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PubMed1977

[Effects of capsaicin on spontaneous unit discharges in medial thalamic single neurons of cats (author's transl)].

The effect of capsaicin was studied in gallamine triethiodide immobilized adult cats. Single neurons were recorded from the medial thalamus with a stainless steel microelectrode. Out of 21 neurons recorded in this experiment, 10 were responsive to both nociceptive (pinch) and non-nociceptive (hair bending and/or tapping) stimuli. Six neurons were responsive to only non-nociceptive stimuli and 5 were not responsive to these stimuli. Out of 10 neurons responding to both nociceptive and non-nociceptive stimuli, 9 were responsive to both bradykinin (3 microgram) and capsaicin (3 microgram). Out of 6 neurons responding to only non-nociceptive stimuli, 5 were not responsive to either bradykinin and capsaicin. All neurons responding to bradykinin were also responsive to capsaicin. The latency for bradykinin and capsaicin was 7.64 +/- 1.12 sec and 0.97 +/- 0.07 sec, respectively. The increased in firing frequency produced by capsaicin was depressed by morphine. However, these depressant effects of morphine on single unit activity were antagonized by naloxone.

Action Potentials↗
PubMed1980

Excitatory effects of dihydrocapsaicin on nociceptive neurons in the medial thalamus.

Effects of capsaicin and dihydrocapsaicin, which are pungent substances contained in Capsicum annuum L., were studied in 32 gallamine triethiodide immobilized cats. Single units were recorded from the medial thalamus using stainless steel microelectrodes. Of the 56 neurons recorded, 28 were responsive to both noxious (pinching) and non-noxious (hair and/or tapping) stimuli, while 16 were activated only by non-noxious stimuli. The remaining 12 neurons did not respond to any natural stimulus. Somatic receptive fields of nociceptive and non-nociceptive neurons were found to be widely distributed over the whole body. Twenty-six of 28 nociceptive neurons were activated by an intra-arterial administration of bradykinin, capsaicin and dihydrocapsaicin. Fourteen of 16 non-nociceptive neurons were not activated by these substances. The mean latency and duration of bradykinin were 8.7 and 12.5 sec, those of capsaicin were 1.2 and 6.1 sec and those of dihydrocapsaicin were 1.3 and 5.0 sec, respectively. The increase of firing frequency produced by capsaicin and dihydrocapsaicin was inhibited by morphine and this inhibition was antagonized by naloxone. However, the activity of medial thalamic neurons with non-noxious stimuli was not affected by these drugs. These results suggest that the pain-conducting fibers were selectively activated by capsaicinoids as well as by bradykinin.

Action Potentials↗
PubMed1982

Potentiating effects of prostaglandin E2 on bradykinin and capsaicin responses in medial thalamic nociceptive neurons.

Potentiating effects of prostaglandin E2 (PGE2) on bradykinin and capsaicin responses were studied in 34 gallamine triethiodide immobilized cats. Single neurons were recorded from the medial thalamus by using stainless steel microelectrodes. The animals were given agents into the femoral artery through a retrogradely inserted cannula. Of the 22 neurons responding to bradykinin, 13 were potentiated by the injection of PGE2, and the remaining 9 neurons were ineffective. Nine of the 17 neurons responding to capsaicin were also potentiated by PGE2. PGE2 significantly shortened the mean latency of bradykinin to fire the neuronal activity without changing the duration, but with the injection of capsaicin, there was no change in latency and duration in the presence of PGE2. Aspirin suppressed the increased activity of the medial thalamic neurons produced by bradykinin, and this suppression was antagonized by arterial infusion of PGE2. However, the activity of medial thalamic neurons with capsaicin was scarecely affected by aspirin. These results suggest that the bradykinin-induced activity of medial thalamic neurons may be mediated by PGE2 and that the mechanism of activation of nociceptive neurons produced by capsaicin is different from that of bradykinin.

Action Potentials↗
PubMed1988

Two types of gastric excitatory responses to stimulation of the vagal trunk in cats: efferent and afferent responses.

Experiments were performed on cats anesthetized with pentobarbital sodium and gallamine triethiodide. Gastric motility was recorded by a balloon method. The excitatory response to electrical stimulation of the vagal trunk was composed of an initial response during the stimulation period and a late response following stimulation. The maximal excitation of the initial response was elicited by a short pulse duration and that of the late response by a long pulse duration. The initial response was inhibited by treatment with hexamethonium or atropine. The late response was hexamethonium-resistant. This hexamethonium-resistant response was inhibited by atropine, hemicholinium and morphine, and enhanced by physostigmine. Treatment with (D-Pro2, D-Trp7,9)-substance P did not affect the hexamethonium-resistant response. Treatment with morphine inhibited the late response without affecting the initial response. From these results, it was suggested that the initial excitatory response was probably due to the activation of the parasympathetic cholinergic fibers. The late response might be due to the activation of the vagal afferent cholinergic fibers, since the pharmacological nature of the late response was similar to that in the cat with supranodose vagotomy (surviving afferent fibers) in our previous reports.

Afferent Pathways↗
PubMed1988

Medullary inspiratory neurons with stable respiratory rhythm and little correlation to phrenic high-frequency oscillation.

Respiratory neurons with a highly stable rhythm have been proposed to be involved in the central neural mechanism responsible for the respiratory rhythmogenesis. In the present study it was examined whether the stably discharging inspiratory neurons are related to the high-frequency oscillation (HFO) in the phrenic nerve activity. Experiments were performed on 27 vagotomized rabbits anesthetized with diethyl ether, immobilized with gallamine triethiodide, and ventilated artificially. Spike-triggered averaging was used to evaluate the degree of the correlation between inspiratory unit spikes and the phrenic HFO. Twenty out of the 35 inspiratory units examined were related to HFO and were located in the medullary reticular formation (n = 19; n, number of units) and in the vicinity of the nucleus tractus solitarius (n = 1). The correlation to HFO decreased after the intravenous injection of thiamylal. The inspiratory units with little correlation to HFO were located in the reticular formation of the pons (n = 3) and medulla (n = 12). The inspiratory neurons with a stable respiratory rhythm (n = 4) had little correlation to HFO and located in the lateral region of the medullary reticular formation. These results suggest that the central neural mechanisms responsible for phrenic HFO are not directly related to the respiratory rhythmogenesis.

Action Potentials↗
PubMed1981

Effect of cepharanthine on neuro-humoral excitatory responses of gastric movement in dog.

In order to clarify the role of histamine in the neuro-humoral excitatory mechanism in the stomach, the effect of cepharanthine (an inhibitory agent of histamine release from mast cells) on excitatory response of gastric movement and increase in gastric mucosal histamine content caused by nerve stimulation (vagus and splanchnic nerves) or administration of tetragastrin were investigated in dogs. The animals were anesthetized with pentobarbital sodium and immobilized with gallamine triethiodide. The following results wee obtained. Increase of gastric mucosal histamine content caused by vagal and splanchnic nerve stimulation and administration of tetragastrin was inhibited by administration of cepharanthine. Cepharanthine inhibited the tonic contraction of the innervated antral pouch or isolated antral circular muscle strip caused by stimulation of vagus nerve. Tonic contraction of the innervated antral pouch caused by electrical stimulation of the splanchnic nerve after nicotinization of celiac and superior mesenteric ganglia was inhibited by administration of cepharanthine. Cepharanthine inhibited motor excitatory response of the denervated corpus pouch caused by stimulation of vagus and splanchnic nerves and by administration of tetragastrin. These results support the theory that cepharanthine inhibits the release of histamine from histamine-secreting cells in the gastric mucosa. It is suggested that histamine plays an important role in the neuro-humoral excitatory mechanism of gastric movement.

Alkaloids↗
PubMed2002

Synthesis and structure-activity relationships of neuromuscular blocking agents.

The first use of neuromuscular blocking agents (muscle relaxants) in clinical practice (1942) revolutionised the practice of anaesthesia and started the modern era of surgery. Since 1942 introduction of tubocurarine (18) neuromuscular blocking agents have been used routinely to provide skeletal muscle relaxation during surgical procedures allowing access to body cavities without hindrance from voluntary or reflex muscle movement. After the introduction of tubocurarine and the depolarizing suxamethonium chloride (4) (1949) several nondepolarizing steroidal and nonsteroidal neuromuscular blocking agents with different onset time and duration of effect were introduced e.g. gallamine triethiodide (1) (1949), methocurine (2) (1949), alcuronium chloride (3) (1963), pancuronium bromide (9) (1968), vecuronium bromide (11) (1982), pipecuronium bromide (10) (1982), atracurium besylate (5) (1982), doxacurium chloride (6) (1991), mivacurium chloride (8) (1992), rocuronium bromide (12) (1994) cisatracurium besylate (7) (1996), and rapacuronium bromide (13) (2000). SZ 1677 (14) a steroid type nondepolarizing neuromuscular blocking agent under development (preclinical phase). This review article deals with a comprehensive survey of the progress in chemical, pharmacological and, in some respects, of clinical studies of neuromuscular blocking agents used in the clinical practice and under development, including the synthesis, structure elucidation, pharmacological actions, structure activity relationships studies of steroidal and nonsteroidal derivatives.

Androstanes↗
PubMed1975

Responses of cortical vestibular center produced by stimulation of vestibular nuclei and visual association area in the cat.

(1) The cortical projection of the vestibular nuclei (LVN, MVN and IVN) was investigated by the evoked potential and unit discharge analyses in the cat anesthetized with alpha-chloralose and/or immobilized with gallamine triethiodide. (2) This projection field coincided well with that of the vestibular nerves, being principally contralateral by LVN stimulation but nearly symmetrical by either MVN or IVN stimulation. (3) Of 11 units responsive to vestibular nuclei stimulation, 6 reacted to stimulation of the visual association cortex (anterior part of the Clare-Bishop area). The response pattern of the cortical vestibular units by C-B stimulation was a sequence of excitation, inhibition and rebound. (4) Interaction of visual information with the cortical vestibular neurons was discussed.

Animals↗
PubMed1998

In-line affinity chromatographic removal of specific antibody from rabbits with experimental myasthenia gravis as a prelude to immunotherapy.

Myasthenia gravis is an autoimmune disease in which antibodies are produced against one's acetylcholine receptors, resulting in complement-mediated membrane destruction and internalization of antibody-receptor complexes. Symptoms range from weakening of extraocular muscles to severe impairment of movement and breathing. Prior to administering a therapeutic agent to eliminate antibody-producing lymphocytes, it will be necessary to remove specific antibody from the circulation. This process was investigated in an animal model of ex vivo specific immunoadsorption using awake, conscious rabbits. Following arterial blood separation, plasma was pumped upward through an affinity column containing covalently-bound acetylcholine receptor. Treated plasma was returned to the rabbit. Within a one-hour ex vivo procedure, specific antibody levels could be lowered from 16.2 ng/ml to less than 0.6 ng/ml, a reduction of more than 95%. By washing the column, at least four exchanges could be performed before specific antibody removal significantly diminished. The effects of specific antibody removal upon muscle function varied among individual rabbits, but if symptoms were not severe following passive transfer of purified monoclonal antibody to induce myasthenia, removal of 60% of the total specific antibody resulted in clinical improvement, as monitored by an animal's response to gallamine triethiodide.

Animals↗
PubMed1977

Studies of methods for in situ observation of gastric motility in domestic turkeys.

The normal gastroduodenal contraction cycle of turkeys is believed to be controlled and coordinated by the myenteric plexus which lies just under the serosa of the muscular stomach. Methods which would permit direct application of chemical and physical stimuli to these gastric nerves were studied in intact and decerebrate turkeys using both radiographic and direct observations to monitor contraction cycles. In intact turkeys, general anesthetics (sodium pentobarbital, halothane; and ketamine hydrochloride) inhibited gastric motility. A local anesthetic (lidocaine hydrochloride) injected into the skin and abdominal muscles caused a depression of motility. In both intact and chronically decerebrate turkeys laparatomy (after local anesthetic in intact birds) and a neuromuscular blocking agent (gallamine triethiodide) also depressed gastric motility. Motility was slightly reduced by artificial respiration and exposure of the serosal surface of the stomach and intestines to air via an abdominal fistula.

Anesthesia, General↗
PubMedDate not supplied

Mu opiate receptor antagonist blocks electroacupuncture inhibition on noxious blood pressure response in rabbits.

A pressor blood pressure response was elicited by strong electric shock stimulation of the front paw in rabbits anesthetized with chloralose and urethane, immobilized by gallamine triethiodide and maintained by artificial ventilation. The pressor response showed a gradual decline in 3-4 successive trials. Naloxone or TCTAP, a specific mu receptor antagonist, administered intraventricularly (icv) at that time could facilitate the pressor response (n = 8, P < 0.02; n = 7, P < 0.01), suggesting the involvement of mu receptors in the declination of the pressor response. Electroacupuncture could inhibit the pressor response (n = 7, P < 0.01), and the inhibition was readily blocked by TCTAP (n = 7, P < 0.01). No obvious changes were observed in the normal saline control group. The results suggest that acupuncture is able to inhibit the pressor response via the activation of the opioid peptidergic system, of which the mu receptor is an important component.

Animals↗
PubMed1999

Non-NMDA receptors mediate both pressor and depressor actions of the cardiovascular-reactive areas in the brainstem of cats.

L-glutamate (Glu), an important excitatory transmitter in the central nervous system, is mainly mediated via two kinds of ionotropic Glu receptors: N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA)/kainate (non-NMDA) receptors. Microinjection of Glu (0.1 M, 30 nL) into gigantocellular tegmental field (FTG), dorsomedial medulla (DM) and rostral ventrolateral medulla (RVLM) induced increases of the systemic arterial pressure (SAP) and the sympathetic vertebral nerve activities (VNA), while its microinjection into caudal ventrolateral medulla (CVLM) induced decreases of SAP and VNA. In this study, the 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a non-NMDA antagonist, was used to examine the effects of non-NMDA receptors on Glu-induced cardiovascular responses. Cats were anesthetized intraperitoneally with a mixture of urethane (400 mg/kg) and alpha-chloralose (40 mg/kg) and paralyzed with gallamine triethiodide (4 mg/kg, i.v. per hour). CNQX blocked the Glu-induced pressor responses in FTG, DM and RVLM but potentiated the depressor responses in CVLM. These results suggest that non-NMDA receptors modulate the central pressor and depressor responses in an opposite direction. On the other hand, activation of DM and RVLM neurons by application of AMPA (5 mM, 30 nL) evoked pressor responses. These AMPA-induced responses were significantly blocked by CNQX. Interestingly, CNQX itself induced pressor responses in many stimulated points of the pressor areas (FTG: 6/9; DM: 13/24; RVLM: 6/13), indicating a tonic release of Glu mediating depressor effects. In conclusion, non-NMDA receptors within the pressor (FTG, DM and RVLM) and depressor (CVLM) areas may play different modulatory roles in cardiovascular integration. The depressor mechanism mediated by non-NMDA receptors is tonically activated by the release of endogenous Glu in these pressor and depressor areas.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1975

Effects of regional intravenous anaesthesia on blood flow.

Forearm blood flow after regional i.v. anaesthesia in volunteers was compared with the predicted blood flow after arterial occlusion alone, using venous occlusion plethysmography. After arterial occlusion alone for 20 min, marked hyperaemia occured after cuff release. Flows returned to normal within 5 min. Both prilocaine and bupivacaine reduced the hyperaemic response to arterial occlusion. Forearm muscle paralysis using gallamine triethiodide was also associated with a statistically significant but smaller reduction in the hyperaemic response.

Adult↗
PubMed1975

Plasma shedding by the canine oxyntic and pyloric glandular mucosa induced by topical action of acetylcholine. Effect of atropine and physostigmine.

Irrigation of the canine oxyntic or pyloric glandular mucosa in vagally denervated pouches with a solution of acetylcholine causes the mucosa to shed plasma proteins and the potential difference across the mucosa to fall. The response is dose-related with the threshold concentration of acetylcholine bromide ranging from 0.1 to 1 g per 100 ml. Topical application or intravenous injection of atropine prevents both plasma shedding and decline in potential difference. The minimal effective intravenous dose of atropine sulfate is about 0.007 mg per kg. The effect of irrigation with low concentrations of acetylcholine is enchanced by concurrent irrigation with physotigmine. The action of topical acetylcholine is not affected by concurrent irrigation with hexamethonium chloride (0.5 g per 100 ml) or by intravenous injection (5 mg per kg). Topical application of gallamine triethiodide (0.5 g per 100 ml) or d-tubocurarine (0.15 g per 100 ml) does not prevent the effects of acetylcholine in causing plasma shedding. Topical application of succinylcholine chloride (1 g per 100 ml) does not cause plasma shedding or a fall in potential difference.

Acetylcholine↗
PubMed2002

Pulmonary C-fiber activation enhances respiratory-related activities of the recurrent laryngeal nerve in rats.

The purpose of the current study was to characterize the response of the recurrent laryngeal nerve (RLN) to pulmonary C-fiber activation. Male rats of Wistar strain were anesthetized by urethane (1.2 g/kg, i.p.). Tracheostomy was performed. Catheter was inserted into the femoral artery and vein. Additional catheter was placed near the entrance of the right atrium via the right jugular vein. The animal was then paralyzed with gallamine triethiodide, ventilated and maintained at normocapnia in hyperoxia. Activities of the phrenic (PNA) and recurrent laryngeal nerves (RLNA) were monitored simultaneously. Two experimental protocols were completed. In the first experiment, various doses of capsaicin were delivered into the right atrium to activate pulmonary C-fibers with vagal intact. Low dose of capsaicin (1.25 microg/kg) produced apnea, a decrease in amplitude of PNA, an enhancement of RLNA during apnea and recovery from apnea, hypotension, and bradycardia. High dose of capsaicin (5 and 20 microg/kg) evoked the same tendency of response for both nerves and biphasic changes in blood pressure. Dose dependency was only seen in the period of apnea but not observable in nerve amplitudes. After bilateral vagotomy, low dose of capsaicin produced an increase in PNA without apnea, no significant change in RLNA, and hypertension. These results suggest that activation of vagal and nonvagal C-fibers could produce different reflex effects on cardiopulmonary functions. The reflex responses evoked by these two types of afferents might play defensive and protective roles in the airways and lungs.

Animals↗
PubMed2003

Arginine vasopressin produces inhibition upon respiration without pressor effect in the rat.

The purpose of the current study was to examine where arginine vasopressin (AVP) inhibits respiration by direct action on the areas of the ventrolateral medulla (VLM) in the rat. The animal was anesthetized by urethane (1.2 g/kg, i.p.), paralyzed with gallamine triethiodide, and artificially ventilated. Catheterization of the femoral artery and vein, and bilateral vagotomy were performed. The rat was then placed upon a stereotaxic instrument in a prone position. The phrenic nerve was separated and cut peripherally. Phrenic nerve activity (PNA) was monitored at normocapnia and hypercapnia in hyperoxia. Microinjection of AVP into various subregions of the VLM was then performed. In response to AVP microinjection, a transient period of apnea and then a significant decrease in PNA amplitude were observed. Arterial blood pressure was unchanged. This inhibition of PNA with AVP treatment was site-specific, attenuated by raising CO2 concentration, and totally abolished by pretreatment with AVP V1A receptor antagonist. Data of the present study indicate that endogenous resource of AVP may produce an inhibitory effect upon respiration via AVP receptors presented on neurons within the VLM.

Animals↗
PubMed1992

[Corticofugal modulation of somatosensory area II on acupuncture effect in nucleus ventralis posterolateralis of the thalamus].

In order to explore whether cortical somatosensory area 11 (SII) was involved in descending modulation of the effect of electroacupuncture (EA) on nucleus ventralis posterolateralis (VPL), the present study was designed to investigate the influence of topical application of lidocaine at SII on the EA effects in VPL nucleus. Experiments were performed on 23 adult cats anaesthetized with pentobarbital sodium (35-40 mg/kg i.p.) and immobilized with gallamine triethiodide. The single unit activities of VPL neurons were extracellularly recorded using glass microelectrodes. The results were as follows: 1. The nociceptive responses of VPL were obviously attenuated after EA at "Huantiao (G30)" and "Yanlingquan (G34)". The difference was statistically significant at 0-10 minutes after cessation of EA (n = 13, P < 0.001 or P < 0.05), then it was gradually recovered. The results showed that EA could inhibit the nociceptive responses of VPL neurons. 2. The inhibitory effect of acupuncture on nociceptive responses were reduced or abolished after topical application of lidocaine (n = 14, P > 0.05). However, it exerted marked inhibition at 0-10 minutes after cessation of EA in the saline control group (n = 14, P < 0.05). There was a statistical difference between these two groups (P < 0.05). The results showed that SII was involved in descending modulation of acupuncture effect in VPL nucleus.

Acupuncture Analgesia↗
PubMed1992

Correlation of cardiovascular and respiratory responses to glutamate excitation of pressor areas of the medulla in cats.

Cardiorespiratory responses, including changes of systemic arterial pressure (SAP), renal or splanchnic sympathetic nerve activity (SNA) and phrenic nerve activity (PNA), were elicited by microinjection of monosodium glutamate solution (0.5 M, 100 nl) into the dorsal (DM) and rostral ventrolateral medulla (RVLM) in 15 vagotomized cats anesthetized by urethane-chloralose and paralyzed by gallamine triethiodide. Artificial ventilation was adjusted to keep the end-tidal CO2 concentration at 4.0-0.5%. Sixty two pressor and 17 non-pressor sites were stimulated. Most of the stimulations inhibited the PNA. The responses of SNA was variable, showing increases, decreases or no change. Inhibition of SNA during SAP increase was not secondary to baroreceptor activation as the inhibition persisted in carotid sinus/aortic denervated animals. Although various combinations of changes of SNA and PNA were observed, their temporal courses were similar in many instances. Attenuation of SNA and PNA was synchronized, suggesting that these changes are coupled in the stimulating sites. The findings suggest that some neurons in DM and RVLM act as a functional unit to modulate cardiorespiratory functions whereas others simply coexist in the same area independent from each other.

Animals↗