naloxone and Reflex--Abnormal

The role of endogenous opioids on the reflex cardiovascular control of chronic uraemic patients was investigated. The opiate antagonist naloxone administered intravenously caused a significant increase in the abnormal Valsalva manoeuvre ratio in nine chronic uraemic patients, but it had no effect in six diabetic patients with normal renal function, whose response to the Valsalva manoeuvre was similar to that of chronic uraemic patients. Naloxone had no effect in eight normal subjects. The increase in the Valsalva ratio observed in uraemic patients was due to restoration of the parasympathetically mediated reflex bradycardia of the release phase of the manoeuvre. Naloxone did not modify supine and standing blood pressure and heart rate in any group. Endogenous opioids may be involved in the defective autonomic control of heart rate in uraemic patients.

Topics: Adult; Autonomic Nervous System Diseases; Blood Pressure; Chronic Disease; Diabetes Mellitus; Drug Evaluation; Heart Rate; Humans; Male; Middle Aged; Naloxone; Reflex, Abnormal; Uremia; Valsalva Maneuver

In pre-clinical models intended to evaluate nociceptive processing, acute stress suppresses reflex responses to thermal stimulation, an effect previously described as stress-induced "analgesia." Suggestions that endogenous opioids mediate this effect are based on demonstrations that stress-induced hyporeflexia is enhanced by high dose morphine (>5 mg/kg) and is reversed by naloxone. However, reflexes and pain sensations can be modulated differentially. Therefore, in the present study direct comparisons were made of opioid agonist and antagonist actions, independently and in combination with acute restraint stress in Long Evans rats, on reflex lick-guard (L/G) and operant escape responses to nociceptive thermal stimulation (44.5 degrees C). A high dose of morphine (>8 mg/kg) was required to reduce reflex responding, but a moderate dose of morphine (1 mg/kg) significantly reduced escape responding. The same moderate dose (and also 5 mg/kg) of morphine significantly enhanced reflex responding. Naloxone (3 mg/kg) significantly enhanced escape responding but did not affect L/G responding. Restraint stress significantly suppressed L/G reflexes (hyporeflexia) but enhanced escape responses (hyperalgesia). Stress-induced hyperalgesia was significantly reduced by morphine and enhanced by naloxone. In contrast, stress-induced hyporeflexia was blocked by both naloxone and 1 mg/kg of morphine. Thus, stress-induced hyperalgesia was opposed by endogenous opioid release and by administration of morphine. Stress-induced hyporeflexia was dependent upon endogenous opioid release but was counteracted by a moderate dose of morphine. These data demonstrate a differential modulation of reflex and operant outcome measures by stress and by separate or combined opioid antagonism or administration of morphine.

Topics: Acute Disease; Adaptation, Physiological; Analgesics, Opioid; Animals; Conditioning, Operant; Disease Models, Animal; Displacement, Psychological; Dose-Response Relationship, Drug; Escape Reaction; Female; Morphine; Naloxone; Narcotic Antagonists; Opioid Peptides; Rats; Rats, Long-Evans; Reaction Time; Reflex; Reflex, Abnormal; Restraint, Physical; Stress, Psychological

The effect of an experimental neuropathy on the viscero-somatic inhibition was studied in lightly anesthetized rats. In controls, colo-rectal distension at noxious intensities produced a multisegmental prolongation of the withdrawal response induced by noxious stimulation of the skin. In rats with a spinal nerve-ligation induced neuropathy this viscero-somatic inhibition was significantly reduced within the neuropathic segment (the hindlimb) but not outside of it (the tail). Naloxone, an opioid antagonist, attenuated this viscero-somatic inhibition in controls and it did not restore the inhibition in neuropathic rats. The results indicate that somatic neuropathy produces a segmental attenuation of viscero-somatic inhibition and this attenuation cannot be explained by a nerve injury-induced release of endogenous opioids. The decreased inhibition of somatic signals may contribute to the hypersensitivity observed in neuropathic conditions.

Topics: Animals; Colon; Hot Temperature; Hyperalgesia; Male; Naloxone; Narcotic Antagonists; Neural Inhibition; Neurons, Afferent; Nociceptors; Pain; Pain Measurement; Pain Threshold; Peripheral Nervous System Diseases; Physical Stimulation; Rats; Rats, Wistar; Reaction Time; Reflex, Abnormal; Skin; Spinal Cord; Spinal Nerves; Visceral Afferents

In decerebrated rabbits, reflexes evoked by electrical stimulation of the toes in the ankle flexor tibialis anterior were enhanced for > 30 min after application of 20% mustard oil to the base of the toes, whereas responses of the ankle extensor medial gastrocnemius to stimulation of the heel were depressed for > 20 min by the same stimulus. Applied to the heel, mustard oil had inconsistent effects on the flexor reflex but potentiated the extensor response for approximately 1 h. Intrathecal co-administration of naloxone (25 microg) with the selective alpha(2)-adrenoceptor antagonist RX 821002 (200 microg) enhanced both reflexes to more than twice pre-drug values and reduced or abolished all effects of mustard oil. These data confirm that the location of a noxious stimulus is an important determinant of the subsequent adaptive changes in reflexes, and indicate roles for endogenous opioids and noradrenaline in these processes.

Topics: Adaptation, Physiological; Adrenergic alpha-Antagonists; Animals; Decerebrate State; Electric Stimulation; Female; Heel; Male; Mustard Compounds; Naloxone; Narcotic Antagonists; Rabbits; Reflex, Abnormal; Stimulation, Chemical; Toes

The cardiovascular responses to muscular contraction induced by ventral root (L7 and S1) stimulation were studied in unanesthetized decerebrate cats before and after the administration of the opiate antagonist naloxone. Intravenous naloxone (1.0-2.0 mg/kg) did not alter the heart rate or arterial pressure responses to either tetanic or repeated twitch contractions. However, naloxone did increase resting arterial pressure.

Topics: Animals; Blood Pressure; Cardiovascular System; Cats; Decerebrate State; Endorphins; Heart Rate; Muscle Contraction; Naloxone; Physical Exertion; Reflex, Abnormal; Spinal Nerve Roots

Topics: Adult; Blood Pressure; Enkephalin, Methionine; Heart Rate; Humans; Male; Middle Aged; Naloxone; Pressoreceptors; Reflex, Abnormal; Renal Dialysis; Uremia; Valsalva Maneuver