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PubMed1985

Effect of locus coeruleus stimulation on regional cerebral oxygen consumption in the cat.

Regional cerebral oxygen consumption was determined during stimulation of the intra-axial noradrenergic pathway to quantitate the metabolic effects of this manipulation on cerebral oxygen extraction, cerebral blood flow (CBF) and its regional distribution. Regional arterial and venous oxygen saturation were examined microspectrophotometrically. Regional CBF was examined using radioactively tagged microspheres (15 +/- 3 microns in diameter). Oxygen consumption was calculated as the regional product of CBF and oxygen extraction. Bipolar concentric electrodes were stereotaxically implanted bilaterally in the locus coeruleus of alpha-chloralose anesthetized, artificially respired adult mongrel cats. The control group was killed after hemodynamic and CBF measurements were taken. The experimental group was sacrificed after these same measurements were taken before and during 10 min of bilateral locus coeruleus stimulation. The cats' heads were simultaneously sawed in 3 places and quickly frozen in liquid nitrogen-cooled propane. Systolic blood pressure was significantly increased during treatment. The heterogeneity of venous oxygen saturation was significantly reduced by stimulation. Average CBF and oxygen consumption were significantly decreased to 57% and 59% of control, respectively. Oxygen consumption was significantly reduced in the hypothalamus from 1.5 +/- 0.3 to 0.9 +/- 0.3 ml O2/min/100 g and from 3.5 +/- 0.9 to 1.2 +/- 0.4 ml O2/min/100 g in the cerebellum by treatment. Changes in the neuronal and/or synthetic cerebral activity produced regional decreases in cerebral oxygen consumption and secondarily altered CBF. These changes are probably due to interaction of the intraparenchymal noradrenergic pathways with other systems or processes in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Intracranial potentials correlated with an event-related potential, P300, in the cat.

Intracranial recordings of long-latency, event-related potentials were obtained from paralyzed, artificially respirated cats. A modified oddball paradigm was employed in which cats were presented with a randomized series of two tones, a 'frequent' 4 kHz stimulus and a 'rare' 1 kHz stimulus. A tail shock was administered 700 ms after onset of the rare tone. Under these circumstances the stimulus elicited a positive component at the vertex similar to the human P300. Intracranial potentials associated with the rare tone usually manifested components of greater amplitude than did potentials associated with the frequent tone. A positive component occurring in latency between 200 and 350 ms only accompanied the presentation of the rare stimulus. The P300 component, which was positive at the dura, appeared as a negative component within a few millimeters of the surface over a wide area of the marginal and suprasylvian gyri. Changing the probability of the rare stimulus resulted in a reduction in the amplitudes of both the intracranial negative component and the P300 recorded at the skull. Components of large amplitude associated with the rare stimulus were obtained from the region of the hippocampus. These components reversed polarity, sometimes more than once, as the electrode was advanced. Substantial latency differences were often observed between the P300 recorded at the skull and P300-like intracranial components associated with the rare stimulus. These results suggest that the cortices of the marginal and suprasylvian gyri and the hippocampal region contribute to the generation of the cat P300.

Animals↗
PubMed1985

Chemical stimulation of the area postrema induces cardiorespiratory changes in the cat.

The purpose of our study was to determine the cardiorespiratory effects of exciting cell bodies of the area postrema of the cat. This was accomplished by local application of L-glutamic acid (bilateral application of 5 microliter of a 250-1000 mM solution) and kainic acid (bilateral application of 5 microliter of a 40 mM solution) to the area postrema of chloralose-anesthetized cats while monitoring arterial pressure, heart rate, tidal volume and respiratory rate. These excitatory amino acids activate neuronal cell bodies but not axons of passage. L-Glutamic acid produced a dose-dependent increase in arterial pressure, decreases in respiratory rate and minute volume and, occasionally, ventricular tachyarrhythmias. Kainic acid produced effects similar to those seen with L-glutamic acid except the changes in respiratory activity were more pronounced with each animal exhibiting respiratory arrest. In artificially respired animals, kainic acid produced similar cardiovascular changes as those occurring in spontaneously breathing animals (i.e. increases in arterial pressure of 61 +/- 5.7 mm Hg, and in heart rate of 32 +/- 8.3 beats/min). Finally, application of kainic acid to the area postrema abolished the pressor and tachycardic responses to bilateral occlusion of the carotid arteries. These results suggest that activation of cell bodies in the area postrema can result in pronounced cardiorespiratory changes.

Animals↗
PubMed1991

On the mechanism of spontaneous recovery of neuromuscular transmission after acetylcholinesterase inhibition in the rat neuromuscular junction.

Neuromuscular transmission shows a significant degree of spontaneous recovery after being impeded by acetylcholinesterase inhibition. Part of this recovery can be ascribed to de novo synthesis of acetylcholinesterase but another part is independent of enzyme activity. To unravel the mechanism underlying this synaptic adaptation to acetylcholinesterase inhibition we have compared a number of electrophysiological parameters in diaphragms taken from animals that were sacrificed within 15 min after a 2 x LD50 dose of the acetylcholinesterase inhibitor diisopropylfluorophosphate and from similarly treated animals killed after being kept alive for 3 h under artificial respiration. We found no differences in the quantal content. There was a significantly smaller degree of endplate potential rundown at tetanic stimulation and the miniature endplate potential amplitude was smaller in the 3-h adapted animals. In addition, the desensitization induced by carbachol appeared to be less in this group. It is likely that these synaptic changes, demonstrating the plasticity of the neuromuscular synapse, are involved in the spontaneous recovery of neuromuscular transmission after acetylcholinesterase inhibition.

Animals↗
PubMed1992

Rostral ventrolateral medullary neurons projecting to locus coeruleus have cardiorespiratory inputs.

This study was designed to characterize some of the properties of the rostral ventrolateral medullary (RVLM) cells with axonal projection to the locus coeruleus (LC) in urethane anesthetized, vagotomized, paralyzed and artificially respirated rats. The vast majority of RVLM units antidromically (AD) activated from LC (RVLM-LC units) were silent and unresponsive to peripheral chemoreceptor stimulation or nociceptive stimulation. Twenty seven spontaneously active RVLM-LC neurons, AD activated from LC with currents below 30 microA (17 +/- 2 microA) were analyzed. AD mapping (n = 18) indicated that the lowest threshold for AD activation occurred within the LC itself. Axonal branching within or close to LC was suggested by the presence of sudden jumps in AD latency. Maximal AD latencies ranged from 7 to 37 ms. Most spontaneously active RVLM-LC neurons displayed marked central respiratory modulation characterized by either a post-inspiratory or an inspiratory pattern. The majority of the tested neurons were affected (excited or inhibited) by brief peripheral chemoreceptor stimulation (N2 inhalation). Most cells were inhibited by raising arterial pressure but none exhibited any detectable pulse synchrony. Reticulospinal sympathetic premotor neurons of RVLM were not found to project to LC (sample of 9) and very few RVLM cells with on-off respiratory discharges appeared to project to LC (2 out of 110). This study suggests that much of the information conveyed by the RVLM to LC could be of a mixed cardiorespiratory nature.

Afferent Pathways↗
PubMed1992

Glutamate, NMDA and NMDA receptor antagonists: cardiovascular effects of intrathecal administration in the rat.

Selected excitatory amino acids and antagonists were tested for their effects on arterial pressure and heart rate when administered intrathecally at the second (T2) or ninth (T9) thoracic spinal levels in urethane-anesthetized Sprague-Dawley rats with spontaneous or artificial respiration. Intrathecal administration of glutamate (1 mumol) and N-methyl-D-aspartic acid (NMDA; 2 nmol) at T9 increased arterial pressure and heart rate. The response began within 1 min, peaked at 2-3 min and persisted for 8-15 min. The maximum changes were 20-25 mm Hg for arterial pressure and 40-50 beats/min for heart rate. These responses were prevented by systemic administration of hexamethonium (10 mg/kg). Responses to administration of NMDA at the two spinal levels were essentially the same. Effects elicited by NMDA but not by glutamate were blocked by pretreatment with the NMDA receptor antagonists, D,L-2-amino-5-phosphonovaleric acid (APV; 10 nmol, intrathecal administration) and ketamine (7 mg/kg, i.v.). Intrathecal administration of APV (10, 50 and 200 nmol) at T2 produced dose-dependent decreases in arterial pressure without changing heart rate. The results support the hypothesis that NMDA receptors are involved in regulation of sympathetic output at the spinal level. They also indicate that in this preparation there is a tonic activation of NMDA receptors in sympathetic pathways to the vessels but not to the heart. Finally, the persistence of the response to glutamate in the presence of NMDA receptor antagonists suggests the involvement of non-NMDA receptors in spinal control of sympathetic output.

2-Amino-5-phosphonovalerate↗
PubMed1990

Cochlear potentials and auditory evoked potentials in the caiman (Caiman crocodilus (L.)).

Brain-stem auditory evoked potentials (BAEPs) and round window compound action potentials (CAPs) in response to rarefaction and condensation clicks were recorded from anaesthetized and artificially respired caiman. The recorded wave forms were substantially different from the brain-stem and round window potentials recorded in mammals, including man. In particular, wave latencies were much longer than in mammals. Wave amplitudes increased and latencies decreased significantly and reversibly with increases in stimulus intensity and body temperature. The latencies of the first positive wave (P1) in the BAEP and the first negative wave (N1) in the CAP are correlated and co-vary with stimulus level and body temperature. BAEP P1 thus represents the response of the auditory nerve. The cochlear microphonic (CM) latency in caiman is unaffected by stimulus intensity and by cooling of the animal.

Action Potentials↗
PubMed1978

Successful oxime therapy one hour after soman intoxication in the rat.

The bisquaternary mono-oxime HI-6, and to a lesser extent HS-6, caused functional recovery of neuromuscular transmission in vivo and in vitro when given 60 min after soman, i.e. when the soman-cholinesterase (AChE) complex is said to be fully "aged". Atropinised rats, with the tracheas intubated, received 4 X LD50 soman i.v. and were kept alive by artificial respiration. 60 min later HI-6 was administered and after an additional 15 min the tracheal tube was removed. Nearly all animals survived for 24 h. After 6 X LD50 soman followed by HI-6, HI-6, respiratory failure was delayed for hours but almost all animals died within 24 h. Against equal doses of soman, HS-6 was less effective. In experiments with isolated rat phrenic nerve-diaphragm preparations, HI-6 given 60 min after soman produced functional recovery which could be abolished by a second dose of soman, suggesting that HI-6 had reactivated the AChE and that this enzyme was then reinhibited by the second dose of soman. HI-6 reactivates purified bovine erythrocyte AChE when added immediately after inhibition by soman, but does not reactivate tabun-inhibited AChE. Accordingly, no functional recovery of neuromuscular transmission was found in rat diaphragm when HI-6 was administered 60 min after tabun. Furthermore, functional recovery was not obtained with HI-6 after exposure diaphragms to S 27, which carries a hydroxyl group instead of an alkoxy group--i.e. it is "pre-aged"--and instantaneously forms an inhibitor--enzyme complex identical to the "age" soman--enzyme complex. These results exclude the possibility that the functional recovery was caused by a direct pharmacological effect of the oxime. The functional recovery of diaphragms treated with II-6 60 min after exposure to soman was not accompanied by a return of histochemically detectable AChE activity. The capacity of the isolated diaphragm to hydrolyze (3H)-acetylcholine, however, seemed to be reactivated to a very small (1--2%) extent by HI-6, 60 min after exposure to soman. It is concluded that soman-inhibited cholinesterase in intact rat tissue "ages" much more slowly than does soman-inhibited purified cholinesterase, so that even after 60 min enough "non-aged" inhibited AChE is still susceptible to reactivation to be lifesaving.

Animals↗
PubMed1982

A new non-depolarizing myorelaxant with high activity and specificity.

The curare-like activity and mode of action of tercuronium (p,p"-bistriethylammonium-p-terphenyl dibenzen-sulphonate) have been investigated in experiments with cats, rabbits, mice and pigeons as well as with rat phrenic diaphragm preparations. The curare-like activity of tercuronium was higher than that of tubocurarine and was close to that of pancuronium bromide. The curare-like activity of tercuronium was higher than that of tubocurarine and was close to that of pancuronium bromide. The neuromuscular blocking doses (ED95) of tercuronium, (+)-tubocurarine and pancuronium in cats, for example, were 0.08 microM/kg, 0.4 microM/kg and 0.04 microM/kg respectively. The time of development and duration of action were similar to those of (+)-tubocurarine and pancuronium. Tercuronium is a nondepolarizing myorelaxant. In experiments with cats the antagonism of neostigmine (0.1 mg/kg) to tercuronium was more pronounced than in the case of (+)-tubocurarine, pancuronium or gallamine. Tercuronium affected neither the arterial pressure nor the heart rate when given in neuromuscular blocking doses. Tercuronium did not block transmission through autonomic ganglia and had no atropine-like action. Only a 10-fold increase in the dose of tercuronium produced the ganglion blocking effect in cats. Under artificial respiration, cats and rabbits tolerated tercuronium in a dose 200 times exceeding its myoparalytic dose. It is concluded that tercuronium is distinguishable from (+)-tubocurarine by its high neuromuscular blocking activity as well as by its specificity and more pronounced neostigmine antagonism.

Anesthesia↗
PubMed1984

Dopamine agonists increase pallidal unit activity: attenuation by agonist pretreatment and anesthesia.

Intravenous administration of a single bolus dose of 1 mumol/kg of the dopamine agonists, pergolide and lisuride, caused marked increases in the unit activity of globus pallidus neurons in awake, paralyzed, locally anesthesized and artificially respired rats. These agonist effects were similar to those observed after administration of 1 mumol/kg apomorphine to awake, paralyzed rats; in rats anesthetized with chloral hydrate, however, responses to apomorphine were markedly attenuated. Subsequent administration of haloperidol reversed the effects of pergolide and pretreatment with haloperidol blocked the effects of lisuride. LSD (1 mumol/kg i.v.) did not effectively stimulate pallidal neuronal activity, suggesting that the ability to stimulate pallidal firing rates correlates better with dopamine, as opposed to serotonin, agonist potency. The ability of a non-excitatory dose of apomorphine to attenuate responses of pallidal neurons to a normally excitatory 1 mumol/kg dose of this agonist administered subsequently, was reconfirmed. Pretreatment with this 'priming' dose of apomorphine also attenuated the rate increases produced by d-amphetamine (8.7 mumol/kg) and enhanced the rate inhibitory effects of haloperidol. The 'priming' effect appears related to the dopamimetic effects of apomorphine; a non-excitatory dose of a second dopamine agonist, lisuride (0.07 mumol/kg i.v.), similarly blocked the effect of excitatory doses of lisuride (1 mumol/kg i.v.) on pallidal activity.

Action Potentials↗
PubMed1984

Depressor and bradycardic effect following intrathecal injection of [NMePhe3,D-Pro4]morphiceptin in rats.

The intrathecal injection of 1.25, 2.5 and 5 micrograms of [ NMePhe3 ,D-Pro4] morphiceptin (MC), a highly selective mu receptor agonist, in pentobarbital-anesthetized rats resulted in a dose-dependent decrease of mean arterial pressure, reaching a maximal effect 1 h after its administration. A marked bradycardic effect paralleled the depressor effect. These effects were totally reversed by prior intrathecal injection of 10 micrograms of naloxone. The effect of MC was fully present in bilaterally vagotomized rats and in rats under artificial respiration. These results provide evidence for the opioid control of blood pressure and heart rate via mu receptors in the spinal cord.

Animals↗
PubMed1987

Verapamil in a new model of severe local myocardial ischaemia due to combined coronary occlusion and stenosis.

The effect of verapamil was studied in a new canine model of local myocardial ischaemia. In this model in addition to the critical construction of the left circumflex coronary artery, the left anterior descending branch was suddenly occluded. Experiments were performed in the anaesthetized, thoracotomized and artificially respired dog. The model represents a severe form of myocardial ischaemia and mimics the clinical situation in which usually more than one coronary artery is involved in the stenotic process. Verapamil (0.15 mg kg -1 i.v.) moderated the extent of the ischaemic changes (indicated by the ST segment elevation in the epicardial and endocardial ECG) as well as their consequences e.g. the incidence and severity of early postocclusion and reperfusion arrhythmias. This beneficial effect was probably due to the drug-induced favourable haemodynamic action (reduction of left ventricular end-diastolic pressure and slight increase in left ventricular dP/dtmax) and to the electrophysiological effects (e.g. decreased inhomogeneity of electrical activation, diminution of extrasystolic activity) and blood flow changes (enhanced blood supply to the ischaemic subepicardium).

Animals↗
PubMed1990

A novel in vivo test for drugs affecting central serotonergic and adrenergic systems.

In urethane-anaesthetized rats, myoclonic twitches of the anterior digastricus muscle were evoked by L-5-hydroxy-tryptophan (L-5-HTP, 50-100 mg/kg iv.), the serotonin (5-HT) receptor agonist, quipazine (1-8 mg/kg i.v.) and the 5-HT releaser, fenfluramine (4-8 mg/kg i.v.). The effect of L-5-HTP or quipazine on the frequency of twitches was inhibited by the 5-HT receptor antagonist cyproheptadine. Also L-DOPA (100 mg/kg i.p.) or the alpha 1-adrenoceptor agonist, cirazoline (0.3-3 mg/kg i.v.) evoked twitches of the muscle which were inhibited by the alpha 1-adrenoceptor antagonist, prazosin. In decerebrate, artificially respired rats, neither L-5-HTP nor L-DOPA evoked the twitches. The frequency of twitches evoked by fenfluramine but not by L-DOPA was increased by the alpha 2-adrenoceptor agonist, clonidine (0.2 and 0.4 mg/kg i.v.); clonidine's effect was abolished by the alpha 2-adrenoceptor antagonist, yohimbine. The beta 2-adrenoceptor agonist, salbutamol (0.01-1 mg/kg i.v.) had no effect on fenfluramine-induced twitches. It is concluded that (1) activation of 5-HT receptors or alpha 1-adrenoceptors in the brain of urethane-anaesthetized rats evokes twitches of the anterior digastricus muscle, and (2) this preparation can be utilized as a test to study the action of compounds on central 5-HT and adrenergic systems.

5-Hydroxytryptophan↗
PubMed1992

The effect of Ca2+ channel modulators on vagally induced bronchoconstriction in the guinea-pig.

The effects of N- and L-type voltage operated calcium channel (VOCC) antagonists were examined on the bronchoconstriction induced by vagal stimulation in artificially respired guinea-pigs. Vagal stimulation produced a reproducible and consistent bronchoconstrictor response which corresponded to an increase in pulmonary inflation pressure equivalent to (10.4 +/- 1.0%) of the maximum. This vagally induced rise in pulmonary inflation pressure was reduced (54% P less than 0.001) by pretreatment with atropine (1 mg/kg i.v.) and almost completely blocked by pretreatment with capsaicin (54.5 mg/kg s.c.) and atropine. omega-Conotoxin GVIA (CgTx) (5-20 micrograms/kg i.v.) caused a dose and time-related inhibition of the vagal response but did not affect either methacholine or substance P (SP)-induced bronchoconstriction. Combination studies with CgTx, atropine and capsaicin pretreatment revealed that CgTx effectively blocked both the atropine-sensitive cholinergic component and the capsaicin-sensitive non-adrenergic non-cholinergic (NANC) component of the vagal response. Selective L-type VOCC antagonists nicardipine, diltiazem and verapamil, at doses which had significant cardiovascular effects, did not reduce the rise in pulmonary inflation pressure to vagal stimulation. This study indicates that N-type VOCCs are important in controlling the release of neurotransmitters from both the cholinergic and NANC neurones within the airways of guinea-pigs.

Animals↗
PubMed1983

A new series of steroidal antidysrhythmic agents.

With the aim of finding an antidysrhythmic agent suitable for intravenous or oral administration we have examined a range of steroids carrying basic substituents. The primary screen involved control of cardiac dysrhythmias induced by intravenous infusion of aconitine into pentobarbitone-anaesthetised artificially-respired rats. The best activity was found among a series of 11 alpha-alkylamino steroids and structure-activity studies included modification of the alkylamino group and variation of substituents in ring A and at the 17-position. Good oral and intravenous activity was found among 17 beta-methoxycarbonyl-5 alpha-androstanes and methyl 2 beta-ethoxy-3 alpha-hydroxy-11 alpha-(3-methylbutylamino)-5 alpha-androstane-17 beta-carboxylate hydrochloride (CCI 22277) was selected for more detailed pharmacological study.

Aconitine↗
PubMed1983

Cholinergic mechanisms within the caudate nucleus mediate changes in blood pressure.

Microinjections of 10 micrograms of carbachol into the caudate nucleus induced changes in the blood pressure of cats anesthetized locally, paralyzed and artificially respired. These responses were dependent on the site of injection. Carbachol, microinjected at rostral levels of the caudate nucleus, elicited pressor responses while a decrease in blood pressure was observed following injections at caudal levels. Both of these effects were blocked by prior microinjection of atropine. Microinjections of carbachol outside the caudate did not affect the resting blood pressure. However, injections of carbachol into the lateral ventricle always produced pressor responses independent of the site of injection along the antero-posterior extension of the ventricle. On the other hand, microinjections of dopamine (20 micrograms) into the caudate nucleus failed to modify blood pressure. From this study, it is concluded that within the caudate nucleus there are two different muscarinic mechanisms, which when activated, mediate changes in blood pressure, possibly through the sympathetic nervous system.

Acetylcholine↗
PubMed1977

Chemoreceptor influence on pulmonary blood flow during unilateral hypoxia in dogs.

Dogs anesthetized with 30 mg/kg pentobarbital were artificially respired after differential cannulation of the main stem bronchi. Following median sternotomy, blood flow was monitored by electromagnetic flow probes on the left pulmonary artery (QL) and on the pulmonary trunk or aorta, QT. Following 10 min of bilateral 100% O2, QL was 42.5 +/- 7% of QT. When 6% O2, was substituted as the gas mixture inspired by the left lung while the right lung remained on 100% O2, PaO2 was above 70 mm Hg and QL fell to 24.5 +/- 5% of QT. Room air was then used to ventilate the right lung while the left lung remained on 6% O2. This caused PaO2 to fall to 42.3 +/- 3 MM Hg and QL to rise to 38.3 +/- 6% QT. This increase in blood flow to the unilaterally hypoxic lung during systemic hypoxemia did not occur in dogs after peripheral chemoreceptor denervation. Therefore, interference with the local response to alveolar hypoxia during systemic hypoxemia appears to be mediated by the arterial chemoreceptors.

Animals↗
PubMed1984

Cardiotoxic effects of the venom of the burrowing asp, Atractaspis engaddensis (Atractaspididae, Ophidia).

The venom from the snake Atractaspis engaddensis has a very high lethal potency, with an i.v. LD50 of 0.06-0.075 micrograms per g body weight in mice. The action of the venom is rapid and death results from seemingly neurotoxic effects. However, even at high concentrations, the venom does not block contractions of skeletal muscles that are directly or indirectly stimulated. The most prominent action of the venom is seen in the function of the heart in anesthetized mice, with or without artificial respiration. The changes observed in the ECG are similar to those recorded in human victims and are the result of an A-V block that is caused by an apparent direct action of the venom on the heart.

Animals↗