PubMed Health⌕ Search

Biomedical subjects

A S Rice

Publications and source records attributed to A S Rice.

At least 19 recordsLinked to original sources
PubMed1998

The endogenous cannabinoid anandamide, but not the CB2 ligand palmitoylethanolamide, prevents the viscero-visceral hyper-reflexia associated with inflammation of the rat urinary bladder.

Anandamide, an endogenous ligand at the CB1 cannabinoid receptor and palmitoylethanolamide (a putative endogenous ligand at the CB2 receptor) have both been shown to possess anti-hyperalgesic properties in models of somatic and visceral inflammation. In the turpentine-inflamed rat urinary bladder a reversal of the inflammation-associated viscero-visceral hyperreflexia (VVH) was observed when the cannabinoids were administered 135 min after the induction of inflammation. Therefore, in this study we determined the efficacy of these two N-acylethanolamides in the prevention of VVH in the same model, using a prophylactic dosing regimen. Palmitoylethanolamide did not prevent the VVH (in the dose range 10-30 mg/kg, i.a), but anandamide attenuated the response in a dose related manner, with a threshold of 25 mg/kg (i.a). These findings provide further support for an acute anti-nociceptive and anti-hyperalgesic role for CB1 receptor agonists, with CB2 agonist effects only becoming important once the effects of inflammation are established.

Amides↗
PubMed1998

The modulatory effects of bradykinin B1 and B2 receptor antagonists upon viscero-visceral hyper-reflexia in a rat model of visceral hyperalgesia.

This study assessed the relative involvement of the two bradykinin (Bk) receptors (B1 and B2) in the viscero-visceral hyper-reflexia (VVH) and plasma extravasation observed in an animal model of cystitis. The effects of the competitive receptor antagonists des-Arg9[Leu8]-Bk (B1) and HOE 140 (B2) were tested both in prophylactic (pre-inflammation administration) and therapeutic (post-inflammation administration) scenarios. Compared with control animals, des-Arg9[Leu8]-Bk had no effect on the hyper-reflexic response of the bladder to inflammation unless it was administered 5 h after inflammation. However, HOE 140 was able to attenuate the inflammation-induced viscero-visceral hyper-reflexia (VVH) at doses of 1 mg/kg, 2 mg/kg and 7.5 mg/kg. This effect was apparent whether the drug was administered before, or after inflammation. In contrast, neither compound was effective in attenuating the intravesical plasma extravasation induced by turpentine. The data therefore suggest that the VVH and tissue inflammation responses are mediated via different mechanisms. In addition, the turpentine-induced VVH appears to be mediated, at least partially, by the B2 receptor in the early phase, with the B1 receptor only becoming important later.

Adrenergic beta-Antagonists↗
PubMed1998

The anti-hyperalgesic actions of the cannabinoid anandamide and the putative CB2 receptor agonist palmitoylethanolamide in visceral and somatic inflammatory pain.

This study assessed the effects of two N-acylethanolamides in established rat models of visceral and somatic inflammatory pain. (1) The therapeutic effects of the cannabinoid anandamide and the putative CB2 agonist palmitoylethanolamide were tested in a model of persistent visceral pain (turpentine inflammation of the urinary bladder). Both anandamide (at a dose of 25 mg/kg) and palmitoylethanolamide (at doses of 10-30 mg/kg) were able to attenuate the viscero-visceral hyper-reflexia (VVH) induced by inflammation of the urinary bladder. (2) The effects of the same compounds on the behavioural response to subcutaneous formalin injection were assessed. The characteristic biphasic response was observed in control animals. Anandamide (dose range 5-25 mg/kg) and palmitoylethanolamide (dose range 5-10 mg/kg) both reduced the second phase of the response. The results confirm the analgesic potential of endogenous ligands at cannabinoid receptor sites. The anti-nociceptive effect of the putative CB2 receptor agonist, palmitoylethanolamide, is particularly interesting since it is believed to be a peripherally mediated effect. This observation might be exploited to separate central psychotropic effects from peripheral analgesic actions of the cannabinoids, under inflammatory conditions.

Amides↗
PubMed1998

Prediction of drinking outcomes for male alcoholics after 10 to 14 years.

This study reports on the long-term outcomes of 360 men who were hospitalized for alcoholism during 1980 to 1984 and followed at 12 months and again 10 to 14 years later. At the 10/14-year follow-up, 96 (26.7%) men were confirmed as deceased; 255 (70.8%) men participated in the assessment/interview battery completed during baseline hospitalization. The battery consisted of psychosocial, alcohol-related, and psychiatric measures. Two distinct but highly correlated outcome measures were selected: a clinical rating scale and a factor score. Overall, predictors from baseline and 12-month follow-up included age at intake hospitalization, alcoholism severity, social stability, drinking days, and antisocial personality disorder. Approximately 37% of the assessed survivors were either totally abstinent or drinking nonabusively throughout the 10/14-year follow-up, whereas another 37% continued to drink abusively. Men who abstained or reduced alcohol intake reported better physical health at follow-up than those who continued to drink. Although our findings did not directly link alcoholism to death, they strongly indicate that chronic alcohol abuse may lead to premature death.

Adult↗
PubMed1997

The role of nerve growth factor in a model of visceral inflammation.

There is growing evidence that nerve growth factor may be an important mediator of the sensory disorders associated with inflammation. This hypothesis was tested in a rat model of cystitis. In this model, an experimental inflammation is created in anaesthetized rats with an irritant chemical. Within 1 h, bladder reflexes, activated by the sensory innervation of this viscus, become exaggerated, mimicking the disorders seen in humans with chronic cystitis. The development of this hyper-reflexia following experimental inflammation was quantified using the technique of repeated cystometrograms. By several measures, bladder reflex excitability increased about three-fold after 5 h. Firstly, the study investigated whether inflammatory changes can be prevented by pharmacological antagonism of nerve growth factor. A synthetic fusion protein was used, consisting of the extracelluar domain of the high-affinity nerve growth factor receptor, trkA, coupled to the Fc portion of an immunoglobulin. Previous work has shown that this molecule can sequester nerve growth factor and reduce its bioavailability both in vitro and in vivo. Treatment of animals with the fusion molecule at 1 mg/kg, immediately before inflammation of the bladder, largely, and very significantly, prevented the expected increases in reflex excitability of this organ. Pretreatment with a related fusion protein, capable of sequestering the neurotrophin brain-derived neurotrophic factor and neurotrophin-4/5, but not nerve growth factor, was without effect. Similarly, a control fusion molecule, without neurotrophin-sequestering capacity, did not reduce the inflammation-induced hyper-reflexia. Systemic treatment with the nerve growth factor-sequestering molecule, but not control molecules, partially and significantly reversed established inflammatory changes, by about 30-60%, depending on outcome measure. The nerve growth factor-sequestering protein had no significant effects on bladder reflex excitability in the uninflamed state. It was also without significant effect on capsaicin-induced contractions of the urinary bladder. Administration of exogenous nerve growth factor into the lumen of the urinary bladders of normal anaesthetized rats produced a rapid and marked bladder hyper-reflexia similar to that seen with experimental inflammation. These findings are consistent with other circumstantial evidence that nerve growth factor may interact with visceral sensory systems. Together, the data strongly suggest that nerve growth factor produced in inflamed tissues is a critical mediator of the sensory disorders associated with inflammation.

Animals↗
PubMed1995

Topical spinal administration of a nitric oxide synthase inhibitor prevents the hyper-reflexia associated with a rat model of persistent visceral pain.

The effects of a neuronal selective nitric oxide synthase (NOS) inhibitor, L-Ng-nitro arginine p-nitroanilide (L-Napna), upon the hyper-reflexia of a rat model of persistent visceral pain was investigated. A baseline cystometrogram (CMG) was performed by measuring intravesical pressure during vesical inflation. L-Napna (125-1000 micrograms) or vehicle (control) was then administered topically onto the exposed spinal cord, followed by another CMG. The bladder was then inflamed with turpentine and a final CMG performed. Neither L-Napna nor vehicle affected vesical reflexes in the absence of inflammation. However, following inflammation, a vesical hyper-reflexia was demonstrated in the control animals, which was prevented by L-Napna. Therefore, spinal NOS does not have a role in the generation of normal bladder reflexes, however it does modulate them during vesical inflammation.

Amino Acid Oxidoreductases↗
PubMed1995

Ketorolac for early postoperative analgesia.

STUDY OBJECTIVE: To determine the efficacy and speed of onset of analgesia of a single dose of intravenous (IV) or intramuscular (IM) ketorolac tromethamine following major orthopedic surgery. STUDY DESIGN: Double-blind, randomized, placebo-controlled trial. SETTING: A district general hospital in England. PATIENTS: 112 patients aged 18 to 80 years suffering moderate or severe pain following orthopedic surgery. INTERVENTIONS: Patients were randomized to receive 30 mg ketorolac IV, 30 mg ketorolac IM, or placebo following surgery. MEASUREMENTS AND MAIN RESULTS: Verbal pain intensity scores were performed prior to admission to the study, then frequently for the first 45 minutes following administration of study medication, and subsequently at hourly intervals. Times to request for further analgesia were noted. Patient assessment of overall acceptability and pain relief of the study medication was recorded. There was no statistical difference in speed of onset of analgesia between the ketorolac groups and placebo. Median (range) times to first analgesic following study drugs were: ketorolac IV 45 minutes (9 to 1440 minutes), ketorolac IM 34 minutes (10 to 1440 minutes), placebo 24 minutes (10 to 615 minutes). There was a statistically significant difference between the ketorolac groups and placebo (ketorolac IV vs. placebo, p < 0.01; ketorolac IM vs. placebo, p = 0.03). Patient assessment of overall acceptability and pain relief was significantly better for IV ketorolac compared with placebo (p < 0.01). By 6 hours, 78% of the IV ketorolac group and 95% of the IM ketorolac and placebo groups required further analgesia. CONCLUSIONS: Despite high patient acceptability compared with placebo, the use of ketorolac as the sole analgesic failed to control postoperative pain following major orthopedic surgery. IV administration of ketorolac conferred no advantages over the IM route with regard to efficacy or speed of onset.

Adolescent↗
PubMed1995

Speed of onset of analgesic effect of intravenous ketorolac compared to morphine and placebo.

The speed of onset of analgesia following intravenous ketorolac, morphine and placebo was investigated in a single-dose, double-blind, randomized, parallel group study of 105 patients. The onset of analgesia was defined as the time at which the pain intensity score reached 50% of the baseline score in 25% of patients. Post-operative patients with moderate or severe pain were dosed and followed for 1 h. Pain reduction by at least 50% occurred in 25% of patients within 40 min (placebo), 15 min (morphine 5 mg), 6 min (morphine 10 mg) and 20 min (ketorolac 10 mg). The pain reduction time for morphine (10 mg) was significantly shorter than that for ketorolac (P = 0.01) or placebo (P < 0.01).

Adult↗
PubMed1993

The electrophysiological consequences of electrode impalement of peripheral nerves in the rat.

Peripheral nerve fascicles are deliberately impaled during microneurography experiments. We have assessed conduction block under these circumstances. First we recorded compound action potentials (CAP) in the sural nerve following stimulation of the sciatic nerve. The insertion of injection and microneurography electrodes between stimulation and recording sites produced a 20% decrease in the size of the CAP, which was maintained for the 10 min duration of impalement. After withdrawal, the conduction block partially resolved. In other experiments, single-unit action potentials were recorded from L4 and L5 dorsal roots following peripheral nerve stimulation. Microneurography electrodes inserted into the sciatic nerve produced conduction block in 50% of these axons. When axons were blocked, anodal stimulation through the tungsten electrode became more effective than cathodal stimulation. These results suggest that a temporary conduction block occurs in a significant number of myelinated fibers near the site of an inserted electrode.

Action Potentials↗
PubMed1992

Metabolic acidosis and fatal myocardial failure after propofol infusion in children: five case reports.

OBJECTIVE: To examine the possible contribution of sedation with propofol in the deaths of children who were intubated and required intensive care. DESIGN: Case note review. SETTING: Three intensive care units. SUBJECTS: Five children with upper respiratory tract infections aged between 4 weeks and 6 years. RESULTS: Four patients had laryngotracheo-bronchitis and one had bronchiolitis. All were sedated with propofol. The clinical course in all five cases was remarkably similar: an increasing metabolic acidosis was associated with brady-arrhythmia and progressive myocardial failure, which did not respond to resuscitative measures. All children developed lipaemic serum after starting propofol. These features are not usually associated with respiratory tract infections. No evidence was found of viral myocarditis, which was considered as a possible cause of death. CONCLUSION: Although the exact cause of death in these children could not be defined, propofol may have been a contributing factor.

Acidosis↗
PubMed1992

Peripheral nerve injury caused by injection needles used in regional anaesthesia: influence of bevel configuration, studied in a rat model.

We have studied the immediate and long term (up to 28 days) effects of short and long bevelled needle impalement of the rat sciatic nerve. Three techniques were used to assess neural trauma and its consequences: stained longitudinal nerve sections were assessed by light microscopy and scored for injury; the extravasation of Evan's Blue dye, after antidromic electrical nerve stimulation, was used as a test of unmyelinated fibre function; the flexion withdrawal times from a noxious stimulus were measured. The results of all three experiments suggested that, should a nerve fascicle become accidentally impaled during regional anaesthesia, the lesions induced by short bevelled needles are more severe, more frequent and take longer to repair than those induced by long bevelled needles. Nerve injury induced by short bevelled needles was associated with persisting signs of injury 28 days after the injury. These results suggest that the current practice of using short bevelled needles to prevent nerve injury complicating regional anaesthesia be reassessed.

Anesthesia, Conduction↗
PubMed1991

Plasma concentrations of bupivacaine after supraclavicular brachial plexus blockade in patients with chronic renal failure.

The plasma concentrations of bupivacaine and the latency and duration of anaesthesia after supraclavicular block with 30 ml of 0.5% bupivacaine were measured in 10 patients with chronic renal failure and in 10 patients with normal renal function. No significant difference was found between the two groups in respect of pharmacokinetic parameters, or in block latency or duration.

Adult↗
PubMed1991

A double-blind study of the speed of onset of analgesia following intramuscular administration of ketorolac tromethamine in comparison to intramuscular morphine and placebo.

A double-blind, randomised, parallel group, placebo-controlled study was performed in 85 patients to compare the speed of onset of analgesia following the intramuscular administration of a single dose of 30 mg of ketorolac tromethamine, 10 mg of morphine or placebo. A new, sensitive, method was used to measure the latency of analgesia. The onset of analgesia was defined by the time taken for the pain intensity score to reach a specified percentage of the baseline value. Twenty-five percent of patients achieving a 50% reduction in baseline pain intensity score appears to be the most appropriate parameter to assess the speed of onset of analgesia of ketorolac and morphine in the postoperative setting. Paired comparison demonstrated that ketorolac had a significantly faster onset of analgesia (p = 0.03) when compared to placebo, whilst comparison of morphine to placebo analgesic latency (p = 0.06) just failed to reach significance. There was no significant difference between the analgesic onset time of ketorolac and morphine (p = 0.73). Intramuscular ketorolac and intramuscular morphine have comparable analgesic onset times in the postoperative pain context. However, the sensitive method of measuring onset of analgesia described, highlights the slow onset of analgesia when analgesics of known efficacy are given by the intramuscular route in the postoperative period. More attention should be given to the speed of onset of analgesia in future assessments of analgesics.

Adult↗
PubMed1987

Comparison of trichloroethylene and enflurane as adjuncts to nitrous oxide and relaxant anaesthesia.

Forty women who underwent gynaecological surgery were randomly allocated to receive trichloroethylene, enflurane, or enflurane plus fentanyl as adjuncts to nitrous oxide/relaxant anaesthesia with controlled ventilation. No serious cardiac dysrhythmias were seen in any group. Each patient was observed postoperatively for 4 hours by a nurse blind to the technique used, and questioned at 24 hours by a similarly blinded anaesthetist. Recovery after trichloroethylene was not significantly prolonged although postoperative analgesia by visual analogue was better, opiate analgesia was required less frequently and there was less nausea and vomiting than in either of the enflurane groups. We argue for the continued use of trichloroethylene by this technique, because it costs one hundred times less than enflurane and because of the potential morbidity of the postoperative opiate dosage required after enflurane.

Adjuvants, Anesthesia↗