellular stores of glutathione and improves the contractile state of postischemic myocardium.

Background: The use of dextran solutions (DX) for hemodilution (HD) is considered being detrimental due to their effects on plasma viscosity., Methods: 14 splenectomized beagles (12.7 +/- 1.3 kg) were anesthetized and randomly assigned to HD to 20 vol% hematocrit (hct) with either 3 or 6% DX-60. The effects of HD upon nutritional organ blood flow (radioisotope-labelled microspheres, phi 15 microns), local tissue oxygenation (pO2 multiwire surface electrode), plasma and blood volume (131I-labelled dog albumin distribution), and macrohemodynamics were evaluated with regard to actual changes in hct and plasma viscosity, respectively., Results: Normovolemic HD with either solution resulted in equivalent changes in macrohemodynamics, and plasma and blood volume. Despite the increase in plasma viscosity associated with HD using 6% DX-60 (up to 1.45 +/- 0.10 mPa.s), blood flow rose in all organs studied (p < 0.05). After HD by means of 3% DX-60, plasma viscosity remained unchanged (1.09 +/- 0.04 mPa.s) but was not associated with higher organ blood flow as compared to 6% DX-60. In both groups, elevated pO2 values on the surface of liver and skeletal muscle (p < 0.01) as well as the shift in the pO2 histograms toward higher pO2 values indicated a more homogeneous tissue perfusion upon HD, independent of the diluent applied., Conclusion: In comparison to 6% DX-60, the solution of 3% DX-60 is of equivalent efficacy as volume substitute and in the induction of normovolemic HD. The main advantage of 3% DX-60 solution, however, is the fact that twice as much volume can be administered before the recommended maximal daily dose of 1.5 g/kg DX is reached. Of the rheological factors influencing oxygen delivery, hematocrit thus plays the predominant role, while plasma viscosity is of minor importance.

The use of modified haemoglobin solutions as blood substitutes has been investigated extensively during the past decades. Ultrapurified, polymerised bovine haemoglobin (upbHb) is a promising new substance in this respect. It was the aim of the present investigation to study the cardiovascular and respiratory effects of massive blood replacement with upbHb in a new model of conscious rats with continuous haemodynamic monitoring. METHODS. The right femoral artery and vein of 13 male Sprague-Dawley rats were catheterised during halothane-N2O-O2 anaesthesia. A thermistor catheter was placed in the descending aorta via the left femoral artery for measuring cardiac output by the thermodilution method. After recovery from anaesthesia blood replacement was achieved by arterial blood withdrawal and simultaneous venous infusion of upbHb in equal amounts. The haematocrit was lowered to < 3% and the animals were then left undisturbed in a rat restrainer while breathing room air. RESULTS. The animals showed no signs of disturbed behaviour patterns, distress, or adverse reactions. There were no significant changes in cardiac index and oxygen delivery during the investigation period of 4 h. A marked increase in mean arterial pressure (MABP) and systemic vascular resistance (SVR) of 30% was observed while stroke volume remained unchanged. Blood gases, acid-base status, and plasma glucose showed no major changes. Plasma oncotic pressure increased during the investigation period. CONCLUSIONS. The results indicate that there is adequate oxygenation and sufficient systemic oxygen delivery in conscious and drug-free rats after isovolaemic haemodilution with upbHb to a final haematocrit of < 3%. In contrast to previous haemodilution studies, which have tested non-oxygen-carrying solutions, no changes in cardiac index were observed. The cause of the increase in MAP and SVR remains to be established.

The transfusion of autologous blood protects surgical patients from both the transfusion transmitted diseases (AIDS, posttransfusion hepatitis) and the immunosuppressive effects of homologous blood. Nevertheless, the use of autologous blood is still unsatisfactory, mainly because of the elaborated logistics, organization and technique required and the often insufficient amounts of autologous blood gained. Today, the major growth-factors of erythropoiesis are available as recombinant analogues. In the studies reviewed here, we investigated the effects of rhu-EPO and IL-3 on perioperative erythropoiesis in two canine models of acute isovolemic hemodilution. Different therapeutic concepts are compared with respect to preoperative changes in hematocrit, the volume of autologous blood gained and the duration of postdilutional anemia.