Biomedical subjects

S G Kamerling

Publications and source records attributed to S G Kamerling.

29 records · Page 2Linked to original sources

PubMed1988

Dose-related effects of detomidine on autonomic responses in the horse.

1. Detomidine is a novel veterinary sedative analgesic which is thought to act by stimulation of alpha 2 adrenoreceptors. The present study was undertaken to determine the direction, time course, and dose-response relationship of detomidine on specific autonomic responses in the unanaesthetized horse. 2. Detomidine was administered intravenously to eight adult thoroughbred racehorses at doses of 0.010-0.040 mg kg-1, according to a double-blind Latin square crossover design. Cardiac and respiratory rates, pupil diameter and rectal temperature were monitored for 180 min postinjection. 3. Detomidine produced prolonged dose-related bradycardia and bradypnoea. This was accompanied by a briefer period of dose-related mydriasis. Response duration, rather than peak was consistently increased as a function of dose. 4. Rectal temperature was not altered in a dose-dependent fashion. Low doses of detomidine produced late onset hypothermia, while high doses produced early and late onset hyperthermia. 5. These data indicate the uniqueness in autonomic response by the horse to alpha 2 adrenoreceptor stimulation.

Animals↗

PubMed1988

Cortical somatosensory-evoked potentials in the horse.

Cortical somatosensory-evoked potentials (SEP) were recorded from thoracic and pelvic limbs in 15 horses (13 Thoroughbreds and 2 Quarter Horses). Ulnar nerve SEP were evoked by electrical stimulation of the lateral palmar branch of the ulnar nerve at the level of the metacarpophalangeal joint. Recordings were taken between electrodes at 2 cm lateral to the vertex (contralateral to the stimulated limb) and the midpoint of the interorbital line. Four peaks were found in all recordings: N1, P1, N2, and P2. Latencies to the peaks were 39.0 +/- 2.7, 45.5 +/- 5.3, 50.4 +/- 5.2, and 62.3 +/- 3.7 ms (mean +/- SD), respectively. Tibial nerve SEP were evoked by stimulation of the lateral plantar nerve branch of the tibial nerve at the level of the metatarsophalangeal joint. Recordings were taken between electrodes at the vertex (contralateral to the stimulated limb) and the midpoint of the interorbital line. Four peaks were also found in all tibial nerve SEP recordings: N1, P1, N2, and P2. Latencies to the peaks were 64.6 +/- 11.8, 84.5 +/- 9.7, 121.2 +/- 11.6, and 134.0 +/- 11.1 ms, respectively. Amplitude variability was high for the ulnar nerve and the tibial nerve SEP. There was no effect of sex seen on peak latency or amplitude, and peak latencies were not affected by body length.

Animals↗

PubMed1986

Dose-related effects of ethylketazocine on nociception, behaviour and autonomic responses in the horse.

Sensitive methods for measuring the analgesic, physiological and behavioural effects of opioids in the horse have recently been developed. Fentanyl, a prototypic mu-opiate receptor agonist, has been previously shown to produce a syndrome characterized by marked analgesia and locomotor stimulation as well as tachycardia, tachypnoea and behavioural arousal. To determine whether other opiate receptors mediate some of the actions of the narcotic analgesics in the horse, an agent with activity at kappa- and to lesser extent mu-receptors was studied using a vigorous experimental protocol. Like fentanyl, ethylketazocine (EKC) (0.0025-0.012 mg kg-1 i.v.) produced marked dose-related analgesia to noxious thermal stimuli. Modest dose-related increases in locomotor activity, pupil diameter and rectal temperature were also observed. However, in contrast to fentanyl, EKC failed to produce any change in cardiac or respiratory rates and produced behavioural sedation rather than arousal. These data suggest that mu- and possibly kappa-receptors can mediate the actions of narcotics in the horse.

Analgesics, Opioid↗

PubMed1985

A method for studying cutaneous pain perception and analgesia in horses.

Pain perception and its alteration by analgesic drugs is difficult to measure in the horse. The latency to onset of flexion of a limb in response to a noxious thermal stimulus has been used as a nociceptive end point for analgesic studies in many species. While this method has been employed in the horse, it may be confounded by the spontaneous locomotor activity observed after administration of narcotic analgesics. Consequently, an alternative method of assaying narcotic analgesia that did not involve the equine locomotor apparatus was developed. This report describes the use of the heat-evoked skin-twitch reflex as a reproducible measure of pain threshold and its alteration by the narcotic analgesic fentanyl. This method is compared with the heat-evoked hoof-withdrawal reflex, and the apparatus necessary to elicit both reflexes in the horse is described. Fentanyl, administered at intravenous doses of 0.010, 0.005, and 0.0025 mg/kg, produced a dose-related prolongation of the skin-twitch reflex but failed to alter the latency to hoof withdrawal following noxious thermal stimulation. The skin-twitch reflex is therefore a more sensitive assay of narcotic analgesia in the horse than is the hoof-withdrawal reflex.

Analgesia↗

PubMed1985

Dose-related effects of fentanyl on autonomic and behavioral responses in performance horses.

The dose-related effects of intravenously administered fentanyl (0.010, 0.005, 0.0025 mg/kg) and saline were studied in mature performance horses using a rigorous experimental protocol. Fentanyl produced a dose-related prolongation of the skin twitch reflex latency but did not increase the hoof withdrawal reflex latency. Dose related increases in stepping frequency, cardiac and respiratory rats were observed following fentanyl, while changes in rectal temperature and pupil area were not. These data indicate that fentanyl, a prototypic mu-agonist, produces a syndrome characterized by analgesia, locomotor and sympathetic stimulation in the horse.

Animals↗

PubMed1984

Differential effects of phenylbutazone and local anesthetics on nociception in the equine.

The effects of procaine, mepivacaine and phenylbutazone on pain perception in the equine were studied using two behavioral assays of nociception; the thermal evoked hoof withdrawal reflex and skin twitch reflex. Pain perception threshold was measured as the latency from onset of thermal stimuli to reflex withdrawal of the forelimb or contraction of the cutaneous musculature. Procaine 2% and mepivacaine 2% prolonged the hoof withdrawal reflex latency when administered locally by producing a block of the palmar and metacarpal nerves. Significant analgesia lasted 90 min and 210 min for procaine and mepivacaine, respectively. Phenylbutazone (7.3 mg/kg) failed to alter pain thresholds measured over a 36 h post-treatment period. However, pain thresholds rose over time with successive trials. These data suggest that in the equine (1) phenylbutazone does not alter normal cutaneous pain perception, and (2) successive presentation of painful stimuli increases nociceptive thresholds.

Analgesia↗

PubMed1984

The effects of naloxone on endotoxic and hemorrhagic shock in horses.

The effects of naloxone on the cardiovascular, hematologic and metabolic derangements associated with endotoxic and hemorrhagic shock were studied in unanesthetized horses. In the first of 3 experiments blood glucose and lactate levels, hematocrit, white, red and differential white cell counts, rectal temperature and clinical signs were obtained before and after endotoxin (10 micrograms/Kg) administration in 5 horses. In the second experiment, two groups of 3 horses received either intravenous naloxone (0.04 mg/Kg) or saline, 7 minutes prior to endotoxin. In a third experiment two groups of 4 horses received either saline or naloxone (0.20 mg/Kg) immediately following acute hemorrhage. In the second and third experiments, pulse, mean arterial and right ventricular pressures, and heart rate were also observed. Endotoxin and acute hemorrhage produced hypothermia, leukopenia, lymphopenia, neutropenia, elevations in hematocrit, blood glucose and blood lactate, and clinical signs of shock. Naloxone (0.040 mg/Kg IV) significantly lowered endotoxin-induced increases in right ventricular pressure and heart rate, and at a higher dose (0.20 mg/Kg) antagonized the decrease in pulse and heart rate, and tachycardia observed after acute hemorrhage. These results suggest endogenous opioids are involved in the pathogenesis of shock. Naloxone appeared to attenuate some of the cardiovascular responses associated with shock and thus may be of therapeutic value in shock management.

Animals↗

PubMed1983

Possible medullary kappa hyperalgesic mechanism. I. A new potential role for endogenous opioid peptides in pain perception.

The kappa-agonist, ethylketazocine, produces hyperalgesia in the acutely decerebrated dog as indicated by a shortening of the skin twitch reflex latency whereas fentanyl is inactive. Naloxone produces analgesia and antagonizes the hyperalgesic effect of ethylketazocine. Spinal cord transection decreases the latency of the skin twitch reflex and allowed the analgesic effect of fentanyl and ethylketazocine on this nociceptive reflex to become manifest. These observations indicate that there is a non-opioid analgesic and kappa hyperalgesic mechanism present in the pontine-medullary region of the dog brainstem. It suggests that the hyperalgesic mechanism is mediated by an endogenous kappa-opioid peptide and that the analgesic effect of naloxone is in part related to antagonism of the activity of this hyperalgesia producing opioid peptide.

Animals↗

PubMed1983

Medullary kappa hyperalgesic mechanisms II. The effects of ethylketazocine administered into the fourth cerebral ventricle of the conscious dog.

Ethylketazocine (EKC) (2 micrograms/100 microliter/min for 15 min) was infused into the fourth cerebral ventricles of conscious dogs. The drug produced hyperalgesia, respiratory depression, miosis, increased EEG electrogenesis and behavioral sedation. Hyperthermia and tremulousness were observed in some animals. These pharmacologic effects reflect the action of EKC on pontomedullary periventricular sites which control nociception, autonomic function and arousal.

Analgesics, Opioid↗

PubMed1982

Interaction between nicotine and endogenous opioid mechanisms in the unanesthetized dog.

Nicotine produced a distinct reproducible syndrome in the conscious dog when injected intravenously or intracerebroventricularly. Intravenously administered nicotine (40 micrograms/kg/min for 20 minutes) increased cardiac and respiratory rates and produced analgesia, miosis, hypothermia, behavioral restlessness and emesis. When microinjected into the third cerebral ventricle, nicotine (100-200 micrograms) similarly increased cardiac and respiratory rates and pupillary diameter; and produced behavioral restlessness, emesis, erratic analgesia and maintained wakefulness and a desynchronized EEG. Microinjection of nicotine (5-25 micrograms) into the periaqueductal gray failed to alter any of the parameters studied. Intravenous pretreatment with the opioid antagonist naltrexone (2 mg/kg) influenced the action of intravenous nicotine on certain physiological systems. While naltrexone alone produced a significant degree of tachycardia, miosis, and analgesia, it potentiated the tachypnea and antagonized the miotic response evoked by nicotine. Methionine-enkephalin was detected in perfusates obtained from the lateral cerebral ventricles of conscious dogs. Nicotine produced a non-significant decrease in enkephalin levels. These observations suggest that there are interactions between endogenous opioid and nicotinic processes. However, they are complex and may differ from one functional system to another.

Animals↗

PubMedDate not supplied

Models for assessing the relationship between drug concentration and drug effect in performance horses.

The actions of most drugs are dependent upon achieving adequate plasma concentrations. Plasma concentrations are influenced by the degree to which a drug is absorbed, distributed, metabolized and excreted. Pharmacokinetic assessment reflects changes in these variables as a function of time. Pharmacodynamics refers to specific drug effects or mechanisms of drug action. Individual drug pharmacokinetics provides information on which to base a therapeutic dose, route of administration and dosing interval. However, not all drug actions temporally correlate with plasma kinetics. To resolve this discrepancy, pharmacodynamic models of drug action have been developed. In this review several pharmacodynamic models of anti-inflammatory and central nervous system effects are discussed in relationship to individual drug pharmacokinetics in the horse. The use of appropriate statistical models can minimize error and maximize the detection of drug effects over time. Data are presented showing the value of pharmacodynamic models in assessing and predicting the onset, peak and duration of drug action. Penetration of drugs into inflamed tissue or the brain may not temporally correlate with plasma kinetics. Therefore, drug kinetics in tissues or compartments associated with a particular effect may be a better predictor of efficacy than plasma concentrations. Recent studies have shown that exercise can affect drug disposition and influence both pharmacokinetics and pharmacodynamics. In competitive athletes, plasma or urine concentrations of drugs are determined to regulate use. Some jurisdictions are advocating the establishment of specific drug thresholds based upon plasma or urine concentrations. However, drug effects may occur during low or undetectable plasma concentrations. Urine concentrations are often dissociated in time from those in plasma. Therefore, the use of appropriate pharmacodynamic models, and the exercising horse, can complement plasma pharmacokinetics in determining drug efficacy and drug thresholds.

Animals↗