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EDITORIALS

From SIVA to ISAP!—A Logical Evolution

Address correspondence to Paul F. White, PhD, MD, Department of Anesthesia and Pain Management, University of Texas, Southwestern Medical Center, 5161 Harry Hines Boulevard, Room CS2.202, Dallas, TX 75390-9068.

The Society for Intravenous Anesthesia (SIVA) achieved affiliation status with the International Anesthesia Research Society (IARS) in 1999. A special section in the journal Anesthesia & Analgesia devoted exclusively to Intravenous Anesthesia was also established. This issue of the journal marks an important name change for the Society, from SIVA to the International Society for Anaesthetic Pharmacology (ISAP). This editorial is intended to explain the background to this evolutionary change.

In the early 1980s, a small group of academicians interested in a specific type of IV anesthesia, namely "neurolept anesthesia," formed the Society for Neurolept Anesthesia (SONLA). Subsequently, with the virtual demise of neurolept anesthesia and the increasing interest in total IV anesthesia (TIVA), the name of the Society was changed to SIVA. Although the primary focus of the Society has been IV anesthesia (1), the interests of our membership have always been much broader. The important contributions of the SIVA membership to the practice of anesthesia and critical care medicine (including pharmacokinetics and dynamics of IV anesthetics, IV drug delivery systems, cerebral function monitoring, and understanding of anesthetic drug interactions), can be applied to an even broader array of pharmacological drugs. Many members of our Society are actively involved in studying the clinical pharmacology of inhaled anesthetics, cardiovascular drugs, antiemetics, and blood substitutes, to name but a few. The importance of understanding the pharmacology of these drugs has increased as our clinical responsibilities now routinely extend beyond the traditional hospital-based operating room (OR) and critical care units.

Anesthesiologists are clinical pharmacologists par excellence. We use drugs that are extremely potent and have very narrow therapeutic windows. As stated by Professor Mushin (2) "we take our patients on a journey from life towards death that is called anesthesia". Importantly, anesthesiologists are frequently called upon to apply their pharmacological expertise (and other skills) outside the OR in areas where there is less technological support (e.g., office-based surgery centers, diagnostic suites, pain clinics, and even drug detoxification centers). Since the inception of the speciality, anesthesiologists have made many valuable contributions to the broader field of pharmacology which have allowed a wide variety of procedures to be performed safely outside the conventional OR.

Many of the key developments in the field of pharmacokinetics and pharmacodynamics owe much to the pioneering work of anesthesiologists. The concept of effect site modelling was first applied by Hull et al. in the UK (3), using pancuronium and muscle twitch tension as the measured effect. This approach was subsequently extended and refined by Sheiner et al. at the University of California at San Francisco (4). Pharmacokinetic-dynamic modelling has been used to characterize the pharmacodynamics of a wide variety of anesthetic and nonanesthetic drugs, and is increasingly used in the early development of new drugs. During induction of anesthesia with rapid administration of drugs, blood (and brain) concentrations change very rapidly. Conventional compartmental pharmacokinetic models (5,6) are inadequate in describing these changes. Anesthesiologists have been in the forefront of developing models that can describe the front-end kinetics of these drugs (7–11).

The mechanisms by which anesthetic drugs produce their clinical effects have long intrigued anesthesiologists and pharmacologists alike. Research in the past decade by anesthesiologists and basic scientists working in academic anesthesia departments has elucidated many of the potential mechanisms involved in producing the anesthetic state. This research has also provided considerable insight into the molecular biology and physiological functions of a wide range of ion channels and receptors thought to be potential sites of anesthetic actions, both within the central nervous system (anesthetic) and elsewhere (nonanesthetic side effects) (12,13). One interesting result of this research has been the realization that IV and inhaled anesthetics, once thought to produce anesthesia by different mechanisms, share many common mechanisms, specifically at the GABA_A receptor (14–17). This is but one aspect of the breaking down of barriers between inhaled and IV anesthesia.

The wide diversity in the pharmacological interests of the members of SIVA has been reflected in the scientific programs at our annual meetings. It has also given rise to discussions about whether the name of the society should be changed to reflect this wider interest. The SIVA Board of Directors decided at their last meeting that the next logical step in this evolutionary process was to change the name of the organization to the International Society for Anaesthetic Pharmacology (ISAP). It was the feeling of the SIVA Board of Directors that the "new" name more accurately reflects the research interests of our membership in the pharmacology of all types of anesthesia-related drugs. In addition to pharmacokinetics and dynamics of anesthetic drugs, the contributions of our members to the advancement of anesthesia also include studies involving new formulations of "old drugs" and purified isomers, as well as novel drugs (e.g., organ-protective drugs, blood substitutes, nitric oxide, neurokinin-1 and NMDA antagonists) and alternative routes of drug administration (e.g., aerosols, transmucosal, transcutaneous). With a broader-based society focusing on education and research programs related to the pharmacology of drugs used in the diverse venues where anesthesiologists work, the Board members felt that the name ISAP more accurately reflects the interests of these clinical and academic anesthesiologists, as well as research pharmacologists working in allied fields. This change was approved by the general membership of the Society at our annual meeting in San Francisco.

As an international-based organization from its inception, the Board of Directors wanted to continue this international tradition by including the word "International" in the new name of the Society. In addition, we have adapted the international spelling of "anaesthesia." We would like to encourage all our colleagues worldwide who are interested in advancing our understanding of the pharmacology of anesthesia-related drugs, to join this dynamic organization. We would also extend a special invitation to attend the ISAP panel entitled "Pharmaco-economics: Are Newer Techniques Worth the Money?" and the hands-on workshops on "TIVA techniques" at the upcoming International Anesthesia Research Society meeting in Fort Lauderdale, Florida, March 16–20, 2001.

References

1. White PF, ed. Textbook of intravenous anesthesia. Philadelphia: Williams and Wilkins,1997:1–617.
2. Mushin WW. Signs of anaesthesia. In: Evans FT, Gray TC, eds. General anaesthesia. London: Butterworths, 1959.
3. Hull CJ, Van Beem HBH, McLeod K, et al. A pharmacodynamic model for pancuronium. Br J Anaesth 1978; 50: 1113–23.[Abstract/Free Full Text]
4. Sheiner LB, Stanski DR, Vozeh S, et al. Simultaneous modelling of pharmacokinetics and pharmacodynamics: applications to d-tubocurarine. Clin Pharmacol Ther 1979; 25: 358–71.[Web of Science][Medline]
5. Fisher DM. (Almost) everything you learned about pharmacokinetics was (somewhat) wrong! Anesth Analg 1996;83:901–3.
6. Krejcie TC, Avram MJ. What determines anesthetic induction dose? It’s the front-end kinetics, doctor! Anesth Analg 1999;89:541–5.
7. Upton RN, Ludbrook GL. A model of the kinetics and dynamics of induction of anaesthesia in sheep: variable estimation for thiopental and comparison with propofol. Br J Anaesth 1999; 82: 890–9.[Abstract/Free Full Text]
8. Kuipers JA, Boer F, Olofsen E, et al. Recirculatory and compartmental pharmacokinetic modelling of alfentanil in pigs: the influence of cardiac output. Anesthesiology 1999; 90: 1146–57.[Web of Science][Medline]
9. Ludbrook GL, Upton RN. A physiological model of induction of anaesthesia with propofol in sheep: 2. Model analysis and implications for dose requirements. Br J Anaesth 1997; 79: 505–13.[Abstract/Free Full Text]
10. Krejcie TC, Henthorn TK, Niemann CU, et al. Recirculatory pharmacokinetic models of markers of blood, extracellular fluid and total body water administered concomitantly. J Pharmacol Exp Ther 1996; 278: 1050–7.[Abstract/Free Full Text]
11. Avram MJ, Krejcie TC, Henthorn TK. The relationship of age to the pharmacokinetics of early drug distribution: the concurrent disposition of thiopental and indocyanine green. Anesthesiology 1990; 72: 403–11.[Web of Science][Medline]
12. Bovill JG. Mechanisms of Anaesthesia: Time to say farewell to Meyer-Overton. Curr Opin Anaesthesiol 2000; 13: 433–6.
13. Durieux ME. Muscarinic signalling in the central nervous system. Anesthesiology 1996; 84: 173–89.[Web of Science][Medline]
14. Moody EJ, Harris BD, Skolnick P. Stereospecific actions of the inhalation anesthetic isoflurane at the GABAA receptor complex. Brain Res 1993; 615: 101–6.[Web of Science][Medline]
15. Tanelian DL, Kosek P, Mody I, Maclver MB. The role of the GABA_A receptor/chloride channel complex in anesthesia. Anesthesiology 1993; 78: 757–76.[Web of Science][Medline]
16. Hara M, Kai Y, Ikemoto Y. Enhancement by propofol of the -aminobutyric acid_A response in dissociated hippocampal pyramidal neurons of the rat. Anesthesiology 1994; 81: 988–94.[Web of Science][Medline]
17. Banks MI, Pearce RA. Dual actions of volatile anesthetics on GABA_A IPSCs. Dissociation of blocking and prolonged effects. Anesthesiology 1999; 90: 120–34.[Web of Science][Medline]

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