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The Development of Concepts of Mechanisms of Anesthesia

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The Development of Concepts of Mechanisms of Anesthesia 1 The Development of Concepts of Mechanisms of Anesthesia Donald Caton and Joseph F. Antognini INTRODUCTION Even before Morton's demonstration of surgical anesthesia in Boston, on October 16, 1846, phy­ sicians and scientists had begun to explore mechanisms by which drugs affect the central nervous system. In large part, this was an outgrowth of a revolution in therapeutics that had begun in wake of the Enlightenment. As philosophers and politicians threw out old patterns of religious, political, and economic thought, so physicians discarded a system of medical practice that had been in place for almost fifteen hundred years. Modem medicine began during this era and with it new disciplines such as physiology, pharmacology, and biochemistry (1). The discarded system of practice, called "Galenic Medicine", for the early Greek physician who established it, maintained that the body was composed of four elements (earth, air, fire, and water), which combined in various proportions to produce four humours (blood, black bile, yellow bile, and phlegm). Health was a state in which humours stayed in proper balance: disease a condition in which that balance had been upset by some internal or external disturbance. Physicians were to discern the character of the imbalance and institute appropriate restorative measures such as bleeding, purging, or cupping (2,3). In the centuries following Galen's death, physicians modified his original scheme in response to new discoveries in other areas of science. As engineers began to exploit hydraulics, for example, physicians attributed all disease to fluctuations of hydrostatic pressure. After the discovery of elec­ tricity, they exchanged hydraulics for energy imbalance to explain disease. Despite changing theory, however, therapy remained the same. Even at the beginning of the nineteenth century, physicians recommended many methods familiar to Galen, modified only in that they used them with less restraint. At the time of the American Revolution, for example, physician Benjamin Rush became known for his propensity to bleed patients to the point of death (4). The movement away from Galenic medicine began with French physicians. Early in the nine­ teenth century, they began to question and then discard Galenic concepts of disease and therapy. Coincidentally, they created a new system based on careful clinical observation, supplemented by post mortem dissection and statistical analysis (5). From this, they developed the idea that disrup­ tions in the structure of specific organs would induce functional changes recognizable to a clinician as distinctive patterns of signs and symptoms. In the context of this discussion, studies of neurologi­ cal disorders proved to be particularly important. The association of localized lesions with specific From: Contemporary Clinical Neuroscience: Neural Mechanisms of Anesthesia Edited by: Joseph F. Antognini et al. © Humana Press Inc., Totowa, NJ 3 4 Caton and Antognini deficits led them to reject the concept that the central nervous system was a homogenous mass in favor of the concept that it consisted of many components, each with a different function. Physi­ ologic data soon confirmed this. Scottish physician Charles Bell showed, and French physiologist Fran~ois Magendie demon­ strated, that dorsal and ventral nerve roots of the spinal cord have different functions. Legallois rec­ ognized the importance of the cerebellum for the coordination of motor activity. Johannes Muller established the idea that different receptors respond to different stimuli-pain, light touch, or tempera­ ture, for example. Coincidentally, anatomists showed the nervous system to be a collection of highly differentiated cells, ganglia, and pathways. These concepts influenced physiologists and physicians who were just beginning their studies of drug action (6). Significant among early studies of drug action was work by French physiologist Fran~ois Magendie (1783-1855). In 1810 he began experiments on the plant upas tieute, a member of the styrchnos family (7,8). Natives of Borneo and Java used a dried extract of the plant, which caused convulsions and cardio-pulmonary arrest, on the points of their arrows to kill small game much as Indians of South America used curare. Magendie showed: • That the poison worked most quickly when placed directly on the spinal cord or brain rather than on a peripheral nerve. • That the onset of action varied directly with the time it took for the drug to reach the brain. For example an intravenous injection killed more rapidly than intra-muscular injection. • That the circulation had to be intact for poison to work. Dogs died quickly after an injection of the poison into a severed limb, but only when he left its arterial and venous connections intact. Magendie's experiments influenced the next generation of physicians when they began to study mechanisms of anesthetic drugs. EARLY STUDIES IN ANESTHESIA: ATTEMPTS TO ASCERTAIN ITS SITE OF ACTION Important though they were, Magendie's experiments had little impact on the practical American physicians who first demonstrated the anesthetic effects of nitrous oxide and ether. Crawford Long, Horace Wells, and William Thomas Greene Morton simply wanted to relieve pain. They showed no particular interest in the mechanisms that brought this about. Their pragmatic approach was typical of early nineteenth century American physicians and scientists, who distrusted theory and had little interest in any innovation for which they could not find an immediate use. Accordingly, most early studies of mechanisms of anesthesia emerged not from the United States but from Europe among physicians and scientists who were better attuned to theory and scientific inquiry (9,10). At first, physicians appeared to be most concerned about establishing the site of action of anesthe­ sia. They attacked this problem in much the same way that Magendie had dealt with strychnine. Here the influence of clinical and pathological studies of neurological disorders becomes apparent. As physicians used ether, for example, they recognized that anesthetized patients exhibit an orderly sequence of clinical signs, starting with a disturbance of consciousness, followed by a loss reflex activity, and finally a paralysis of respiratory and cardiac activity. From this they reasoned that some parts of the nervous system were more susceptible than others. In fact, within months of the announcement of Morton's demonstration in Boston, French physiologist Pierre Flourens described anesthesia as a progressive depression of the nervous system beginning with the cortex, followed by the cerebellum, and finally the brain stem and spinal cord (11). Others confirmed his findings, among them Nicolai Pirogoff (12-14). Born in Moscow, Pirogoff (1810-1881) trained there before moving to Dorpat, Estonia to con­ tinue his studies. The University in Dorpat, staffed at that time by German speaking physicians, was to have a seminal influence on the development of experimental pharmacology and on early concepts of mechanisms of anesthesia. From Dorpat, Pirogoff moved to Saint Petersburg, where he became Mechanisms of Anesthesia 5 chief surgeon in the medical school. He was teaching there when he first learned about Morton's work with ether (15). Within a year, Pirogoff published a book about anesthesia. In it he describes his use of ether, but he also describes more than forty-five experiments that he performed to elucidate its site and mechanism of action. For example, Pirogoff demonstrated that direct application of ether on a peripheral nerve caused partial anesthesia. He speculated, however, that this response might be due less to the pharmacological action of the drug than to a temperature change in the nerve caused by direct application of the liquid. Pirogoff then proceeded to demonstrate that ether had a more potent effect on the brain than on peripheral nerves, and that it worked better when distributed by the circulation rather than by direct application to the cortex. Pirog off examined individual nerves look­ ing for microscopic anatomical changes that might explain how ether blocked the conduction of impulses (14). He suggested two possibilities. First, that ether might have some "chemical action on nervous tissue." Second, he thought that "ether vapor in the capillary system surrounding nervous tissue" might exert a "greater or lesser degree of compression on the component fibers of the brain and nerves, partly by the force of expansion or partly by passage into the cerebrospinal fluid." In fact, neither of Pirog off's suggestions was particularly new. Pharmacology textbooks from the eighteenth century had speculated that morphine induced some physical change in nerve fibers, thereby inhibit­ ing function (16). Similarly, surgeons had long known that pressure on a nerve could render a limb anesthetic. In fact, one English surgeon, James Moore, tried to popularize this method for painless amputations (17,18). In effect, Pirogoff simply substituted gaseous pressure for the mechanical force that Moore had used (19). Establishing the central nervous system as the primary target of anesthesia was no small achieve­ ment. Even after Magendie's work with strychnine, physicians continued to debate the primary site of action of morphine. Most believed that it affected the brain, but others believed that morphine had its most profound effect on peripheral nerves. For this reason, textbooks recommended that morphine be administered as close as possible to an injured part. In
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