naloxone and Hyperthyroidism

This study was conducted to determine the effect of thyroid hormone on opiate receptor ligand-binding and pain sensitivity. Specific opiate receptor-binding was performed on brain homogenates of Swiss-Webster mice. There was a significant increase in 3H-naloxone-binding in thyroxine-fed subjects (hyperthyroid). Scatchard analysis revealed that the number of opiate receptors was increased in hyperthyroid mice (Bmax = 0.238 nM for hyperthyroid samples vs. 0.174 nM for controls). Binding affinity was unaffected (Kd = 1.54 nM for hyperthyroid and 1.58 nM for control samples). When mice were subjected to hotplate stimulation, the hyperthyroid mice were noted to be more sensitive as judged by pain aversion response latencies which were half that of control animals. After morphine administration, the hyperthyroid animals demonstrated a shorter duration of analgesia. These findings demonstrate that thyroxine increases opiate receptor number and native pain sensitivity but decreases the duration of analgesia from morphine.

Topics: Animals; Brain; Etorphine; Hyperthyroidism; Ligands; Male; Mice; Mice, Inbred Strains; Morphine; Naloxone; Pain; Receptors, Opioid; Thyroxine

Topics: Diabetes Complications; Diabetic Coma; Drug Combinations; Endocrine System Diseases; Glucose; Humans; Hyperthyroidism; Insulin; Male; Middle Aged; Naloxone; Potassium; Shock; Somatostatin; Thyroid Hormones

The anesthesiologist uses a wide spectrum of drugs, including inhalational general anesthetics, barbiturates, benzodiazepines, narcotics analgesics and their antagonists, and neuromuscular blocking drugs. All of these drugs in sufficient dose impair the ventilatory response to chemical stimuli, and may cause inadequate gas exchange. The effect of depression of ventilatory control depends on the magnitude of depression and the coexistence of functional abnormalities in the respiratory system. The functional abnormalities are the result of preexistent pulmonary disease or other disease processes that impair respiratory function, the anticipated effects of major surgery (e.g., pulmonary resection), and the complications of anesthesia and surgery. From a functional viewpoint, the mechanisms of the effects of these disease processes on ventilatory control are: (1) interference with the neurophysiological control of automatic ventilation; (2) impairment of peripheral or central chemoreceptor function; (3) impairment of respiratory muscle function; (4) increase in the mechanical load to breathing as a result of increased resistance or decreased compliance of the respiratory system; and (5) increase in the ventilatory requirements as a result of ventilation/blood flow maldistribution, metabolic acidosis, or increased metabolic rate. As a result of current trends in the use of multiple drugs and controlled ventilation during anesthesia, the patient is at greatest risk during the early postoperative period in the recovery room. In addition to the functional abnormalities described above, the probability of impaired gas exchange and respiratory failure is increased as a result of impaired metabolism and elimination of drugs as a result of hepatic and renal insufficiency, and acute changes in acidbase status, which alter the ionization and distribution of drugs.

Topics: Anesthetics; Anti-Anxiety Agents; Autonomic Nervous System; Barbiturates; Benzodiazepines; Carbon Dioxide; Fentanyl; Halothane; Humans; Hyperthyroidism; Hypoxia; Lung Diseases, Obstructive; Meperidine; Methoxyflurane; Morphine; Naloxone; Neuromuscular Blocking Agents; Neuromuscular Diseases; Obesity; Pulmonary Edema; Pulmonary Fibrosis; Respiration; Scoliosis