Anesthesia and Analgesia in Laboratory Animals

Richard Fish, Peggy J. Danneman, Marilyn Brown, Alicia Karas, Richard Fish, Peggy J. Danneman, Marilyn Brown, Alicia Karas

• Editorial: Academic Press
• Año: 2011
• ISBN:
  9780080559834
• Edición: 2
• Categoría: Medicine
• Categoría: Veterinary Medicine

Anesthesia and Analgesia in Laboratory Animals focuses on the special anesthetic, analgesic, and postoperative care requirements associated with experimental surgery. Fully revised and updated this new edition provides the reader with agents, methods, and techniques for anesthesia and analgesia that ensure humane and successful procedural outcomes.

• Provides researchers with the most comprehensive and up-to-date review of the use of anesthesia and analgesia in laboratory animals
• Thoroughly updated with new material on ferrets, birds, reptiles, amphibians, fish, and invertebrates
• Includes hot topic areas such as pain research, ethical issues, legal issues, and imaging studies

Chapter 1 Anatomy, Physiology, and Effects of Pain

George J. DeMarco, Peter J. Pascoe

I. Definitions

A. Pain

II. Anatomy and Physiology of Nociception

A. Nociception

III. Neuropharmacology of Nociception

A. Excitatory Neurotransmitters and Receptors

B. Inhibitory Neurotransmitters and Receptors

IV. Neonatal Development and Pain

A. Pain in the Neonate

B. Developmental Effects of Pain

V. Physiologic Effects of Pain

A. Neuroendocrine Response

B. Cardiovascular Effects

C. Pulmonary Compromise

D. Miscellaneous Effects

VI. Neuroplasticity and Pain: Peripheral and Central Sensitization

A. Peripheral Sensitization

B. Central Sensitization

VII. Pathophysiology of Chronic Pain

A. Role of Neuroplasticity and Sensitization

B. Etiologies

References

I. DEFINITIONS

A. Pain

Pain has been defined by the International Association for the Study of Pain (IASP) as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Merskey and Bogduk, 1994). The IASP has also added the following comments: “The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain-relieving treatment,” and “pain is always subjective.” Irrespective of statements regarding verbal communication, this is a human description for pain, based on the experience of physicians. Molony and Kent have used the following for an animal-specific definition of pain: “an aversive sensory, emotional experience representing an awareness by the animal of damage or threat to the integrity of its tissues (note, there may not be any damage); it changes the animal’s physiology and behavior to reduce or avoid damage, reduce the likelihood of recurrence, and to promote recovery; nonfunctional pain occurs when the intensity or duration of the experience is not appropriate for the damage sustained (especially if none exists) and when physiological and behavioral responses are unsuccessful in alleviating it.” This definition is predicated on animal pain having similar purpose and significance but not in equivalence to human pain (Molony, 1997; Molony and Kent, 1997). It puts pain in the context of an evolutionary survival mechanism by which the animal recognizes and learns to avoid injury. This definition also addresses forms of pain that serve no known function and situations where the animal has exhausted its ability to adapt or compensate and is condemned to suffer.

Although neither definition has been universally accepted for animals, it is interesting that both human and animal definitions squarely cast pain as an experience. The scientific and philosophical arguments for or against animal pain are beyond the scope of this work. Although the debate continues, the consensus among veterinarians and a growing number of neuroscientists is that animals do feel pain, and this volume is predicated on this concept.

1. Acute Pain

Acute pain usually has a proximate cause and often serves an essential protective function by associating potentially damaging noxious stimuli with an unpleasant sensation (Woolf, 2004). It can last from seconds to days, and perhaps longer; some have suggested somewhat arbitrary time frames even up to 3 months for humans. Acute pain can be further characterized as physiologic or clinical. Physiologic pain, sometimes referred to as nociceptive pain, is an early-warning system that aids in protecting the body from tissue damage by physical, thermal, or chemical threats (Woolf and Salter, 2000). This type of pain is initiated by the activation of high-threshold nociceptive neurons by noxious stimuli that produce minimal tissue damage, is highly localized to the site of nociceptor activation, and is transient. Another important feature of physiologic pain is that neurophysiologic and subjective responses are closely tied and proportional to the intensity of the inciting stimulus (Casey et al., 1996; Cervero and Laird, 1996; Granovsky et al., 2005). Nociceptive pain initiates physiologic and avoidance behaviors accompanied by protective reflexes, all of which serve to prevent or limit tissue damage. (Nociception is discussed in detail below. Note that the term, nociceptive pain, is also commonly used to distinguish pain arising from nociceptors, from neuropathic pain (NP), i.e., some kind of centrally mediated pain resulting from nerve injury or changes in central processing.)

Clinical pain refers to prolonged unpleasant sensations arising from significant tissue damage. In contrast to physiologic pain, clinical pain induces augmented or abnormal signal processing, may be spontaneous, and may be characterized by hypersensitivity, hyperalgesia, and allodynia (see definitions below), pain at the site of injury (primary allodynia and/or hyperalgesia), and pain in surrounding noninjured tissues (secondary mechanical allodynia and/or hyperalgesia) (Merskey and Bogduk, 1994). The primary causes of clinical pain are tissue inflammation or damage to peripheral or central neurons (neuropathic); thus, the number and type of initiating conditions or events (trauma, surgery, infection) are quite extensive. In some cases, such as cancer-associated pain, amputations, or vertebral disk prolapse, both inflammatory and neuropathic mechanisms are at work. Clinical pain may serve a useful biologic function by coupling pain to tissue healing, thus, helping limit further injury during the recovery process. However, in many instances, excessive inflammation develops or damaged nervous tissue functions abnormally, and clinical pain becomes a disease, serving no benefit to the individual. Any potential benefits of clinical pain should not be taken as evidence that pain is an acceptable means of restraint or that it should be untreated. Besides ethical considerations, it is generally accepted that untreated pain significantly increases morbidity and mortality.

2. Chronic Pain

In human medicine, chronic pain has been defined as “pain which persists past the normal time of healing” (Bonica, 1953). This definition has significant shortcomings since healing may never occur in chronic-pain-associated diseases like arthritis, may never be recognized, as in forms of NP, or may remit and relapse over time. A more useful definition is that chronic pain is said to be present when the pain continues beyond the stage where it is useful to protect the region, or is persistent and may not have a clearly identifiable cause. The IASP has adopted temporal endpoints based on common medical experience to classify chronic pain. The IASP regards 3 months of pain as the most expedient point at which the transition from acute to ...