Recently, it came to my attention that William S. Burroughs used a number of substances with commonality to both the human and veterinary pharmacopeia. Within a veterinary context, some of these substances are primarily indicated in the treatment of dogs and cats, others in the treatment of horses and cattle. All of them were utilized by Burroughs in an attempt to escape the constant shadow of opiate addiction. An account of his experiences with these drugs can be found in The British Journal of Addiction (vol. 53;2, 1956), and forms the appendix of his novel, Naked Lunch.

Burroughs became fascinated by the mechanics and technicalities of addiction. Furthermore, he was intrigued by the public perception of drug addiction. "People believe what they want to believe without regard for the facts," he observed. What follows, in several parts, is a listing of the veterinary drugs utilized by Burroughs, some impressions regarding their effects, and, as a tribute to Honest Bill, the objective data:

Opiates:

Junk plagued Burroughs for fifteen years. It formed the basis for his wanderings through a myriad of psychoactive substances. Its definition was total need. "Wouldn?t you? Yes you would," Burroughs wrote. By his own account, his use of opiates was extensive: opium, morphine, heroin, diluadid, eukodal, pantopon, diocodid, diosane, demerol, dolophine, palfium, dionine, paracodine, codeine, and methadone. Morphine, codeine, and meperidine (demerol) are commonly used for pain management in both small and large animals. Morphine and codeine are natural opiate alkaloids, found in the milky, viscous fluid of unripe opium poppy (Papaver somniferum) seedpods. Meperidine is a synthetic opiod. All are scheduled narcotics.

Opiates and their derivatives act at a series of receptors, designated Mu, Kappa, Sigma, Delta, and Epsilon, that are scattered across tissues in the body. The concentration of these receptors is particularly high in neural tissue, but can be found as well in the gastrointestinal and urinary tracts and in smooth muscle. Opiates act at their receptors much the same way a key would open a lock. If the opiate binds to the receptor in a fashion that provokes a cascade of biochemical events resulting in a characteristic action, it is known as an agonist. However, there are opiates that have a high affinity for receptors, but provoke no action at those receptors, known as antagonists. As a key broken off in a lock, they neither open the lock nor allow other keys to open the lock. Although individual opiates have specific affinity for one or more opiate receptors, the effects resulting from stimulation of these receptors are not consistent across species.

Morphine and meperidine have primary activity at the Mu receptor. While these opiate agonists have analgesic properties across species, they tend to elicit excitement in horses, cattle and cats but are responsible for the characteristic euphoria and sedation experienced by humans and observed in dogs. Intravenous administration of morphine provokes defecation in the dog, while other species experience constipation. These "Mu agonists" are some of the most potent analgesics known.

A walk through the small animal orthopedic surgery wards in any major veterinary teaching hospital will turn up a significant number of patients receiving fentanyl, a synthetic Mu agonist. Fentanyl is typically delivered via a transdermal patch in which a semi-permeable membrane enables continuous release of the opiod across the skin for a period of seventy-two hours.

There is little doubt that had fentanyl been available during the years of Burroughs opiate addiction, he would have readily used it. It is marketed, seperately from the transdermal patch, as an injectable solution, and is known on the street in this form as "China white." In humans, the potential exists for significant respiratory depression, with the possibility of muscular spasm leading to respiratory arrest. This fairly significant detail seems not to have curbed the abuse of fentanyl.

My experience with the fentanyl solution remains limited to perineural injection of the product on a humane, experimental basis in a recumbent horse with end-stage laminitis. The condition is defined by deviation, or pulling away, of the most distal bony digit from its normally close association with the sensitive lamina lining the hoof wall. The process is thought to be exquisitely painful; akin to a tearing away of one's fingernail from the underlying skin, with the added pain of one's entire body weight resting upon this disrupted structure. End-stage denotes a perforation of the distal digit through the sole of the hoof, resulting in exposed bone as the weight bearing surface. Horses in this condition are generally reluctant or unable to walk and are frequently recumbent. There is no humane course of treatment when the laminitis has progressed to this stage.

This patient was admitted with severe laminitis in all four hooves -- the distal digit having perforated through the sole in two of the hooves -- significant muscle wasting and pressure sores over forty percent of the body resulting from prolonged recumbency. We couldn't have euthanized the horse fast enough if the needle and euthanasia solution had come preplaced in its vein. Sadly, legal action prevented the hospital from doing so until nearly three days following admission. The interim was filled with novel attempts at providing profound analgesia bordering on a state of semi-consciousness. Perineural infiltration of fentanyl at the palmar digital nerves, which supply sensory information originating from the region of the hoof, seemed a logical approach. The efficacy of this endeavor was difficult to assess given the multi-faceted analgesic coverage employed, including the fentanyl transdermal patch to ensure opiod delivery to the brain. However, the fixed stare, gape-mouthed expression and absence of movement, save for the rhythmic expansion and contraction of the chest with respiration, hinted at a mental state less than full awareness. Given the conditions, that might have been the best for which we could have hoped.

Butorphanol, a potent mixed agonist/antagonist opiod analgesic with limited use in humans due to its strong antagonist effect, has found wide use amongst large animal veterinarians. Abdominal pain in horses, frequently referred to as colic, represents one of the most common and potentially life threatening equine emergencies. Butorphanol is astoundingly effective at controlling colic pain originating from the gastrointestinal tract. It is common to send a violently painful thousand pound horse into a state of euphoria with as little as ten to fifteen milligrams of butorphanol. A profound respect for this drug is attained when these horses are opened at surgery, and you comprehend the wall this drug constructs to block out pain originating from, in severe cases, meters of purple-black dead bowel. Typically, a sedative/analgesic combination given intravenously is the initial response to mild or moderate colic. However, intramuscular injection of butorphanol is appropriate in violently thrashing horses that cannot be kept standing and in which venous access is precluded by the liklihood of a hoof in the face. A central tenet of opiod use in horses that all veterinary students learn is that they are not to be given intravenously rapidly without prior sedation. At low doses, this may provoke only mild excitement or head tremors, but higher doses can result in seizure activity. Although I haven?t witnessed such an event, reports exist of horses flipping over backward after receiving an overdose of intravenous butorphanol.

Physical and psychological dependence are known sequellae to repeated opiate use. The potential for dependency seems to vary directly with each opiate's analgesic potency. Regular use of opiates leads to development of tolerance, in which increasing quantities of opiate are required to achieve a consistent effect. This phenomenon accounts for the addict?s ever-growing appetite for junk. Although the therapeutic range for treatment of severe pain with morphine may reach its upper limit at sixty milligrams intravenously daily based on average weight, the junkie will readily consume hundreds of milligrams of morphine daily. Dosages that endanger life are defined by the LD50 or median lethal dose. That is, the dose of a compound at which fifty percent of the test subjects experimentally receiving that dose will likely die. Although the LD50 for morphine in humans has not been established, it is thought to be in the range of several hundred milligrams to several grams.

And so the chronic junkie courts death regularly. Because nothing shy of sublime is acceptable. Because you could be standing on exposed bone and rotting from the inside, and that would be fine. Because once you cross the threshold, nothing else matters, and leaving the abyss is a long and uncertain journey.

Read Part Two.

Read Part Three.