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PubMed1995

A study on the cause of death due to waglerin-I, a toxin from Trimeresurus wagleri.

Waglerin-I, a lethal toxin isolated from the venom of Trimeresurus wagleri, consists of 22 amino acid residues with a proline-rich sequence. In the present study, we investigated the cause of death and the possible site of action of this toxin. In anesthetized mice, i.v. administration of waglerin-I at 0.5 microgram/g produced respiratory failure within 5 min. The blood pressure could be maintained by the application of artificial respiration immediately after respiratory arrest. Waglerin-I at 4 microM reversibly blocked the indirect twitch of the mouse phrenic nerve-hemidiaphragm preparation, but had no effect on the direct twitch. It is concluded that respiratory failure, resulting from neuromuscular block, is the primary cause of death due to waglerin-I in mice. In contrast to the results obtained in mice, in anesthetized rats no toxic effects on respiration and blood pressure were observed except for a transient hypotension up to 10 micrograms/g (i.v.). In accordance with the in vivo experiments, waglerin-I at concentrations up to 40 microM did not block the indirect twitch of the rat diaphragm. It thus appears that rats are resistant to the toxic effects of waglerin-I.

Animals↗
PubMed1996

Sir Joseph Fayrer MD FRS (1824-1907) Indian Medical Service: snakebite and mortality in British India.

Whilst Professor of Surgery at the Calcutta Medical College, Dr Fayrer studied all aspects of snake poisoning. His work, The Thanatophidia of India being a Description of the Venomous Snakes of the Indian Peninsula, with an Account of the Influence of their Poison of Life; and a Series of Experiments was published in 1872. Collating information from official Government records of death due to snakebite, Fayrer recorded a mortality of 11,416 persons for the year 1869 in the Presidency of Bengal and estimated a mortality of more than 20,000 for all British India. In 1872, working in London with Lauder Brunton, Fayrer studied the physiological action on Naja naja venom in more detail. Respiratory paralysis was due to a curare-like blockade of the neuromuscular junction, and they believed, a central effect also; artificial respiration was ineffective in producing recovery. A large dose of cobra venom was observed to induce tetanic contraction of the heart both in vivo and in vitro. As President of the Medical Board of the India Office in London from 1873 to 1895, Sir Joseph Fayrer was much concerned with cholera epidemics which resulted in an average mortality of over 200,000 persons annually. In 1885, he represented the Indian Government at the fourth International Conference on Cholera, a fore-runner of the World Health Organization.

Animals↗
PubMed1976

Structure-activity relationships in a series of 11-deoxy prostaglandins.

A series of 11-deoxy prostaglandin derivatives and some naturally occurring prostaglandins have been investigated in the anaesthetized artificially respired guinea-pig for their effect on blood pressure, bronchial resistance (overflow pressure at constant volume), tracheal segment pressure, and on intestinal and uterine smooth muscle. The compounds were administered intravenously. Prostaglandins E1, E2 and F2alpha produced responses that were qualitatively similar to those in the literature. Prostaglandin A2 (100 mug) was a bronchoconstrictor, although it decreased tracheal segment pressure and blood pressure. Prostaglandin B2 (100 mug) caused double elevations in blood pressure, tracheal segment pressure and bronchial resistance. The intensity of bronchoconstriction produced by PGB2 was of the same order as with PGF2alpha. A number of structure-activity relationships were found. 11-Deoxygenation lowered the biological activity of the natural prostaglandins PGE1 and PGF1alpha. The vasodepressor and bronchodilator responses of 11-deoxy PGE1 were converted to vasopressor and bronchoconstrictor by epimerisation at C-15. Introduction of a methyl group at C-15 of 11-deoxy PGF1alpha both increased and prolonged vasopressor and bronchoconstrictor activity. At C-9 both the keto and beta-hydroxy group imparted vasodepressor and bronchodilator activity, while the alpha-hydroxy led to vasopressor and bronchoconstrictor activity. Extension of the omega sidechain by two methylene groups radically reduced the activity of 11-deoxy PGF1alpha and its derivatives. These experiments indicate that steric differences in the prostaglandin structures studied can result in diametrically opposed profiles of biological activity. Further, small variations in the prostaglandin molecule can lead to differences in potency and/or profile of activity in the guinea-pig.

Airway Resistance↗
PubMed1979

Some biological activities of a series of 9a-homo-9,11-epoxy prostanoic acid analogues.

A number of stereochemical variants at C-8, C-12 and C-15 of 9a-homo-9,11-epoxy prostaglandins (PGs) have been examined for in vivo activity on blood pressure, bronchial resistance, tracheal segment pressure, heart rate and on intestinal and uterine contractility in artificially respired anaesthetised guinea-pigs; and on blood pressure and blood platelet aggregation in rats (using the extra-corporeal filter-aorta loop technique). In vitro tests for smooth muscle activity were carried out on the isolated rat fundus strip, the guinea-pig tracheal chain and the rat uterus. The following was found: 1. In the guinea-pig, in vivo, all the homo-epoxy PGs were vasopressor and bronchoconstrictor following bolus injections of 250 micrograms i.v. The effects on heart rate, and intestinal and uterine contractility were equivocal. The configurations at the chiral centres, C-8, C-12 and C-15 play an important role in determining potency. The 15-(S)-hydroxy derivatives were the most potent in stimulating vascular and respiratory muscle. The 8-iso configuration appeared to enhance potency amongst the 15-(S)-hydroxy compounds. The 15-(R)-hydroxy configuration markedly reduced constrictor potency. The same pattern of activity was seen on rat blood pressure, in vivo. The 15-(S)-hydroxy configuration combined with the 8-iso configuration had the most potent constrictor activity, while the 15-(R)-hydroxy group negated this and even led, in the case of the natural configuration at C-8 and C-12, to vasodepression. 2. In vitro, the activity on the rat fundus and guinea-pig tracheal chain followed the same pattern. The 15-(S)-hydroxy derivatives were very much more potent than the 15-(R)-hydroxy derivatives at contracting the smooth muscle preparations. Uterine muscle appeared to be relaxed by the PGs with the natural configuration at C-8 and C-12, with the 15-(R)-hydroxy compound exhibiting greater activity. 3. Inhibition of ADP-induced rat blood platelet aggregation after "intra-arterial" administration was shown only by the derivatives with a single change in the natural configuration either at C-8 or at C-15. Additional changes either resulted in inactivity or, in the case of the 8,12-di-iso-15-(S)-hydroxy compound, even reversed the effect to aggregation. The inhibition of aggregation was long lasting with both the 8-iso-15-(S)-hydroxy derivative and the 8,12-nat-15-(R)-hydroxy derivative. In the case of the latter compound, GBR-30731, activity increased during the 30 min after administration. GBR-30731 deserves further investigation as a platelet aggregation inhibitor because of its relatively low smooth muscle stimulant (sometimes even relaxant effects) and its long lasting platelet aggregation inhibiting activity.

Animals↗
PubMed1977

Failure to elicit conditioned taste aversion by severe poisoning.

In an attempt to assess the universal validity of the conditioned taste aversion (CTA) paradigm, various types of poisoning (UC) were associated with the gustatory CS. Water deprived rats were habituated for two days to the drinking box, where water was available for 15 min. On Day 3, access to the CS (0.1% saccharin 15 min) was followed after 30 min by a sublethal dose of the poison (0.15 M LiCl, 4% body weight; 0.1 M sodium malonate, 1% body weight; pyrrolopyrimidine drug BW 58-271, 15 mg/kg; sodium cyanide 4 mg/kg; sodium iodoacetate 40 mg/kg; sodium fluoride 30 mg/kg; gallamine triethiodide 40 mg/kg). Rats injected with the last drug were maintained under artificial respiration until muscular paralysis disappeared. After 4 days of recovery, water deprivation schedule was resumed on Days 8 and 9. During the retention test on Day 10 saccharin consumption dropped by 60% in the LiCl poisoned rats, but not CTA developed in animals poisoned by pyrrolopyrimidine, gallamine, malonate and cyanide. CTA of intermediate intensity was evoked by iodoacetate and fluoride. The absence of CTA was not due to the amnesic effect of poisoning, since LiCl administration to NaCN poisoned rats produced CTA of usual intensity. It is concluded that CTA is not related to the overall severity of poisoning but rather to the effect of the poison on specific interoceptors.

Animals↗
PubMed1982

Differential effects of LSD serotonin and l-tryptophan on visually evoked responses.

Alterations in photically-evoked cortical responses were assessed in immobilized artificially respired cats following intraraphe microinjections of LSD and serotonin (5-HT) and IV administration of LSD and l-tryptophan. Both systemic (10-100 micrograms/kg; N = 5) and intraraphe (0.25 microgram; N = 10) LSD significantly increased the amplitudes of the three primary components of the visual evoked response (VER). In contrast, the same VER components were significantly depressed following intraraphe 5-HT (30 micrograms; N = 4) and IV l-tryptophan (100 mg/kg; N = 6), a serotonin precursor that elevates raphe 5-HT levels. Intraraphe cinanserin (180 micrograms; 30 minute pretreatment) completely reversed LSD-induced enhancements in all three components (p less than 0.01). Depressions of VER following intraraphe 5-HT (30 micrograms) were also antagonized by cinanserin, although to lesser degree (p less than 0.05 for first 2 components only) than with LSD. The depressive effects of l-tryptophan (100 mg/kg) were unaffected by cinanserin. Modification of raphe neuronal activity can significantly alter photically evoked responses, and may explain the perceptual disturbances associated with LSD, i.e., depression of an area (raphe) normally inhibiting forebrain areas of the visual system.

Animals↗
PubMed1985

A method for studies of tracheobronchial microvascular permeability to macromolecules.

Probably because of methodological problems, little is known about permeability to macromolecules and edema formation in the tracheobronchial microcirculation. A novel atraumatic technique of exposing the guinea pig airway mucosa to mediators has been developed. The intralumenal surface of the trachea and main bronchus is superfused (0.02 ml/min) via a thin plastic tubing introduced into the trachea through the mouth in anesthetized, tilted, and spontaneously breathing guinea pigs. Erythrocytes were labelled in vivo with Technetium 99m and individual hematocrit values and plasma concentrations of Fitc-dextran were determined. By quantification of content of a macromolecular tracer (Fitc-dextran MW 70,000) and blood pool in excised airway tissue the amount of extravasated macromolecules was calculated. In control animals where airways were superfused with saline (0.02 ml/min) during 30 min the extravasated amount of tracer was 0 +/- 14 micrograms/g trachea (n = 15), which was similar to what was found in animals without any superfusion (n = 6). Capsaicin 10(-6) M (total dose 0.1 nmol), probably by activating nerves, produced an extravasation of Fitc-dextran of 223 +/- 32 micrograms/g, n = 8, (p less than 0.005). In guinea pigs intubated for artificial respiration and prepared for vagal stimulation the base-line microvascular values were deranged, and large amounts of macromolecules leaked from the vascular compartment. Still, vagal stimulation in these animals produced further extravasation of macromolecules. It is suggested that atraumatic techniques such as the present superfusion method should be employed in studies of physiological and pharmacological control of permeability to macromolecules in the tracheobronchial microvasculature.

Animals↗
PubMed1992

Somatosensory afferents in the parasympathetic vasodilator reflex in cat lip.

Somato-parasympathetic reflexive vasodilatation elicited by activation of the nociceptors in the oro-facial areas of the cat was investigated. Changes in lower lip blood flow monitored by a laser Doppler flowmeter took place in pentobarbital-anesthetized and artificially respirated cats. Pinch and heat stimulation of the oro-facial areas evoked a blood flow increase similar to that of electrically induced vasodilatation. Sustained increased responses in blood flow were obtained when a 1% capsaicin solution was applied to the tongue. These results show that the C-polymodal nociceptor is a strong candidate for a receptor that provokes somato-parasympathetic vasodilatation. Capsaicin-insensitive nerve fibers, however, also participate because electrical stimulation of the capsaicin-treated tongue evoked vasodilatation. The correlation between noxious stimulation-induced vasodilatation and systemic blood pressure change also is discussed.

Animals↗
PubMedDate not supplied

TRH: cardiovascular and sympathetic modulation in brain nuclei of the rat.

The cardiovascular and sympathetic effects of TRH in discrete cardiovascular-related brain nuclei were studied. Microinjections of TRH were made into the nucleus preopticus medialis (POM) of conscious rats and the nucleus tractus solitarius (NTS) of pentobarbitone-anesthetized, artificially respired rats. POM injections (1 microliter, 0.8-80 nM) elicited dose dependent pressor and tachycardic responses which were accompanied by increased levels of norepinephrine (NE) and epinephrine (EPI) in the plasma. These pressor/tachycardic effects of TRH were also elicited in adrenal demedullated (ADM-x) rats, but completely abolished in ADM-x rats pretreated with bretylium (30 mg/kg, IA). NTS injections (0.1 microliter, 30 and 150 nM) had a short depressor effect on blood pressure (BP) and a delayed increase in heart rate (HR). From these findings we suggest that the POM, a central nucleus in the AV3V region, may be an important forebrain site for autonomic regulation by TRH, mediated through the sympathetic nervous system.

Adrenal Medulla↗
PubMed1983

Immobilization-induced changes in the response of striatal neurons to dexamphetamine.

Bipolar multiple unit recording electrodes were implanted in the striata of male Long-Evans rats 5-7 days prior to experimentation. In subsequent experiments, striatal neuronal activity in response to dexamphetamine (1.0 or 2.5 mg/kg i.p.) was recorded in either freely moving or immobilized, artificially-respired rats. Whereas dexamphetamine produced only excitation of striatal neurons in freely moving animals, a multiplicity of responses, ranging from excitation to inhibition, and including biphasic as well as no change responses were observed in immobilized animals. It is concluded that the absence of dexamphetamine-induced behavior in immobilized animals modifies the striatal neuronal response to dexamphetamine, possibly through alteration of the activity of excitatory striatal afferents.

Animals↗
PubMed1981

Reversal of multiunit activity within and outside the suprachiasmatic nucleus in the rat.

Multiunit activity (MUA) in the suprachiasmatic nucleus (SCN) and adjacent hypothalamic areas were compared in albino rats anesthetized with thiopental, immobilized with succinylcholine chloride and artificially respired. During adaptation to light lasting up to 2 h, MUA in the SCN increased gradually, whereas MUA in the other locations outside the SCN decreased. During adaptation to the dark, MUA in the SCN decreased whereas MUA outside the SCN increased. This reversal was apparent not only when recording in the SCN and adjacent hypothalamus simultaneously, but also while advancing an electrode from the optic chiasm through the SCN to the anterior hypothalamus.

Animals↗
PubMed1987

Light microscopic observations on the morphology of sympathetic preganglionic neurons in the pigeon, Columba livia.

Experiments were performed in anesthetized, immobilized, artificially respirated pigeons (Columba livia). Extracellular recordings from 56 antidromically activated and collided sympathetic preganglionic neurons were obtained. Eleven cells were intracellularly labeled with horseradish peroxidase and reconstructed at the light microscopic level. Electrophysiologically there were no statistical differences between labeled and unlabeled neurons. Four different somatic shapes were observed: fusiform, pyriform, multipolar and stellate. Nine of 11 cells were located within the principal preganglionic cell column (column of Terni), the other two were within nucleus intercalatus spinalis. Principal column neurons exhibited planar, horizontally aligned dendritic arbors with major extensions directed rostrocaudally. Unexpectedly, the majority of these cells also had dendritic branch projections which spanned the entire width of the ipsilateral zona intermedia. Contralateral dendritic terminal arborizations were evident in seven neurons. Intercalatus neurons were multipolar-shaped and exhibited a notably different dendritic arrangement from principal column preganglionic cells. The dendrites of intercalated cells coursed obliquely within the transverse spinal cord axis, giving rise to major dendritic extensions into the base of the dorsal horn, the dorsolateral funiculus, and the dorsal aspects of the ventral horn. Irrespective of somatic subnuclear location, the morphology of preganglionic dendrites was similar: (1) Largely primary, secondary, and tertiary processes were smooth. (2) Fine caliber proximal and distal elements appeared beaded or "varicose." (3) Distal processes gave rise to thin-stalked, spine-like appendages. The axons of preganglionic neurons arose from cell bodies as well as primary and secondary dendrites. The axons of two cells branched intraspinally. The present findings provide detailed descriptions of the somatic structures and accompanying dendritic trees of preganglionic neurons within nucleus intercalatus. The observations also include anatomical evidence showing the intraspinal collateralization of sympathetic preganglionic axons. In general, avian sympathetic preganglionic neurons located within the principal cell column appear to be structurally homologous to their mammalian counterparts within the intermediolateral cell column of thoracic spinal cord.

Animals↗
PubMedDate not supplied

Differential morphine effects on evoked impulse activity in the caudate and central grey.

This study had two primary objectives: (1) to develop a new physiological method for investigating opiate action, based on the effect of morphine on evoked impulse activity in small neuronal populations, and (2) to test the hypothesis that morphine's effects would vary with response site (caudate and central grey), and with stimulation site (sciatic nerve, substantia nigra). Bipolar recordings were made from curarized, artificially respired rats. Morphine increased stimulus thresholds for sciatic evoked responses in both brain areas, with especially marked effects in the central grey. Sciatic stimulation produced phasic (transient) responses in both brain areas to mild stimulation and tonic (sustained) responses to more intense stimulation; the tonic responses were depressed more effectively than phasic responses. Substantia nigra stimulation produced only tonic responses in both areas, and morphine did not alter these stimulation thresholds. Morphine effects were blocked and reversed by naloxone. Thus, clear differential depressive effects of morphine were demonstrated in terms of function (phasic vs. tonic responses), in terms of stimulus site, and in terms of responding site.

Animals↗
PubMed1983

Middle and long latency auditory evoked potentials in cat. I. Component definition and dependence on behavioral factors.

Middle (10-50 ms) and long (50-600 ms) latency auditory evoked potentials (AEPs) were investigated in artificially respired, muscle-paralyzed cats. Similarity to human potentials of comparable latencies was examined in two ways: (1) the similarity of waveform features such as peak amplitude, polarity and latency, and (2) the effects of task-related variables on these various waveform features. Four behavioral variations of a classical pupillary conditioning paradigm were used to vary attention and arousal. Twelve peaks and troughs were identified in the AEP: P10, N13, P17, N22, P31, N41, P55, N70, N100, N140, P260 and N520. Principal components analysis (PCA) defined 7 AEP components, some of which spanned several peaks. Analysis both of peak latencies and amplitudes, and of principal component scores, revealed differential effects of the behavioral manipulations on these components: those with latencies longer than 50 ms were strongly influenced by behavioral variations, while earlier components were relatively immune to these effects. On the basis of these findings, several relationships between cat and human AEP components were suggested. Specifically, peaks P10-P41 in the cat were thought related to human middle latency components, cat P55 to human P50, cat N140 to human N300, and cat P260 to human P300. Cat N520 was comparable to several long latency components in humans. No obvious correspondences between cat AEP components and human N90 and P170 were identified.

Acoustic Stimulation↗
PubMed1983

Middle and long latency auditory evoked potentials in cat. II. Component distributions and dependence on stimulus factors.

The middle (10-50 ms) and long (50-600 ms) latency periods of the auditory evoked potential (AEP) were investigated in muscle-paralyzed, artificially respired cats with respect to two issues: (1) the distribution of components across the skull, and (2) the effects of changing stimulus intensity on component latencies and amplitudes. The distributional data were gathered during a behavioral study in which four behavioral tasks related to classical pupillary conditioning were used to vary attentional and arousal processes. The distributions across the skull surface (averaged across tasks) of 12 peaks and troughs (P10, N13, P17, N22, P31, N41, P55, N70, N100, N140, P260 and N520) and seven principal components derived from the set of waveforms collected during this experiment are reported. Both peak amplitudes and principal component scores were distributed differentially across the skull surface. In the second experiment, acoustic stimulus intensity was varied, and AEPs collected from a vertex and temporal electrode site. In general, increasing stimulus intensity had a stronger influence on the earlier portions of the AEP, where increased amplitude and decreased latency was the rule, than on later ones. The relationships between cat and human AEP components were discussed based on both the data presented in this paper and in previous papers.

Acoustic Stimulation↗
PubMed1992

Effect of reversible hypoxia on the compared time courses of endocochlear potential and 2f1-f2 distortion products.

In order to study the effects of a controlled hypoxia on the cochlear active mechanisms, the 2f1-f2 distortion product (DP) and the endocochlear potential (EP) were recorded simultaneously in the same ear, in guinea pigs artificially respired with gas mixtures containing different percentages of oxygen. The data show an important difference in the behavior of the two parameters. While the EP undergoes a reduction of amplitude starting shortly after the establishment of the hypoxia, reaches a steady state, and recovers monotonically after a return to normoxic conditions, the time course of the DP is more complex. Its level also declines shortly after the beginning of the hypoxia though it slightly lags behind the EP decline. After switching back to normoxic conditions, the DP rises with an eventual delay with respect to the EP, overshoots, and then dramatically falls again. A slow recovery subsequently takes place and normal values are reached within 5 to 10 min. These results indicate a certain independence of the DP versus the EP. During the exposure to hypoxic conditions, differences in the time course and in the variation of amplitude of the two recorded parameters seem to indicate that the DPs could be more related to the OHC physiology than to the EP. The DP post-hypoxia effect observed after a return to normoxic conditions, indicates that a normal EP is not sufficient for the generation of normal DPs. Different hypotheses which could explain the DP post-hypoxia effect are discussed.

Acoustic Stimulation↗
PubMed2004

Relationship between the tooth eruption and regional blood flow in angiotensin II-induced hypertensive rats.

OBJECTIVE: The mechanism of action of vasoactive drugs on tooth movement is unknown. The purpose of the present study was to measure simultaneously the axial movement of the mandibular incisor, regional blood flow at the base of the incisor, and systemic arterial blood pressure in angiotensin II-induced hypertensive rats to determine the possible cause of tooth displacement. DESIGN: The measurements were made under artificial respiration with halothane anaesthesia. In the experimental animals, 2.5 microg of angiotensin II in 1 ml of Ringer's solution was infused at 0.83 ml/h for 12 h from the femoral vein. In the control animals, only Ringer's solution was infused. RESULTS: Angiotensin II caused an increase of the mean arterial blood pressure from 86 to 119 mm Hg, and decreases of the eruption rate from 667 to 494 microm/24 h and the regional blood flow from 262 to 214 mV. There was a positive correlation between the eruption rate and regional blood flow, and a negative correlation between the blood pressure and regional blood flow. CONCLUSION: These results suggest that angiotensin II caused constriction of the peripheral vascular smooth muscle resulting in an increase of arterial blood pressure and a decrease of regional blood flow, followed by a decrease of fluid volume and then a reduction of either the pressure within the socket or of the eruptive force. We assume that the regional vascular pressure within the socket plays an important role in determining the position of the rat incisor.

Angiotensin II↗