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PubMed1988

Hyperglycemic suppression of morphine withdrawal signs in the rat.

Male Sprague-Dawley rats maintained under controlled lighting and temperature conditions were used in this experiment. Morphine dependency was induced by giving increasing doses of morphine by intraperitoneal injection (IP group) or by the ingestion of morphine through drinking water (PO group). Animals were injected with 10, 20, 30 and 50 mg/kg morphine sulfate at days 1, 2, 3 and 4, respectively. Another group of animals received increasing concentrations of morphine through drinking water from 0.1, 0.2, 0.3 to 0.4 mg/ml at 48 h intervals. Morphine dependent animals were given naloxone by the intraperitoneal route to precipitate withdrawal. Glucose (3 g/kg or 10 g/kg) was given 10 min prior to the administration of naloxone to the respective groups. Another two groups of animals were made diabetic by the administration of streptozotocin. In one group, animals received increasing concentrations of 10, 20, 30 and 50 mg/kg morphine sulfate by the IP route at days 1, 2, 3 and 4, while the other group was not treated with morphine but was assessed for withdrawal signs to serve as the control. Withdrawal signs were assessed by observing the presence of diarrhea, tremor, piloerection, hunchbacked posture, teeth chattering, salivation, erection, restless activity, territorial exploring, irritability to handling, vocalization and jumping. Results obtained indicate that glucose administration at 10 g/kg abolished most of the withdrawal signs, and we were unable to induce the same degree of morphine dependency in diabetic animals as compared to the non-diabetic groups. It was concluded from this study that hyperglycemia could suppress morphine withdrawal signs.

Animals↗
PubMedDate not supplied

Conditioned behavioral and physiological changes associated with injections of a narcotic antagonist in morphine-dependent monkeys.

Environmental stimuli which are repeatedly associated with the nalorphine-induced withdrawal syndrome in morphine-dependent monkeys acquire the ability to produce a variety of conditioned behavioral and physiological responses. Morphine-dependent rhesus monkeys were studied under a fixed-ratio schedule where every tenth lever press produced a food pellet. After several pairings of a stimulus (light or tone) with intravenous injection of a dose of nalorphine which produced an immediate and severe withdrawal syndrome, onset of the stimulus alone produced conditioned suppression of lever pressing heart-rate decrease, vomiting and salivation. Conditioned suppression of responding and conditioned heart-rate changes persisted in post-dependent monkeys for one to four months after termination of chronic morphine treatment. No conditioned electrocardiogram, respiration or temperature changes were ever seen. A second group of morphine-dependent rhesus monkeys was studied under a schedule where every lever press produced an intravenous injection of morphine. After 10 pairings of a light with the intravenous injection of a dose of nalorphine which produced marked withdrawal signs and increased responding for morphine, presentation of the light and injection of saline produced conditioned increases in responding for morphine. A third group of morphine-dependent rhesus monkeys was studied under a schedule where every nth lever press (n=1 to 10) terminated a stimulus light associated with periodic injections of nalorphine or naloxone; lever-press responding was engendered and subsequently maintained. Thus, stimuli associated with the nalorphine-- or naloxone--induced withdrawal syndrome can either suppress, enhance or maintain behavior depending on the schedule conditions.

Animals↗
PubMed1976

Physostigmine as an adjuvent to neuroleptanaesthesia in neurosurgical procedures.

The use of physostigmine electively to reverse the effects of droperidal and diazepam has permitted an optimum level of neuroleptanaesthesia in neurosurgical operations where co-operation of the patient is required during part of the procedure. The patient can be put to sleep or readily awakened to be fully co-operative depending on the needs of the surgeon. In this series of seven anaesthetics there were no side effects from the small doses of physostigmine employed. Bradycardia and salivation were not a problem. One child vomited once. Atropine was not necessary. Since a narcotic antagonist is not needed, a reasonable degree of analgesia can be maintained in these patients while they are awake. The latent time for the effect of physostigmine was two to four minutes and the effect of an intravenous dose lasted from 35 to 45 minutes. With physostigmine, these patients wake up gently as though from normal sleep. If neurological assessment is required post-operatively, drowsiness due to drugs can be reversed by giving more physostigmine and the level of consciousness can then be assessed.

Adjuvants, Pharmaceutic↗
PubMed1998

Awake removal of the laryngeal mask airway is safe in paediatric patients.

PURPOSE: It has been suggested that it is safer to remove the Laryngeal Mask Airway (LMA) in paediatric patients when they are deeply anaesthetised than when they are awake. However, the evidence regarding this recommendation is contradictory. The purpose of the study was to compare the incidence of complications (laryngeal spasm, bronchospasm, coughing, retching, excessive salivation and oxygen desaturation) associated with removal of the LMA in children. METHODS: In a randomised study, we studied 165 ASA physical status I infants and children of both sexes, aged 2 mo to 13 yr. All patients were undergoing elective lower limb or perineal surgery. They were randomly assigned to two groups: in 83 the laryngeal mask was removed when recovery of airway reflexes had been demonstrated and the patients had opened their eyes or mouth in the recovery area. In the other 82 patients it was removed with the patient deeply anaesthetised. RESULTS: Two (2.4%) patients developed laryngeal spasm in the anaesthetised group, one patient (1.2%) desaturated and another vomited (1.2%) in the awake group. CONCLUSION: There was no difference in the incidence of airway complications whether the LMA was removed in the anaesthetised or the awake child.

Adolescent↗
PubMed1995

Complications associated with removal of the laryngeal mask airway: a comparison of removal in deeply anaesthetised versus awake patients.

The purpose of the study was to compare the incidence of complications (coughing, biting, retching, vomiting, excessive salivation and airway obstruction) associated with removal of the laryngeal mask airway. The laryngeal mask airway was used in 100 adults undergoing urological procedures. The patients were randomly assigned to two groups. In 50 patients the laryngeal mask was removed by a nurse when the patient responded to commands in the recovery area. In the other 50 patients it was removed by the anaesthetist with the patient deeply anaesthetized in theatre. The majority of patients were elderly men who had relatively short procedures. The incidence of gastric regurgitation was assessed by measurement of pH of secretions at the tip of the laryngeal mask airway. Complications occurred more frequently in the awake patients (P < 0.01). Most were minor and occurred before removal of the laryngeal mask airway during emergence in the recovery room. Airway obstruction occurred in three patients in whom the laryngeal mask was removed in the recovery room. In two of these patients the oxygen saturation decreased below 80% and the other to 90%. No decrease in arterial oxygenation occurred in the anaesthetised patients in whom the laryngeal mask was removed by the anaesthetist. In 14 patients in the awake group the pH of secretions at the tip of the laryngeal mask was < or = 3 compared with only four patients in the anaesthetised group (P < 0.05). It is concluded that it may be safer to remove the laryngeal mask airway whilst the patients are deeply anaesthetised in the operating room than when they are awake in the recovery room.

Adult↗
PubMedDate not supplied

The effect of furazolidone and furaltadone on drug metabolism in rats.

This work examines the effect of oral treatment of rats with the nitrofuran drugs furazolidone (FZ) and furaltadone (F) at doses of 100, 200 and 400 mg/kg for 4 days, or F in the drinking water at concentrations of 0.1, 0.2 and 0.4% w/v for 14 days, on drug metabolism in vivo. FZ at doses of 200 and 400 mg/kg, and F at a dose of 400 mg/kg or at a concentration of 0.4% w/v in water depressed growth and prolonged pentobarbitone-induced sleeping time. Treatment also significantly increased the blood concentration of metronidazole when measured 30 and 40 min after metronidazole administration. Administration of tremorine (25 mg/kg, i.p.) to control vehicle-treated rats produced within 2-3 min tremors, piloerection, profuse salivation, defecation urination and chromodacryorrhesis (red tears). The onset of appearance of these signs was delayed to 7-12 min in rats pretreated with FZ or F (100 mg/kg, 4 days) or cimetidine (50 mg/kg, i.p.) given 45 min earlier. Taken together, these results suggest that FZ and F inhibit drug metabolism in rats. Treatment with these nitrofuran drugs may alter the disposition of certain drugs which may be given concomitantly with them.

Animals↗
PubMed2000

Time course of ultrastructural changes and immunoelectron microscopic localization of neurocalcin in motor endplates of the lumbrical muscles of rats given a single administration of 2,5-di(tert-butyl)-1,4-hydroquinone.

A time-course study of ultrastructural changes and immunoelectron microscopic localization of neurocalcin was performed on motor endplates of the lumbrical muscles of female Wistar rats given a single oral administration of 2,5-di(tert-butyl)-1,4-hydroquinone (DTBHQ) at a dose of 120 mg/kg. Toxic signs such as salivation and muscle weakness of the hind legs appeared from 3 h after DTBHQ administration. No remarkable macroscopic or light microscopic changes were noted in the lumbrical muscles of the treated rats. At the ultrastructural level, neurotoxicity characterized by a decreases or loss of synaptic vesicles and mitochondria was observed after 24 h and at the 1-week time point, nerve endings had disappeared in some of the motor endplates, while many neurite nerve endings suggestive of early stage regeneration were apparent. After 6 weeks, newly formed reinnervated endplates were observed. Immunoelectron microscopically, the synaptic vesicle membranes were heavily labeled for neurocalcin in the control rats, but not at 24 h after DTBHQ treatment. Synaptic vesicle membranes in the DTBHQ group were weakly labeled at 1 week, but strongly at 6 weeks. The results strongly suggest that DTBHQ targets the motor endplates in the rat lumbrical muscles, causing depletion of neurocalcin in the synaptic vesicles followed by their loss.

Animals↗
PubMed2000

Xerostomia in patients with triple A syndrome--a newly recognised finding.

Triple A syndrome is characterised by achalasia, alacrima, adrenal insufficiency and progressive neurological abnormalities including impaired autonomic nervous function. We present five patients with triple A syndrome in whom we describe xerostomia for the first time, a symptom which was presumed to be practically exclusive to Sjøgren syndrome and familial dysautonomia. Conclusion We recommend the investigation of salivation in all patients with triple A syndrome and treatment of xerostomia in order to ease swallowing. Further, our results corroborate earlier doubts that some patients with Sjøgren syndrome, especially those with the so-called "achalasia sicca" syndrome and adrenocortical insufficiency, actually had triple A syndrome. Therefore, adrenocortical function should be assessed in all patients with Sjøgren syndrome, particularly in those with difficulties in swallowing, because even latent adrenocortical insufficiency could be life-threatening for these patients in stressful situations.

Adolescent↗
PubMed1999

Immunoglobulin-binding proteins in ticks: new target for vaccine development against a blood-feeding parasite.

Humans have a long history of trying to control ticks. At first, attempts focused on modifying the habitat, whereas later efforts relied heavily on the use of chemicals. Current research is directed at finding a vaccine against ticks. A strategy of targeting 'concealed antigens' succeeded with the first commercialised vaccine against the cattle tick Boophilus microplus. However, vaccine development against other tick species appears unsatisfactory to date. Vaccination depends on a specific antibody-mediated immunoreaction that damages the parasite. Immunoglobulin molecules of vertebrate hosts can pass through gut barriers into the haemolymph of ectoparasites while retaining antibody activity. Research on the ixodid tick Rhipicephalus appendiculatus revealed that host immunoglobulin-G in the parasite was excreted via salivation, during feeding. Immunoglobulin-binding proteins in tick haemolymph and salivary glands are thought to be responsible for such excretion. The discovery of an immunoglobulin excretion system in ticks indicates that they have a highly developed mechanism to protect themselves from their host's antibody attack. Such a mechanism questions whether immunization strategies will be effective against ticks, unless they circumvent or disable the ticks' immunoglobulin excretion system.

Amino Acid Sequence↗
PubMed2006

[Pharmacological aspects of therapeutic botulinum toxin preparations].

Therapeutic preparations of botulinum toxin (BT) consist of botulinum neurotoxin (BNT), complexing proteins, and excipients. Depending on the target tissue, BNT can block cholinergic neuromuscular innervation of intra- and extrafusal muscle fibres or cholinergic autonomic innervation of sweat, lacrimal, and salival glands and smooth muscles. Indirect CNS effects are numerous; direct ones have not been reported after intramuscular application. Botulinum toxin type A is distributed as Botox, Dysport, Xeomin, Hengli/CBTX-A, and Neuronox and BT type B as NeuroBloc/Myobloc. Differences in potency labelling of therapeutic BT preparations can be corrected by introduction of a conversion factor of 1:3 between Botox and Dysport, of 1:1 between Botox and Xeomin, and of 1:40 between Botox and NeuroBloc/Myobloc. Acute adverse effects of BT can be obligate, local or systemic. Adverse effect profiles of the different preparations are similar. However, BT type B frequently produces additional autonomic systemic adverse effects. Long-term application does not produce additional adverse effects. BNT can be partially or completely blocked by antibodies. Risk factors include the amount of BNT applied at each injection series, the interval between injection series, and the specific biological potency (SBP) of the BT preparation used. The SBP is 5 equivalent mouse units/ng BNT for NeuroBloc, 60 for Botox, 100 for Dysport, and 167 for Xeomin. Xeomin should therefore have a particularly low antigenicity. Clinical confirmation of this predicition, however, is lacking.

Botulinum Toxins↗
PubMed1998

Ultrastructural changes in motor endplates of the lumbrical muscles of rats induced by a microsomal Ca2+ ATPase inhibitor, 2,5-di(tert-butyl)-1,4-hydroquinone.

Female Wistar rats were treated orally for 5 days with 80 mg/kg body weight of 2,5-di(tert-butyl)-1,4-hydroquinone (DTBHQ), a microsomal Ca2+ ATPase inhibitor. Motor endplates of the lumbrical muscles were examined by light and electron microscopy. There was a decrease in body weight in the treated rats from the first day after administration, and toxic signs appeared after the third day, such as adoption of a prone position, salivation, lacrymation, and an abnormal gait and/or muscle weakness. No remarkable macroscopic or light microscopic changes were noted in the lumbrical muscles as well as other peripheral nerves of hind legs of the treated rats killed 1 day after the last DTBHQ treatment. Ultrastructurally, neurotoxicity characterized by loss of synaptic vesicles and mitochondria in the motor endplates, and by destruction of the motor terminals was detected in the lumbrical muscles of the treated rats. These results strongly indicate that DTBHQ targets the motor endplates in the rat lumbrical muscles and suggest that the resultant damage is responsible for the appearance of neurological signs, such as an abnormal gait and loss of muscle control.

Administration, Oral↗
PubMed2002

M(3) receptor antagonism by the novel antimuscarinic agent solifenacin in the urinary bladder and salivary gland.

The antimuscarinic profile of the experimental drug solifenacin/YM905 [(+)-(1 S,3' R)-quinuclidin-3'-yl 1-phenyl-1,2,3,4-tetrahydroisoquinoline-2-carboxylate] for the treatment of overactive bladder was compared with the commonly prescribed agent oxybutynin. In radioligand binding assays, p K(i) values of solifenacin for M(1), M(2), and M(3) receptors were 7.6, 6.9, and 8.0, respectively. These values for oxybutynin were 8.6 (M(1)), 7.7 (M(2)), and 8.9 (M(3)). Solifenacin and oxybutynin antagonized the contractile effect of carbachol (CCh) on isolated guinea pig urinary bladder smooth muscle (detrusor), displaying the negative logarithm of antagonist apparent affinity constant (p K(b) value) of 7.1 for solifenacin and 7.4 for oxybutynin. To study the tissue selectivity between bladders and salivary glands, guinea pig detrusor and mouse submandibular gland cells were stimulated with CCh and monitored for intracellular Ca2+, as determined by Fura 2 fluorescence. Ca2+ mobilization of detrusor cells was inhibited equipotently by solifenacin (p K(i)=8.4) and oxybutynin (p K(i)=8.6), whereas that of the gland cells was antagonized less potently by solifenacin (p K(b)=7.4) than by oxybutynin (p K(b)=8.8), although the M(3) subtype mediated both cell responses. In anesthetized rats, solifenacin (63-2100 nmol kg(-1) or 0.03-1 mg kg(-1)) dose-dependently inhibited CCh-stimulated increases in urinary bladder pressure, while its inhibitory effects on salivation and bradycardia were apparent only at a dose of 2100 nmol kg(-1). In contrast, oxybutynin within a dose range of 77-770 nmol kg(-1) (0.03-0.3 mg kg(-1)) inhibited responses of the bladder and salivary gland slightly more potently than that of the heart. In addition, inhibitory effects of darifenacin indicated a major role of M(3) receptors in the bladder and salivary gland. Therefore, M(3) receptor antagonism by solifenacin could be bladder-selective. This selectivity remains to be elucidated and may provide new approaches to the pharmacotherapy of overactive bladder.

Animals↗
PubMed2005

Why patients with Alzheimer's disease may show increased sensitivity to tropicamide eye drops: role of locus coeruleus.

RATIONALE: Patients suffering from Alzheimer's disease (AD) may show increased sensitivity to tropicamide, a muscarinic cholinoceptor antagonist. AD is associated with a severe loss of noradrenergic neurones in the locus coeruleus (LC), which can be "switched off" experimentally by the alpha(2)-adrenoceptor agonist clonidine. The possibility arises that increased pupillary sensitivity to tropicamide in AD may be due to diminished LC activity. OBJECTIVE: To examine the hypothesis that clonidine may potentiate tropicamide-evoked mydriasis. MATERIALS AND METHODS: Sixteen healthy male volunteers participated in two experimental sessions (0.2 mg clonidine or placebo) conducted 1 week apart. In each session tropicamide (0.01% 10 microl x 2) was applied to the left eye and artificial tear (10 microl x 2) was applied to the right eye. Pupillary functions (resting pupil diameter and light and darkness reflexes), alertness and non-pupillary autonomic functions (blood pressure, heart rate, core temperature and salivary output) were measured. Data were analysed by ANOVA, with multiple comparisons. RESULTS: Tropicamide increased resting pupil diameter, velocity and amplitude of the darkness reflex response, and decreased recovery time of the light reflex response. Clonidine affected all these pupillary measures in the opposite direction with the exception of the recovery time. The mydriatic response to tropicamide was potentiated by pre-treatment with clonidine. Clonidine reduced critical flicker fusion frequency, subjective alertness, blood pressure, salivation and temperature. CONCLUSIONS: The potentiation of tropicamide-evoked pupil dilatation by clonidine may be due to the abolition of the increase in parasympathetically mediated pupil constriction due to reduced LC activity.

Adrenergic alpha-Agonists↗
PubMed1998

The central pattern generator for vomiting may exist in the reticular area dorsomedial to the retrofacial nucleus in dogs.

There is some controversy over whether or not a discrete site that integrates vomiting activities in somatic and autonomic nerves is present in the medulla oblongata. On the basis of our previous studies, we hypothesized that the temporal patterns of muscle contractions in vomiting are generated by a central pattern generator in the retrofacial area of the rostral medulla. To investigate this hypothesis further, the effects of electrical and chemical lesions of the medullary area were observed in decerebrate paralyzed dogs. Efferent activities of the phrenic and abdominal muscle nerves were recorded to recognize fictive vomiting. The right half of the medulla oblongata was transversely severed about 3 mm rostral to the obex. Fictive vomiting responses to vagal stimulation still appeared after hemisection in all 11 dogs. In addition, stimulation of the contralateral reticular area dorsomedial to the retrofacial nucleus produced fictive vomiting even after hemisection. An electrical lesion or injection of kainic acid (0.5-1.0 microl) was applied at the point where reticular stimulation induced fictive vomiting. After this destruction, no activities that corresponded to fictive vomiting could be induced by stimulation of vagal afferents or the reticular site. Salivation was decreased by hemisection, and decreased further, but was not completely abolished, with destruction of the reticular area. Kainic acid is known to selectively destroy neural cell bodies. Therefore, we concluded that neuronal somata in the reticular formation dorsomedial to the retrofacial nucleus play an essential role in the central patterning of vomiting activities in peripheral motor nerves.

Animals↗
PubMed2005

Trigeminal neuralgia and facial nerve paralysis.

The trigeminal nerve is the largest of the cranial nerves. It provides sensory input from the face and motor innervation to the muscles of mastication. The facial nerve is the cranial nerve with the longest extracranial course, and its main functions include motor innervation to the muscles of facial expression, sensory control of lacrimation and salivation, control of the stapedial reflex and to carry taste sensation from the anterior two-thirds of the tongue. In order to be able adequately to image and follow the course of these cranial nerves and their main branches, a detailed knowledge of neuroanatomy is required. As we are dealing with very small anatomic structures, high resolution dedicated imaging studies are required to pick up normal and pathologic nerves. Whereas CT is best suited to demonstrate bony neurovascular foramina and canals, MRI is preferred to directly visualize the nerve. It is also the single technique able to detect pathologic processes afflicting the nerve without causing considerable expansion such as is usually the case in certain inflammatory/infectious conditions, perineural spread of malignancies and in very small intrinsic tumours. Because a long course from the brainstem nuclei to the peripheral branches is seen, it is useful to subdivide the nerve in several segments and then tailor the imaging modality and the imaging study to that specific segment. This is particularly true in cases where topographic diagnosis can be used to locate a lesion in the course of these nerves.

Facial Nerve Diseases↗
PubMed2003

Bio-ecological control of perioperative and ITU morbidity.

BACKGROUND: Perioperative and intensive therapy unit (ITU) morbidity and mortality has remained unchanged during the past several decades, and this at an unacceptably high level. It is most likely, in the EU countries annually, that more than 1 million people suffer severe sepsis and some 300,000 die. Pharmaceutical attempts at prevention and treatment have, despite extensive efforts, hitherto failed to improve outcome more significantly. Much supports the fact that sepsis and its severe consequences are results of a malfunctioning innate immune system, impaired by both lifestyle and disease. A series of mostly simple measures to prevent further deterioration of the immune system, and to boost it, is recommended. Among the measures recommended are some modifications of surgical and postoperative management: restricted use of antibiotics, attempts made to maintain salivation and GI secretions, omission of prophylactic gastric decompression, postoperative drainage and preoperative bowel preparation, restricted use of stored blood, avoidance of overload with nutrients, uninterrupted enteral nutrition but also tight blood glucose control, supply of antioxidants, administration of prebiotic fibre and probiotic lactic acid bacteria. Nutritional control of postoperative morbidity includes use of so-called synbiotics, e.g. a combination of bioactive lactic acid bacteria (LAB) and bioactive plant fibres. RESULTS: Dramatic reduction in (in reality, almost abolishment of) septic morbidity is reported following supplementation of specific bioactive lactic bacteria in combination with prebiotic plant fibres, as tried in controlled studies in connection with extensive abdominal operations, liver transplantation and severe acute pancreatitis.

Critical Care↗
PubMed2005

Treating sialorrhea with transdermal scopolamine. Exploiting a side effect to treat an uncommon symptom in cancer patients.

INTRODUCTION: Sialorrhea is a distressing symptom accompanying oral cancer and many heterogeneous cancer-related conditions (chemotherapy-induced nausea, bowel subocclusion, pharmacologic side effects), but its incidence is low in cancer patients. Conversely, it is frequent in patients with neurological damage, and some therapeutic options have been attempted such as botulinum toxins, anticholinergic agents, and surgical procedures. CASE REPORT: We report the case of an 80-year-old woman with peritoneal carcinomatosis and bowel subocclusion, suffering from distressing nausea and sialorrhea that rapidly improved using transdermal scopolamine. No relevant side effects occurred during the treatment, and the reduction of the abnormal salivation allowed the recovery of oral feeding. CONCLUSIONS: Anticholinergic drugs are classified as secondary options in the treatment of sialorrhea of patients with Parkinson's disease or cerebral palsy, owing to the relevant side effects occurring during prolonged treatments. However, they could be useful in cancer patients with bowel subocclusion, as the reduction of gastrointestinal secretions and intestinal motility (frequent side effects of anticholinergic drugs) could be effective in controlling nausea, vomiting, and abdominal pain. Moreover, the transdermal or sublingual route of administration can be of some interest, avoiding other more invasive parenteral approaches.

Administration, Cutaneous↗
PubMed1998

Xerostomia: aetiology and management in cancer patients.

Although oral complications are common sequelae of cancer/cancer treatment, only sporadic research is published in the literature. It is clear that 'routine' oral hygiene measures are inadequate; a little time and effort may, however, reduce oral discomfort. This is particularly true in the case of xerostomia, which is often thought to be a relatively minor symptom with few deleterious effects. Many patients, however, find xerostomia a significant cause of distress, and for this reason alone, health care professionals require knowledge and appreciation of the pathology and aetiology of the condition and approaches to its management. This paper reviews the physiology of salivation and the aetiology of xerostomia and considers the ways in which the condition can be managed.

Antineoplastic Agents↗