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PubMed1990

Vagal afferent-mediated inhibition of a nociceptive reflex by intravenous serotonin in the rat. I. Characterization.

The effect of intravenous (i.v.) serotonin (5-HT) on nociception and blood pressure was examined in male Sprague-Dawley rats. Intravenous 5-HT produced a dose-dependent (6-192 micrograms/kg, i.v.) inhibition of the nociceptive tail-flick (TF) reflex in lightly pentobarbital-anesthetized (ED50 = 40 micrograms/kg) and conscious rats (ED50 = 44 micrograms/kg). In the lightly pentobarbital-anesthetized rat, the blood pressure response to i.v. 5-HT was typically a triphasic response with a marked Bezold-Jarisch reflex-induced decrease in pressure (associated with a brief period of apnea) followed by a pressor phase and a subsequent delayed hypotension. In the conscious rat, the response was typically biphasic with the late hypotensive phase absent. A variety of anatomical and pharmacological manipulations were performed to characterize the 5-HT-induced inhibition of the TF reflex and associated changes in blood pressure. Prevention of 5-HT-induced reflex apnea by artificial ventilation did not affect inhibition of the TF reflex produced by 5-HT. Pharmacological manipulations were performed to mimic, as closely as possible, the acute increases and decreases in blood pressure associated with i.v. 5-HT. Nitroprusside (8 micrograms/kg, i.v.) produced a decrease in blood pressure of similar magnitude and rate as that associated with the Bezold-Jarisch reflex-induced decrease in pressure produced by 72 micrograms/kg 5-HT, but did not change TF latency from baseline. Similarly, acute increases in pressure produced by phenylephrine (8 micrograms/kg, i.v.), intended to mimic the secondary pressor effect of 5-HT, did not change TF latency. The short-acting ganglion blocker trimethaphan (5 mg/kg, i.v.) closely mimicked the late hypotensive phase produced by 5-HT, but again resulted in no change in TF latency. Pretreatment with the ganglion blocker chlorisondamine (2.5 mg/kg) abolished all depressor responses to 72 micrograms/kg 5-HT, but did not significantly affect the TF reflex. These results indicate that acute changes in blood pressure and respiration associated with i.v. 5-HT do not contribute to inhibition of the TF reflex. This conclusion was confirmed in experiments in which bilateral vagotomy abolished approximately 70% of the 5-HT-induced inhibition of the TF reflex (and all depressor responses), and resulted in a significantly greater pressor response. Finally, low thoracic spinal cord transection (T9-10) abolished the inhibition of the TF reflex produced by i.v. 5-HT. Therefore, 5-HT stimulates vagal afferents and inhibits the TF reflex by activating descending inhibitory systems from the brainstem.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗

PubMed1991

Relaxant effect of capsaicin in the rat gastric fundus.

The effect of capsaicin was studied in precontracted longitudinal muscle strips of the rat gastric fundus. Capsaicin induced a relaxation in the concentration range 10(-7)-10(-6) M. The relaxation induced by 10(-6) M capsaicin was completely prevented by extrinsic denervation of the stomach. The adrenoceptor antagonists phentolamine and propranolol did not influence the effect of capsaicin while hexamethonium potentiated it; this potentiation was not observed with another nicotinic receptor antagonist trimethaphan. Tetrodotoxin did not have a consistent effect as it reduced the capsaicin-induced relaxation in some but not all tissues. The peptidase trypsin consistently reduced the action of capsaicin but vasoactive intestinal polypeptide (VIP) antiserum, desensitization to calcitonin gene-related peptide (CGRP), and CGRP antiserum had no influence. The neuropeptide involved in the relaxant effect of capsaicin in the rat gastric fundus has thus still to be determined.

Animals↗

PubMed1988

Vasomotion in normal and injured spinal cord.

Blood flow in the feline thoracic spinal cord was measured, using a laser-Doppler flowmetry. Rhythmic changes in the spinal cord blood flow were repeatedly observed with a frequency of about three to eight cycles per minute, unrelated to the respiratory or cardiac cycles. These changes were unaffected by hypertension induced by angiotensin II, but disappeared when systemic blood pressure was lowered by trimethaphan or when hypercapnia was induced. CO2 responsiveness of the blood flow and postocclusive reactive hyperemia were also examined, in both the normal and injured spinal cord. CO2 responsiveness was lost 1 h after a 500 gm/cm injury without rhythmic changes, but was partially regained 2 days later, at which time rhythmic changes were frequently observed. Postocclusive hyperemia apparently diminished 1 h after a 500 gm/cm injury, but reappeared 2 days later. Vasomotion in the normal and injured spinal cord is discussed.

Animals↗

PubMed1993

Role of the locus coeruleus in the noradrenergic response to a systemic administration of nicotine.

Experiments were conducted using in vivo microdialysis to ascertain the role of nicotinic receptors in the terminal, or the cell body area, in the hippocampal noradrenaline response provoked by a systemic administration of nicotine. These experiments combined systemic administration of nicotine with local administration of antagonists into the hippocampus via the microdialysis probe, or close to the LC via a cannula, while continuously monitoring extracellular levels of NA in the hippocampus. Systemic administration of nicotine (0.4 mg/kg, s.c.) produced a rapid and prolonged increase in extracellular levels of noradrenaline in the hippocampus of conscious animals, reaching a maximum in the first 10 min sample. In anaesthetised animals the maximum occurred 20 min after administration, but the subsequent response profile was similar. In both anaesthetised and freely moving animals nicotine increased extracellular levels of dihydroxyphenylacetic acid and homovanillic acid in the hippocampus, but failed to alter levels of dopamine or 5-hydroxyindoleacetic acid. In anaesthetised animals intrahippocampal administration of nicotine (250 microM over 10 min via the dialysis probe) significantly increased extracellular levels of noradrenaline; the response was shortlasting, being evident only in the 10 min sample during exposure to the drug. Local administration of nicotine failed to alter extracellular levels of any other amine or metabolite measured. Mecamylamine (25 microM), a nicotinic channel blocker, administered intrahippocampally 10 min prior to an intrahippocampal administration of nicotine completely blocked the increase in noradrenaline. However, intrahippocampal administration of mecamylamine (25 microM) for 10 min, or for the duration of recording, failed to antagonise the effect of a systemic administration of nicotine (0.4 mg/kg, s.c.) on extracellular levels of noradrenaline, dihydroxyphenylacetic acid or homovanillic acid. In contrast administration of mecamylamine (50 microM) close to the locus coeruleus abolished the increase in noradrenaline levels in the ipsilateral hippocampus following a systemic administration of nicotine (0.4 mg/kg, s.c.), while trimethaphan (50 microM), a nicotine receptor antagonist, significantly reduced the response. Administration of mecamylamine also attenuated increases in dihydroxyphenylacetic acid and homovanillic acid, suggesting that the response of these metabolites may be associated with the functional metabolism of noradrenergic neurones. Locus coeruleus administration of kynurenic acid (1 mM), a non-specific excitatory amino acid antagonist, was without effect. Finally, application of nicotine (50 microM) close to the locus coeruleus significantly increased extracellular levels of noradrenaline in the ipsilateral hippocampus.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗

PubMed1993

The paradoxical blood pressure-flow relationship in the brain with an arteriovenous malformation.

The responses of regional cerebral blood flow (CBF) to decrease in arterial blood pressure were studied in eight patients with arteriovenous malformations using the Xe-133 inhalation method. Measurements were performed twice for each study; before and during hypotension induced by trimethaphan camsylate (Arfonad). In all cases, there were regions where cerebral blood flow increased remarkably in response to hypotension. When the studies were repeated in five cases after total resection of the malformations, increase in the cerebral blood flow in response to hypotension was not observed. The underlying mechanisms that operate in such paradoxical blood pressure-flow relationship are discussed.

Adult↗

PubMed1978

Uropharmacology: VII. Ganglionic stimulating and blocking agents.

A classification of the various ganglionic stimulants and blockers is presented, and their pharmacologic effects on the urinary bladder and urethra are discussed. Ganglionic stimulating drugs are of considerable interest in investigational work but are not presently used therapeutically. Ganglionic blockers include hexamethonium, tetraethylammonium, mecamylamine emepronium, pentolinium, chlorisondamine, and pemipidine. Of the numerous ganglionic blocking drugs that have appeared on the therapeutic scene, only mecamylamine, pentolinium, and trimethaphan are currently official.

Animals↗

PubMed1994

Mechanism of long-lasting block of ganglion nicotinic receptors by mono-ammonium compounds with long aliphatic chain.

The effect of long-chain mono-ammonium compounds (long-chain MACs), t-butyldecylammonium (IEM-1078), 2,2,6,6-tetramethyldecylpiperidine (IEM-1559), and diisopropyldecylammonium (IEM-1194), on nicotinic acetylcholine receptors (nAChRs) was studied in sympathetic ganglion neurons using the patch clamp method. Long-chain MACs (1-10 microM) strongly inhibited acetylcholine (ACh)-induced current (ACh-current); the block persisted for hours after washing the drugs out. Short-chain MACs had a much weaker and completely reversible blocking effect. Suppression of ACh-current by MACs was dose- and voltage-dependent; it was absent at low ACh doses or at potentials > or = 60 mV and increased with higher ACh doses or hyperpolarization. The second of two ACh-currents induced by paired application of ACh was inhibited by long-chain MACs more strongly than the first. This use-dependent block also persisted for hours after washing the drugs out. Additional inhibition of the second ACh-current was reduced by lengthening the time interval between ACh applications in the pair. Time constants of the recovery of the second ACh-current in the presence and after washing out of long-chain MACs were similar, ranging from 45 to 140 s at -50 mV for different long-chain MACs, and decreased with de- or hyperpolarization. The use-dependent block produced by long-chain MACs could be prevented by another long-chain MAC with a small ammonium head (IEM-1195, 75-100 microM) or trimethaphan (30 microM), a competitive antagonist of ACh in ganglia. Neither the short-chain MAC (IEM-1405, 100 microM) nor ACh (100 microM) could exert this protective effect. Long-chain MACs did not exert any use-, dose- or voltage-dependent suppression of ACh-current when applied intracellularly. Single-channel conductance was not affected by IEM-1194 (3-10 microM). We suggest that inhibition of ACh-current by long-chain MACs is accounted for by (i) a long-lasting, apparently irreversible, binding of the drug near the channel of nAChR via its long aliphatic chain and (ii) a slow reversible block of the nAChR channel with the MAC's ammonium head.

Acetylcholine↗

PubMed1994

A nicotinic-like receptor mediates suppression of distortion product otoacoustic emissions by contralateral sound.

The purpose of this investigation was to provide in vivo pharmacologic characterization of a cholinergic receptor mediating the suppressive effects of medial olivocochlear (MOC) efferent activation. MOC neurons were activated by contralateral sound and the resulting suppression of ipsilateral distortion product otoacoustic emissions (DPOAEs) was monitored before and after intracochlear perfusions of cholinergic antagonists. Results revealed a dose-dependent blockade of contralateral suppression of DPOAEs by a wide variety of nicotinic and muscarinic cholinergic receptor antagonists, as well as by non-traditional antagonists of cholinergic activity. The nicotinic antagonists, alpha-bungarotoxin, curare and kappa-bungarotoxin, and the glycine antagonist, strychnine, blocked contralateral suppression at nanomolar concentrations and demonstrated similar potencies. IC50 values were 2.38 x 10(-7), 2.79 x 10(-7), 3.81 x 10(-7) and 2.96 x 10(-7) M, respectively. These agents were followed in potency by the nicotinic antagonist, trimethaphan (1.75 x 10(-6) M), the M3 muscarinic antagonist, 4-DAMP (1.88 x 10(-6) M) and the GABAA antagonist, bicuculline (2.39 x 10(-6) M). Increasingly greater concentrations of the muscarinic antagonists, atropine (9.52 x 10(-6) M), AF-DX 116 (2.72 x 10(-5) M) and pirenzepine (8.24 x 10(-4) M) were necessary to block contralateral suppression of DPOAEs. The in vivo pharmacology of this putative outer hair cell cholinergic receptor suggests that it may be a member of the nicotinic family of receptors.

Acoustic Stimulation↗

PubMed1999

Opioid neurotoxicity: fentanyl-induced exacerbation of cerebral ischemia in rats.

We tested the hypothesis that fentanyl would worsen ischemia-induced brain damage. In two sequential protocols forty rats were physiologically monitored and controlled. In protocol 1, rats were randomized (n=10/group) to 30 min of control (N2O plus 0.4% halothane), low dose fentanyl (loading dose [LD] 50 micrograms kg-1, maintenance dose [MD] 2 micrograms kg-1 min-1), or high-dose fentanyl (LD 800 micrograms kg-1, MD 32 micrograms kg-1 min-1). After 15 min of fentanyl or sham infusion trimethaphan 0.5 mg was given i.v. and 3 min later bilateral carotid artery occlusion and blood withdrawal-induced hypotension were maintained for 12 min. At 18 h postischemia rats underwent cerebral perfusion fixation. Brain areas were graded from 0 (normal) to 5. In addition to analysis of specific regions, neuropathologic scores were also summated over all brain regions and analyzed to compute a summed neuropathologic score. In protocol 2, five control and five high-dose fentanyl rats were treated identically except that post-ischemic oxygenation was maintained for 6 h and cerebral perfusion-fixation was performed 6 h post-ischemia. Only the caudate/putamen was examined in protocol 2. Fentanyl worsened lesions in both fentanyl groups' summed neuropathologic scores (P=0.002) in protocol 1 and specifically, in the caudate/putamen (P<0.01) in both protocols. Fentanyl in both high and low doses can exacerbate incomplete forebrain ischemia in rats.

Analgesics, Opioid↗

PubMed1989

Acetylcholine as a possible neurotransmitter in penile erection.

We investigated the erectile response to intracavernous injection of increasing doses of acetylcholine (0.5 to 500 micrograms.) in 10 monkeys. To differentiate between nicotinic (ganglionic) and muscarinic (parasympathetic postganglionic) effects, acetylcholine was likewise administered after 1.6 mg. trimethaphan camsylate and 0.1 mg. atropine, alone or sequentially. Erections were induced by cavernous nerve stimulation before and after atropine. Acetylcholine induced a dose-dependent, triphasic erectile response: a first tumescence phase followed by contraction and a subsequent second phase of tumescence. Atropine reduced but did not abolish the erectile response to acetylcholine: attainment of maximal intracavernous pressure after neurostimulation was both delayed and reduced (mean 25 cm. H2O). Only after combined nicotinic and muscarinic blockade was the erectile response to acetylcholine completely abolished. Histologic staining for acetylcholinesterase in five additional monkeys that had not received acetylcholine showed dense staining within the cavernous erectile tissue and around the cavernous arteries. Our data suggest that acetylcholine is a possible neurotransmitter for penile erection in monkeys.

Acetylcholine↗

PubMed1983

Controlled hypotensive anesthesia to reduce blood loss in radical cystectomy for bladder cancer.

Controlled intraoperative hypotension has been reported to reduce blood loss in major cancer operations. We did a retrospective evaluation on the effects of induced controlled hypotensive anesthesia using enflurane or trimethaphan compared to standard normotensive anesthesia in 37 consecutive patients who were undergoing single stage radical cystectomy with pelvic lymphadenectomy and bilateral ureteroileal cutaneous urinary diversion. Group 1 contained 16 patients who received induced hypotensive anesthesia and group 2 contained 21 patients who received normotensive anesthesia. Average age, pathological stage, and hematocrit values preoperatively and 5 days postoperatively were not significantly different. The average blood loss in group 1 was 821 plus or minus 78 cc and in group 2 it was 1,740 plus or minus 132 cc, a difference of 919 cc (p less than 0.001). Concomitantly, total blood replacement was significantly different. The hypotensive group required an average of 1.38 plus or minus 0.25 units or 700 plus or minus 100 cc and the normotensive group averaged 3.25 plus or minus 0.45 units or 1,600 plus or minus 225 cc (p less than 0.05). In addition, only 69 per cent of the hypotensive group required blood replacement compared to 90 per cent of the normotensive group. Our data demonstrate that controlled hypotensive anesthesia markedly reduces blood loss for radical bladder cancer surgery.

Anesthesia↗

PubMed1975

Deliberate hypotension.

Deliberate hypotension can reduce major blood loss and indelicate operations can produce a drier field increasing the ease of surgery and the likelihood of a good result. The techniques used to induce hypotension can also be used to avoid dangerous hypertension during and after surgery. These benefits must be weighed against the risks of inadequate perfusion: especially cerebral, myocardial, or renal. In previously normotensive patients these risks are minimal when the arterial pressure is held above 80 torr systolic, and may be acceptably small even at mean pressure of 50 to 60 torr. Previously hypertensive patients show signs of cerebral ischemia at higher pressures; they should probably not be subjected to deliberate hypotension, but they also can be harmed by severe hypertension which can be avioded by the proper use of hypotensive agents. For most situations a balanced technique is suitable: after a stable anesthetic level has been achieved using halothane or enflurane, hypotension can be induced with sodium nitroprusside or trimethaphan camsylate. Longer-acting agents such as pentolinium are sometimes desirable, but the shorter-acting agents are easier to control. Careful monitoring with observation of intra-arterial pressure, electroencephalogram, electrocardiogram, and determination arterial blood gas tensions is likely to make for safer conduct. Close postoperative observation is essential. With careful preparation and monitoring deliberate hypotension can be a safe technique for reducing blood loss or facilitating delicate procedures.

Abdomen↗

PubMed1999

Characterization of a recovery global cerebral ischemia model in the mouse.

Transgenic/knockout murine variants allow roles of specific proteins to be studied in cerebral ischemia. Because of the size of mice, however, study of prolonged recovery from global ischemia has been limited. This project characterized an adaptation of the rat two-vessel occlusion model of global ischemia for use in the mouse. C57B1/6J mice (8 weeks old; 21 +/- 1 g) were overnight fasted, anesthetized with halothane, intubated and mechanically ventilated. The right internal jugular vein and femoral artery were cannulated. Pericranial temperature was held at 37.0 degrees C. The carotid arteries were occluded and mean arterial pressure was reduced to 35 mmHg with 0.3 mg intra-arterial trimethaphan and venous exsanguination. Electroencephalographic isoelectricity was confirmed in cohort mice. Ten minutes later ischemia was reversed. Mice were allowed 1, 3 or 5 days survival followed by histologic analysis. Regional cerebral blood flow (CBF) was determined autoradiographically. Outcome effects of intra-ischemic hyperglycemia (approximately 350 mg/dl) or hypothermia (34 degrees C) were also examined. The mortality rate was less than 10% in all recovery groups. Ischemia caused reduction of CBF to < 2% of sham values in cortex, hippocampus, and caudoputamen. CBF was unchanged in thalamus, brainstem and cerebellum. CA1 damage, greater after 3 days vs. 1 day reperfusion, was not further increased at 5 days. Histologic injury was increased by hyperglycemia although seizures did not occur. Hypothermia reduced CA1 damage. This study demonstrates feasibility of using the two-vessel occlusion + hypotension recovery model in the mouse. Recovery intervals of > or = 3 days are required to account for delayed CA1 neuronal necrosis. Histologic outcome can be modulated by known physiologic determinants of ischemic brain damage.

Animals↗

PubMed2002

Hypertension in orthostatic hypotension and autonomic dysfunction.

Disabling orthostatic hypotension dominates the clinical picture of autonomic failure. Nonetheless, severe supine hypertension is observed in about 50% of patients. In patients with multiple system atrophy (Shy-Drager syndrome), supine hypertension is explained by residual sympathetic tone because it can be eliminated with the ganglionic blocker trimethaphan. The cause of hypertension in patients with pure autonomic failure is not known and its understanding may be relevant to essential hypertension. Supine hypertension complicates the treatment of these patients but can be managed by overnight administration of antihypertensive medications.

Humans↗

PubMed1986

The ensemble approach to distance geometry: application to the nicotinic pharmacophore.

We develop an extension of conventional distance geometry techniques that treats two or more molecules as a single "ensemble". This extension can be used to find a common pharmacophore, i.e., the spatial arrangement of essential groups, from a small set of biologically active molecules. The approach can generate, in one step, coordinates for the set of molecules in their "active" conformations such that their essential groups are superimposed. As an example, we show how the nicotinic pharmacophore can be deduced from a set of four nicotinic agonists: nicotine, cytisine, ferruginine methiodide, and muscarone. Three essential groups in each agonist are chosen: the cationic center (A), an electronegative atom (B), and an atom (C) that forms a dipole with B. There is only one pharmacophore possible for the superposition of these essential groups: a triangle with sides 4.8 A (A-B), 4.0 A (A-C), and 1.2 A (B-C). The pharmacophore triangle, which is consistent with previous models in the literature, can also be achieved by the agonist trans-3,3'-bis[(trimethylammonio)methyl]azobenzene and the antagonists strychnine, trimethaphan, and dihydro-beta-erythroidine. An examination of the common volumes of agonists suggests a specific disposition of molecular volume relative to the pharmacophore triangle. We discuss the relative strengths and drawbacks of the ensemble approach vs. other conformational search methods.

Alkaloids↗

PubMed1985

Effect of hypothermic cardiopulmonary bypass on nitroprusside metabolism.

At a rectal temperature of 25 degrees C, six patients undergoing hypothermic cardiopulmonary bypass received intravenous infusions of sodium nitroprusside (SNP) at a rate of 7.3 +/- 1.7 micrograms/kg/min for 20 minutes. Total SNP dose per patient was 11.0 +/- 1.1 mg. Blood samples for serum cyanide (CN-), red blood cell cyanide (RBC CN-), and thiocyanate (SCN-) determinations were drawn immediately before SNP infusion. These determinations were repeated at the end of the infusion, at the start of rewarming, and at a rectal temperature greater than 34 degrees C and 1, 4 (five subjects), and 24 hours (three subjects) thereafter. Extracorporeal blood flow was held constant at 2.4 L/min/m2 and mean arterial pressure was maintained between 50 to 100 mm Hg with phenylephrine (3.62 +/- 0.75 mg) during SNP infusion and trimethaphan (37.8 +/- 15.6 mg) after the end of the infusion. There was a significant increase in RBC CN- after the SNP infusion that lasted until the subjects were rewarmed. One subject developed a peak RBC CN- level of 0.8 microgram/ml. Plasma CN- levels changed little throughout and SCN- levels were elevated only after rewarming. The nonenzymatic release of free CN- from SNP was not inhibited by hypothermia, while the enzymatic detoxification of CN- to SCN- may have been delayed.

Aged↗

PubMed1990

Protective effect of nimodipine against ischemic neuronal damage in rat hippocampus without changing postischemic cerebral blood flow.

The purpose of the present study was to investigate the neuroprotective action of nimodipine. Furthermore, the influence of nimodipine on postischemic local CBF (LCBF) was examined. Forebrain ischemia of the rat was performed for 10 min by bilateral carotid clamping, administration of trimethaphan, and blood withdrawal to obtain an MABP of 40 mm Hg. LCBF was measured after 10 min of postischemic recirculation by injecting [14C]iodoantipyrine in saline solution. Nimodipine (0.1, 0.3, and 1.0 mg/kg) was suspended in miglyol oil and applied orally 60 min prior to ischemia. Histological evaluation was performed 7 days after ischemia. Hippocampal neuronal damage was determined as the percentage of necrotic neurons. After preischemic application of nimodipine, neuronal damage was significantly reduced in the hippocampal CA1 subfield. Postischemic LCBF was not affected by treatment with nimodipine. These findings show that nimodipine is able to protect neurons against ischemic damage. The neuroprotective effect of nimodipine was not mediated by a postischemic cerebral vasodilation, but by a direct action on the neurons.

Animals↗

PubMed1985

Reduced plasma noradrenaline during angiotensin II-induced acute hypertension in man.

1. Plasma noradrenaline and adrenaline concentrations were measured in ten subjects before, during and after intravenous infusion of angiotensin II (ANG II) in order to determine the sympathoadrenal response of ANG II challenge in man. In five subjects ganglionic blockade was additionally performed by intravenous infusion of trimethaphan. 2. During ANG II infusion mean arterial blood pressure increased by 30% (P < 0.001), and plasma noradrenaline decreased by 25% (P < 0.001). Plasma adrenaline decreased less. 3. During ganglionic blockade plasma noradrenaline decreased significantly (P < 0.005) and similarly to the decrease obtained with ANG II infusion. 4. The results indicate that a decrease in sympathoadrenal activity occurs during ANG II-induced acute hypertension in man. This may be elicited by the arterial baroreflex, which seems to dominate any direct sympathoadrenergic facilitating effect of ANG II.

Acute Disease↗