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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.

We addressed the question to which extent cerebral blood flow (CBF) is maintained when, in addition to a high blood viscosity (Bvis) arterial oxygen content (CaO2) is gradually decreased. CaO2) 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). Bvis was reduced in the BR group and was doubled in the BR/PVP. Despite different Bvis, 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 Bvis at decreased CaO2. 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 Bvis 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.