PubMed · 14249567
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M ANDREASSEN. 1965-01-21. [TRASYLOL].. https://pubmed.ncbi.nlm.nih.gov/14249567/
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The pharmacological methods used to achieve systemic hemostasis have generated much discussion due to concerns of serious adverse effects (e.g., thromboembolic complications) and costs of therapy in addition to efficacy considerations. There are a limited number of well-controlled trials involving pharmacological hemostasis for spine surgery. In the largest double-blinded randomized controlled trial to date involving spine surgery, there was a trend toward reduced homologous transfusion in patients receiving aprotinin, but the only statistically significant result ( p<0.001) was a reduction in autologous red cell donations. The findings of this trial are important, since the investigators used a number of restrictive transfusion strategies (e.g., autologous donation, low hematocrit trigger for transfusion, blood-salvaging procedures with the exception of no cell saver) that were not always employed in earlier trials involving hemostatic agents. Smaller studies involving antifibrinolytic agents other than aprotinin have demonstrated reductions in blood loss and transfusion requirements in patients undergoing spine surgery, although the results were not always statistically significant. A very large randomized trial would be required to address comparative medication- and transfusion-related adverse events; such a trial involving patients undergoing cardiac surgery is currently being performed. Additionally, cost-effectiveness analyses are needed to help define the role of these agents based on the data that is available.
Biological processes often involve the surfaces of proteins, where the structural and dynamic properties of the aqueous solvent are modified. Information about the dynamics of protein hydration can be obtained by measuring the magnetic relaxation dispersion (MRD) of the water (2)H and (17)O nuclei or by recording the nuclear Overhauser effect (NOE) between water and protein protons. Here, we use the MRD method to study the hydration of the cyclic peptide oxytocin and the globular protein BPTI in deeply supercooled solutions. The results provide a detailed characterization of water dynamics in the hydration layer at the surface of these biomolecules. More than 95% of the water molecules in contact with the biomolecular surface are found to be no more than two-fold motionally retarded as compared to bulk water. In contrast to small nonpolar molecules, the retardation factor for BPTI showed little or no temperature dependence, suggesting that the exposed nonpolar residues do not induce clathrate-like hydrophobic hydration structures. New NOE data for oxytocin and published NOE data for BPTI were analyzed, and a mutually consistent interpretation of MRD and NOE results was achieved with the aid of a new theory of intermolecular dipolar relaxation that accounts explicitly for the dynamic perturbation at the biomolecular surface. The analysis indicates that water-protein NOEs are dominated by long-range dipolar couplings to bulk water, unless the monitored protein proton is near a partly or fully buried hydration site where the water molecule has a long residence time.
PURPOSE: To describe the utility of vasopressin in the treatment of acute distributive shock clinically compatible with the diagnosis of aprotinin anaphylaxis. CLINICAL FEATURES: A 57-yr-old female patient underwent repeat cardiac surgery to treat prosthetic valve endocarditis. She had received aprotinin during her first surgery 60 days ago. Despite a negative test dose of i.v. aprotinin 20,000 KIU, when aprotinin loading was initiated during the repeat surgery, the patient developed bronchospasm and hypotension secondary to acute distributive shock. Bronchospasm responded to inhaled salbutamol and ipatropium. The hypotension was refractory to high doses of phenylephrine. Two doses of i.v. vasopressin 5 U reversed the vasodilation and reestablished normal blood pressure. CONCLUSION: Vasopressin, in association with alpha-agonists, can reverse acute refractory distributive shock following aprotinin administration.