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BACKGROUND: Colloids are widely used in the replacement of fluid volume, however doubts remain as to their benefits. Different colloids vary in their molecular weight and therefore in the length of time they remain in the circulatory system. Because of this and their other characteristics, they may differ in their safety and efficacy. OBJECTIVES: To compare the effects of different colloid solutions in patients thought to need volume replacement. SEARCH STRATEGY: The Cochrane Injuries Group specialised register, The Cochrane Controlled trials register (all years), MEDLINE (1994-98), EMBASE (1974-98) were searched. Bibliographies of trials retrieved were searched and drug companies manufacturing colloids were contacted for information. SELECTION CRITERIA: Randomised and quasi randomised trials comparing colloid solutions in critically ill and surgical patients thought to need volume replacement. The main outcomes measured were death, amount of whole blood transfused and incidence of adverse reactions. DATA COLLECTION AND ANALYSIS: Two authors independently extracted the data and assessed the quality of the trials. MAIN RESULTS: 46 trials met the inclusion criteria, with a total of 2884 participants. Many of the trials were small. In the majority of trials quality was poor or uncertain. Deaths were obtained from 27 trials. Twenty three trials recorded the amount of blood transfused, however quantitative analysis was not possible due to skewness and variable reporting. Thirteen trials recorded adverse reactions, but none occurred. For albumin or PPF versus hydroxyethyl starch (HES) 20 trials reported mortality. The pooled relative risk (RR) was 1.17 (95% CI 0.91, 1.50). For albumin or PPF versus gelatin 3 trials reported mortality. The RR was 0.99 (0.69, 1.42). For gelatin vs HES 3 trials reported mortality, RR was 0.97 (0.65, 1.44). RR was not estimable in the albumin vs dextran, gelatin vs dextran, and HES vs dextran groups. REVIEWER'S CONCLUSIONS: From this review, there is no evidence that one colloid solution is more effective or safe than any other, although the confidence intervals are wide and do not exclude clinically significant differences between colloids. Larger trials of fluid therapy are needed if clinically significant differences in mortality are to be detected or excluded.
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The use of dextrans in clinical practice are mainly based on the following effects: 1. Plasma volume effects 2. Flow Promotion 3. Antithrombotic effects. The dextrans are the only plasma volume substitute with the antithrombotic effect but this discussion will only deal with their effects on plasma volume and flow. The effect on plasma volume--the colloid supported intravascular volume--can be calculated as ml of water held in circulation per gram circulating colloid--for dextran 70 around 20 ml/g, for albumin 18 ml/g and for plasma protein 12-13 ml/g. After infusion of a plasma volume substitute the volume effect depends on dose injected, molecular weight distribution, rate of disappearance from the intravascular department mainly via the kidneys. The clinical experience of a reliable plasma volume expansion can be demonstrated in animal experiments comparing different infusion fluids. The effect on erythrocyte aggregation depends on kind of substance and molecular weight distribution. The flow promoting effect is mainly due to restoration of plasma volume but also related to hemodilution and aggregation. The vasoconstriction seen in shock can be counteracted essentially with colloid supported plasma volume expansion. The supposed influence of the dextrans on the kidney function in some clinical cases has been investigated experimentally.
Seminal plasma from oligozoospermic ejaculates and ejaculates with high rate of pathological spermatozoa was substituted for seminal plasma from normal ejaculates in experiments carried out in order to improve the ejaculate quality. In these experiments the improvement of ejaculate quality could not be established. The progressive increase of 20% in the motility of spermatozoa was recorded, in 4 out of 7 ejaculates with hypokinetic motility of spermatozoa where plasma was substituted, while in one case the motility remained unchanged. When plasma from normal ejaculates was substituted for plasma from ejaculates of poorer quality, the intensity of the motility of spermatozoa decreased for 10-20% in 3 of cases while in 1 it remained unchanged. Deep freezing of ejaculates after seminal plasma was substituted did not gain satisfactory results except when cases of substitution for plasma from normal ejaculates were concerned.
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The plasma membrane calcium ATPase (PMCA) actively transports Ca(2+) from the cytosol to the extra cellular space. The C-terminal segment of the PMCA functions as an inhibitory domain by interacting with the catalytic core. Ca(2+)-calmodulin binds to the C-terminal segment and stops inhibition. Here we showed that residue Asp(170), in the putative "A" domain of human PMCA isoform 4xb, plays a critical role in autoinhibition. In the absence of calmodulin a PMCA containing a site-specific mutation of D170N had 80% of the maximum activity of the calmodulin-activated PMCA and a similar high affinity for Ca(2+). The mutation did not change the activation of the PMCA by ATP. Deletion of the C-terminal segment further downstream of the calmodulin-binding site led to an additional increase in the maximal activity of the mutant, which suggests that the mutation did not affect the inhibition because of this portion of the C-terminal segment. The calmodulin-activated PMCA was more sensitive to vanadate inhibition than the autoinhibited enzyme. In contrast, inhibition of the D170N mutant required higher concentrations of vanadate and was not affected by calmodulin. Despite its higher basal activity, the mutant had an apparent affinity for calmodulin similar to that of the wild type enzyme, and its rate of proteolysis at the C-terminal segment was still calmodulin-dependent. Altogether these results suggest that activation by mutation D170N does not involve the displacement of the calmodulin-binding autoinhibitory domain from the catalytic core and may arise directly from changes in the accessibility to the calcium-binding residues of the pump.
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