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PubMed1998

Positron emission tomography reveals changes in global and regional cerebral blood flow during noxious stimulation of normal and inflamed elbow joints in anesthetized cats.

In cats the global (gCBF) as well as the regional cerebral blood flow (rCBF) and blood pressure were measured before, during, and after noxious inward and outward rotations of normal and inflamed elbow joints. The animals were anesthetized with halothane and immobilized by gallamine triethiodide. The gCBF as well as the rCBF were measured using positron emission tomography (PET) with a camera specifically designed for use in small animals. Slow intravenous bolus injections of 15O-labeled water were followed by 3-min acquisition of regional radioactivity starting at the time of injection. In all experiments the gCBF as well as the blood pressure were increased by noxious inward-outward rotations of the normal and of the inflamed joint, whereas the blood pressure and the rCBF remained unchanged during bolus injections under control conditions (without any joint movement). Movements of the inflamed joint evoked significantly greater increases in blood pressure and gCBF than corresponding ones of the normal joint. These increases in gCBF were paralleled by increases in rCBF along the complete anterior to posterior axis of the brain. Again, the increases in rCBF were larger, more extensive and more uniform following the stimulation of the inflamed joint relative to the results obtained with stimulation of the normal joint. No significant laterality was seen, but when an atlas-based region of interest (ROI) analysis was carried out and when the individual variations in rCBF were removed with two-way ANOVA, significant differences were disclosed in rCBF between the stimulated condition and the resting condition in a large number of brain regions. In particular, noxious rotation of the normal (right) elbow joint induced a significant increase in rCBF over the cerebral cortex and in the right thalamus and hippocampus. The same stimulation of the (left) inflamed joint induced a significant increase in rCBF throughout the brain; the biggest increase being over the right posterior cortex. It is concluded that under the conditions of the present experiments the generally accepted autoregulation of the cerebral blood flow is not fully functioning, and various factors that may be responsible for this failure (which obscures rCBF differences) are discussed. The more pronounced increases in rCBF when moving inflamed joints instead of normal ones is thought to be a direct consequence of the peripheral sensitization of the articular nociceptors and the consequent central hyperexcitability induced in the articular nociceptive pathways.

Anesthesia↗
PubMed1976

Single unit study of binaural interaction in the auditory cortex of the chinchilla.

The primary aim of this investigation was to systematically compare for various stimulus conditions the relative influences of contralateral and ipsilateral acoustic stimulation on cortical single units in an unanesthetized preparation and to study the effects upon single unit responses of the dominant stimulus cues for sound localization--interaural intensity difference (deltaI) and interaural time difference (deltat). Recordings were obtained from 133 units in chinchillas immobilized by gallamine triethiodide. All units were found to be influenced by input from both ears. Unit thresholds for contralateral stimulation were lower and more discharges were elicited than for ipsilateral stimulation over a range of intensities from unit threshold intensity to 80 dB sound-pressure level. A predominance of contralateral influence was also observed when the number of stimulus-evoked discharges was plotted as a function of the deltaI or deltat. For 62% of the deltaI functions maximal responsiveness occurred for binaural stimuli that were more intense at the contralateral ear. Similarly, of the 36 units that showed sensitivity to deltat parameters for tone stimuli, 22 (61%) were maximally responsive at the contralateral-leading deltat intervals. For click stimuli, maximal responsiveness for all 21 deltat-sensitive units also occured for contralateral-leading stimuli. Certain observations in the study question the generality of the hypothesis that a particular cell invariantly encodes a specific deltat, i.e., that cells have 'characteristic delays'. First, most units tested at more than two frequencies showed maximal responsiveness at different deltat intervals depending upon stimulus frequency. Second, the deltat intervals for maximal responsiveness for half of the units tested were greater than the maximal interaural delays the animal could encounter naturally. Third, deltat functions from the same unit for click and tone stimuli showed poor correspondence. These findings suggest that the encoding of interaural time and intensity might depend on an inter-hemispheric comparison of the activity of neural populations as originally proposed by von Bekesy.

Acoustic Stimulation↗
PubMed1991

Single neurone studies of opioid tolerance and dependence at the ventrobasal thalamic level in an experimental model of clinical pain, the arthritic rat.

The aim of this electrophysiological study was to investigate the effects of an acute injection of morphine (1 mg/kg i.v.) or the opioid antagonist naloxone (0.6-2 mg/kg i.v.) on thalamic ventrobasal (VB) neuronal activities recorded in arthritic rats rendered tolerant/dependent by pretreatment with relatively low doses of morphine. Recordings were performed in animals immobilized by i.v. injections of gallamine triethiodide (Flaxedil) and artificially ventilated under a moderate gaseous anesthesia (mixture of one-third O2, two-thirds N2O, 0.5-0.6% halothane). This level of anesthesia, as checked by the electrocorticogram, was stable and appeared sufficiently deep, since no sign of suffering or stress could be detected. The efficacy of morphine on VB neuronal responses induced by mild stimulation of the joints was greatly reduced in morphine-pretreated arthritic rats, compared to naive animals (mean neuronal inhibition of 35 vs 85%, respectively). This indicates that the tolerance phenomena observed in behavioral studies are reflected at the VB level, on neurons involved in pain processes. In addition, naloxone (0.6, 1 and 2 mg/kg i.v.) induced a dramatic increase in the evoked (52, 88 and 93%) and spontaneous (64, 211 and 292%) VB neuronal activities recorded in morphine-pretreated arthritic rats, while these activities were not significantly altered in naive arthritic rats. The time-courses of the modifications induced by naloxone in morphine-pretreated arthritic animals were similar to those of the naloxone-precipitated morphine withdrawal observed in freely moving rats. These findings may represent the neuronal correlate at the VB level of the withdrawal response and/or the hyperalgesia induced in tolerant arthritic rats by high doses of naloxone.

Animals↗
PubMed1980

Evidence for a primary cortical origin of a middle latency auditory evoked potential in cats.

The origin of the scalp-recorded auditory evoked potential, Pa, was examined in cats anesthetized with chloralose-urethane and immobilized with gallamine triethiodide. This potential is a prominent positive wave which peaks approximately 12--15 msec following click stimuli. Mapping revealed that Pa is distributed on the scalp in the region overlying cortical area AI, contralateral to the stimulated ear. The cortical potential recorded from AI was a surface-positive wave, restricted to the anterior portion of AI. Laminar analysis of the cortical evoked potentials demonstrated the existence of a dipole generator at that area. The onset of this potential coincided with the onset of the scalp-recorded Pa. Comparison of the scalp and the cortex-recorded potentials showed that both the amplitude-intensity function and the amplitude-rate function for the scalp-recorded potential closely paralleled those recorded from AI. Acute and chronic lesion studies showed that extirpation of AI (particularly the anterior part) almost completely abolished the Pa response. This evidence indicates that the scalp-recorded Pa of cats is generated almost entirely from the anterior part of the contralateral AI.

Animals↗
PubMed1977

Pharmacological studies of facial motoneurones in the rat.

Experiments were performed on 39 male albino rats anaesthetized with pentobarbitone sodium and paralyzed with gallamine triethiodide. Facial motoneurones consistently showed a progressive alteration of spike shape and decrease in spike firing frequency during the continuous microelectrophoretic application of the excitant amino acids D,L-homocysteate, L-glutamate, L-aspartate, and kainate, but infrequently during that of N-methyl-D-aspartate. The relative potencies of these excitants on facial motoneurones are reported. The potential usefulness of N-methyl-D-aspartate to produce amino acid-evoked motoneurone action potentials is discussed. The microelectrophoretically-applied depressant amino acid antagonist strychnine selectively and reversibly blocked the depressant effects of glycine on facial motoneurones. The depression of amino acid-induced firing of facial motoneurones by stimuli to the lingual or glossopharyngeal nerves were reversibly antagonized by microelectrophoretically applied strychnine but not by bicuculline.

Action Potentials↗
PubMed1990

Parasympathetic nervous control of intraocular pressure.

Electrical or chemical activation of the oculomotor nucleus (ONC) was performed in pentobarbital anesthetized cats to determine the role of parasympathetic nervous input to the eye in modulating intraocular pressure (IOP). In all animals, the vagosympathetic nerve trunks were sectioned bilaterally at the mid-cervical level. Intracranial stimulation of the ONC produced miosis and a bilateral sustained rise in IOP with little or no cardiovascular response. During stimulation, IOP increased by approximately 35-40%, with an additional small rise seen when the current was turned off. The secondary rise in IOP probably represents the actual pressure level reached which was otherwise masked by intense accommodation due to stimulation. The rise in IOP was not antagonized with gallamine triethiodide. However, both IOP and pupillary responses were blocked by either hexamethonium (1.5 mg kg-1, i.v.) or atropine (0.5 mg kg-1, i.v.). These results provide evidence for a neural parasympathetic mechanism for increasing IOP in cats. In another group, activation of ONC following electrolytic lesion of the preganglionic parasympathetic nerve to one eye, produced a rise in IOP and miosis only on the side with intact oculomotor nerve indicating that the rise in IOP is in part mediated by nerve fibers that travel to the eye along the oculomotor nerve trunk. Microinjection of L-glutamate (2.5 x 10(-7) M) into the ONC produced a bilateral rise in IOP that lasted for more than 15 min. This increase in IOP was greater than 50% of control levels and was accompanied with miosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Cutaneous venodilation in response to systemic hypoxemia in dogs.

Experiments were performed in chloralose anesthetized dogs to test if the saphenous vein (a cutaneous vein) participates in the cardiovascular response to systemic hypoxemia. The saphenous vein was perfused at constant flow with cooled blood (32 degrees C) from the terminal aorta. Sixteen paralyzed (gallamine triethiodide) animals were ventilated with 10% O2 in N2 for 4-min episodes; arterial PO2 was 49 +/- 4 mm Hg after 4 min of ventilation with this gas mixture. Hypoxemia caused a 29% decrease in saphenous vein perfusion pressure (interpreted as a dilation) and an 8% increase in aortic pressure. The hypoxemia induced saphenous venous dilation was abolished by (1) section of the vagus nerves and denervation of the carotid chemoreceptors (afferent pathways), or (2) section of the lumbar sympathetic chain (efferent pathway). These data demonstrate that systemic hypoxemia causes a neurally mediated dilation of the saphenous vein that is dependent upon intact carotid chemoreceptors and/or vagus nerves. It is concluded that saphenous vein dilation is part of the integrated cardiovascular response to hypoxemia in anesthetized dogs. This reflex effect may represent a decompensatory mechanism that compromises cardiac output during hypoxemia in animals with hypothermic extremities.

Animals↗
PubMed1991

Inhibition by talipexole, a thiazolo-azepine derivative, of dopaminergic neurons in the ventral tegmental area.

A microiontophoretic study using rats anesthetized with chloral hydrate and immobilized with gallamine triethiodide was carried out to compare the effect of talipexole (B-HT 920 CL2:2-amino-6-allyl-5,6,7,8-tetrahydro-4H-thiazolo [4,5-d]-azepine-dihydrochloride), a dopamine autoreceptor agonist, on dopaminergic neurons in the ventral tegmental area (VTA) to non-dopaminergic neurons in the VTA. VTA neurons were classified into two types according to the responses to antidromic stimulation of the nucleus accumbens (Acc): type I neurons with a long spike latency (8.69 +/- 0.24 msec) upon Acc stimulation and low spontaneous firing rate (6.80 +/- 1.34/sec), and type II neurons with a short latency (2.76 +/- 0.20 msec) and high spontaneous firing rate (26.77 +/- 7.05/sec), probably corresponding to dopaminergic and non-dopaminergic neurons, respectively. In type I neurons, microiontophoretic application of talipexole and dopamine inhibited antidromic spike generation elicited by Acc stimulation, and talipexole-induced inhibition was antagonized by domperidone (dopamine D-2 antagonist). In type II neurons, however, the antidromic spikes were not affected by either talipexole or dopamine. Furthermore, spontaneous firing was also inhibited by iontophoretically applied talipexole and dopamine in most type I neurons, but rarely affected by either drug. Inhibitory effects of talipexole were antagonized by domperidone. These results suggest that talipexole acts on dopamine D-2 receptors, thereby inhibiting the dopaminergic neurons in the VTA.

Animals↗
PubMed1991

Role of the axon reflex in capsaicin-induced bronchoconstriction in guinea pigs.

To study the axon reflex as a contributing factor to capsaicin-induced bronchoconstriction in vivo, 30 guinea pigs weighing 325 +/- 7 g were randomly divided into four groups: Group 1, control (n = 6); Group 2, bupivacaine (n = 11); Group 3, tetrodotoxin (TTX, n = 10); and Group 4, tachykinin depletion (n = 3). Each animal was anesthetized with pentobarbital sodium, cannulated with a tracheal cannula and venous catheter, paralyzed with gallamine triethiodide, and artificially ventilated. All animals were treated with atropine and phenoxybenzamine, and a ganglionic blocking agent (chlorisondamine) was given to about half of the animals. Capsaicin (16 micrograms/kg) was intravenously injected to induce bronchoconstriction. Immediately upon the capsaicin being induced each animal exhibited a decrease in vital capacity, maximal expiratory flow and respiratory compliance, as well as a more than six-fold increase in residual volume, indicating severe bronchoconstriction. Then, the airway spasm decreased gradually toward the baseline values. The animals in Group 4 indicated a complete abolishment of the capsaicin-induced bronchoconstriction, whereas Group 2 and Group 3 displayed a significantly attenuated constriction at 15 to 20 min after capsaicin injection. Administration of chlorisondamine did not alter the capsaicin-induced bronchospasm. Since it is known that bupivacaine and TTX block nerve conduction, the data suggest that the axon reflex plays a significant role in the late phase of bronchoconstriction, which is apparently mediated via tachykinins.

Animals↗
PubMed1993

Role of vagus nerves in resiniferatoxin-induced bronchoconstriction of guinea pigs.

To study the role of vagal afferent C-fibers in resiniferatoxin (RTX)-induced bronchoconstriction in vivo, 30 guinea pigs weighing 347 +/- 28 g were evenly and randomly divided into five groups: Group 1, control; 2, chronic vagotomy; 3, local capsaicin (acute); 4, local capsaicin (chronic); and 5, systemic capsaicin. Each animal was anesthetized with pentobarbital sodium, cannulated with a tracheal cannula and venous catheter, paralyzed with gallamine triethiodide, and artificially ventilated. All animals were pretreated with atropine and phenoxybenzamine. Immediately after RTX was intravenously injected, each animal in the control group exhibited profound decreases in maximal expiratory flow, dynamic respiratory compliance, and total lung capacity, as well as an increase in functional residual capacity, indicating severe airway constriction. Animals in Groups 2-4 exhibited partial abolishment, while those in Group 5 showed complete abolishment of the RTX-induced bronchoconstriction. In 12 additional animals (6 animals each in control and chronic vagotomy groups), chronic vagotomy caused also suppressive effects on capsaicin-induced airway constriction. At one min, our data demonstrate that 36-51% of noncholinergic bronchoconstriction is due to the vagal component while the remaining constriction is due to the nonvagal component. Thus, the nonvagal component plays a significant role in this type of tachykinin-mediated airway constriction.

Afferent Pathways↗
PubMed1993

Axon reflex in resiniferatoxin-induced bronchoconstriction of guinea pigs.

To study the role of the axon reflex in resiniferatoxin (RTX)-induced bronchoconstriction in vivo, 32 guinea pigs weighing 292 +/- 7 g were randomly divided into five groups: Group 1, control (n = 6); Group 2, chlorisondamine (n = 6); Group 3, tetrodotoxin (TTX, n = 6); Group 4, local capsaicin application (n = 6); and Group 5, systemic capsaicin application (n = 8). Chlorisondamine was used to interrupt ganglionic transmission while TTX was employed to block nerve impulse conduction. In Group 4, capsaicin was locally applied to both cervical vagus nerves 30 min prior to the study whereas capsaicin was given subcutaneously for 5 days starting 9 days before the study in Group 5. Each animal was anesthesized with pentobarbital sodium, cannulated with a tracheal cannula and venous catheter, paralyzed with gallamine triethiodide, and artificially ventilated. All the above animals were treated with atropine (0.2 mg/kg) and phenoxybenzamine (0.5 mg/kg). Resiniferatoxin (2 micrograms/kg) was injected intravenously to induce airway constriction. Immediately upon injection of RTX (at 1 min), each animal in the control group exhibited decreases in maximal expiratory flow, dynamic respiratory compliance, and total lung capacity, indicating severe bronchoconstriction. Then the airway spasm ameliorated gradually with time. Animals in Groups 3 and 4 indicated partial abolishment, while those in Group 5 showed complete abolishment, of the RTX-induced bronchoconstriction. On the other hand, the animals in Group 2 did not display any significant alteration in the RTX-induced bronchospasm. Furthermore, we tested RTX-induced bronchoconstriction in 5 additional animals not pretreated with either atropine or phenoxybenzamine. Compared with the data above, no significant differences in RTX-induced respiratory changes were found. Since it is known that TTX blocks nerve conduction, the data suggest that the TTX-sensitive reflex (the axon reflex) via afferent C-fibers plays a significant role in the RTX-induced bronchoconstriction, which is apparently mediated via tachykinins.

Analysis of Variance↗
PubMed1992

Differential effects on sympathetic nerve activities elicited by activation of neurons in the pressor areas of dorsal and rostral ventrolateral medulla in cats.

Changes of the nerve activity of the sympathetic renal and vertebral nerves were elicited by microinjection of sodium glutamate (50 nmol/100 nl) into the pressor areas of the dorsal (DM) and rostral ventrolateral medulla (RVLM) in cats under urethane-chloralose anesthesia. Animals were bilaterally vagotomized, artificially ventilated, and paralyzed with gallamine triethiodide. The vertebral nerve activity always increased when pressor responses were induced by DM or RVLM stimulation. However, the effects of medullary stimulation on the renal nerve activity were variable. Three types of renal nerve responses concomitant with the pressor responses were observed in either baroreceptor-intact or baroreceptor-denervated cats. They were: (1) augmentation (type I); (2) attenuation (type II); and (3) insignificant change (type III). Type I responses were often elicited by RVLM stimulation whereas type II responses were often elicited by DM stimulation. Findings suggested that neurons integrating these sympathetic nerve activities were not equally distributed in the pressor areas of DM and RVLM. This result supports the notion that neurons located in different pressor areas of the brainstem exert differential effects over different sympathetic nerve activities.

Animals↗
PubMed1993

Lumbosacral spinal neurons in the cat that are candidates for being activated by collaterals from the spinocervical tract.

Lumbosacral spinal neurons activated via the spinocervical tract were stained by intracellular injection of horseradish peroxidase in cats anaesthetized with chloralose and paralysed with gallamine triethiodide. The neurons were activated orthodromically by single shock stimulation of the ipsilateral dorsolateral funiculus at the second to third cervical segment, but not from the rostral part of the first cervical segment. Twenty nine cells were recovered from the histological material and subsequently reconstructed from transverse sections. Sixteen cells (55%) had axons that projected ipsilaterally to the lateral funiculus and their somata were located in two regions of the spinal cord, one group in the dorsal horn (laminae IV-V) and the other in the intermediate gray matter (laminae VI-VII). The axons of 10 of these cells gave off collaterals, and in seven of them the collaterals ramified in the grey matter deep to the cell body. The axons of five cells (17%) projected medially towards the central canal, four crossing the mid line in the ventral white commissure and ascending in the contralateral ventral funiculus. Only one of these cells had an axon collateral that crossed into the contralateral dorsal horn. Of the remaining eight cells, three had no obvious long axons but had many local axon collaterals, the axons of three cells were not stained, one had an axon projecting towards the ipsilateral ventral funiculus and one was a motoneuron and its axon projected into a ventral root. A feature of the dendritic trees of many cells was their wide spread in the mediolateral and/or the dorsoventral directions, although no dendrites reached dorsally into lamina II. Twenty-two cells (76%) were excited by moving hairs and by noxious pinch, three (10%) by hair movement alone, two (7%) by noxious pinch and pressure, and for two cells (7%) no receptive field could be found. It is concluded that not only postsynaptic dorsal column neurons receive input from the spinocervical tract but also other cells in the dorsal and ventral horns and the intermediate gray matter. Possible identities for these cells are discussed.

Animals↗
PubMed1995

Effects of upper cervical spinal cord stimulation on neurons in the lumbosacral enlargement of the cat: spinothalamic tract neurons.

Extracellular microelectrode recordings were made from deep spinothalamic tract neurons in the lumbosacral spinal cord of cats anaesthetized with chloralose and paralyzed with gallamine triethiodide. The effects of upper cervical spinal cord stimulation were tested on 43 spinothalamic tract neurons, by stimulation of the ipsilateral dorsolateral funiculus at C3 and rostral C1 using five or six shocks at 333 Hz. The strength of cervical stimulation was adjusted so that the C3 shock was above threshold for antidromic activation of spinocervical tract neurons but the same strength of shock applied at C1 was below threshold for the same neurons. Four of the 43 spinothalamic cells (9%) were not influenced by upper cervical stimulation. The remaining 39 spinothalamic tract cells (91%) were all excited from the upper cervical cord. Twenty-seven of these (63%) were excited more strongly from C3 than from C1, 4 (9%) were excited more strongly from C1 than from C3, and the remaining eight cells (19%) showed no significant differences between their responses to stimulation at C1 and C3. There were no obvious differences between those spinothalamic tract neurons showing differential effects from C1 and C3 and those showing no such effects. The neuronal systems possibly responsible for the differential effects from C3 and C1 on spinothalamic tract neurons are discussed. We conclude that the most likely candidate system for the greater excitation from C3 compared with C1 is the subset of spinocervical tract neurons with axon collaterals in the lumbosacral enlargement and that the spinothalamic tract is a further ascending path, in addition to the postsynaptic dorsal column path, that receives excitatory input from spinocervical axon collaterals. The greater excitation from C1 compared with C3 is interpreted as due to excitation from C1 and a mixture of excitation and inhibition from C3. The responsible neuronal systems seem likely to be either the spinocervical neurons with axon collaterals operating on the spinothalamic tract via inhibitory interneurons, or cells in the lateral cervical nucleus with axons descending to the lumbosacral cord.

Animals↗
PubMedDate not supplied

Effects of urethane on hippocampal unit activity in the rat.

The effect of urethane on hippocampal single unit activity in rats paralyzed with gallamine triethiodide was examined to determine possible influences of urethane as an anesthetic for electrophysiological recordings. With intravenous injections of urethane (1.0 g/kg body weight), hippocampal units responded initially with a substantial decrease in spontaneous firing rate. Activity in some cells recovered partially after a period of approximately 45 min. The activity of the remainder of cells recorded remained depressed for periods of time up to 1.5 hr. Longer periods of depression were observed in some cells. The difference in susceptibility to urethane in the population of hippocampal cells may offer a selective alteration in patterns of spontaneous activity in the hippocampus and systems efferent to the hippocampus. A knowledge of such alterations may prove important in interpreting the results of electrophysiological recording in preparations under urethane anesthesia.

Animals↗
PubMed1986

Comparison of the effects of hypercapnia on phrenic and hypoglossal activity in anesthetized decerebrate and decorticate animals.

To examine the effects of suprapontine structures on the activity of hypoglossal and phrenic nerves, 13 chloralose anesthetized, paralyzed (gallamine triethiodide) and artificially ventilated cats were studied. In all animals vagi and carotid sinus nerves were cut bilaterally. All animals were first hyperventilated to apnea and then made progressively hypercapnic by rebreathing under hyperoxic conditions. Following midcollicular decerebration, the peak phasic activity of the hypoglossal nerve was significantly depressed and the PCO2 at which apnea occurred (apneic point) increased. However, following high decerebration or decortication the activity of the hypoglossal nerve was increased at higher CO2 levels and there was no change in apneic point. By contrast, peak phrenic nerve activity was not altered by any of the above surgical procedures. Neither systemic blood pressure nor respiratory frequency were significantly altered by these procedures. The results indicate that suprapontine structures can appreciably modify hypoglossal activity.

Anesthesia, General↗
PubMed2000

Glutamatergic transmission in the trigeminal nucleus assessed with local blood flow.

Stimulation of the superior sagittal sinus in humans is pain-producing and in experimental animals leads to excitation of neurons in the caudal trigeminal nucleus and dorsal horns of the C(1/)C(2) cervical spinal cord: the trigeminocervical complex. Neuronal excitation is generally associated with an increase in local blood flow due to flow/metabolism coupling and we have used local blood flow in the trigeminocervical complex to examine the role of N-methyl-D-aspartate (NMDA)-mediated transmission in these neurons. Cats were anaesthetised with alpha-chloralose (60 mg/kg, ip; supplements 20 mg/kg iv) after surgical preparation under halothane (0.5-3%). Animals were paralysed with gallamine triethiodide to prevent possible movement artefact distorting the laser Doppler signals. The superior sagittal sinus was isolated for electrical stimulation (150 V; 250 microsec duration; 0.5, 1, 2, 5, 10 and 20 Hz) and the dorsal surface of the spinal cord exposed at the C(2) level. Blood flow was recorded from the region over the trigeminocervical complex by careful placement of a laser Doppler flow probe. Flow was recorded continuously by an online collection programme and NMDA-mediated transmission modulated by intravenous administration of MK-801 (0.4, 1 and 4 mg/kg, iv) at the stimulation frequency of 5 Hz. Stimulation of the superior sagittal sinus produced a stimulus-locked, frequency-dependent increase in blood flow in the region of the trigeminocervical complex. The mean maximum response was 39+/-4% at 20 Hz. MK-801 had no effect on the resting flow signal but markedly attenuated the SSS-evoked response in a dose-dependent manner. The mean maximum response after 4 mg/kg MK-801 was 13+/-2%. NMDA-mediated transmission is likely to be involved in nociceptive trigeminovascular transmission within the trigeminocervical complex and offers a possible target for both acute and preventative treatment of migraine.

Animals↗
PubMed1997

3.5% hypertonic saline produces sympathetic activation in hemorrhaged rabbits.

The neural mechanisms for pressor effects after hypertonic saline infusion are still unclear. Using direct measurement of the renal sympathetic nerve activity (RNA), we tested the hypothesis that the autonomic nervous system is involved in an acute blood pressure elevation produced by hypertonic saline (HTS) in anesthetized rabbits subjected to hemorrhage. Twenty urethane-anesthetized rabbits were ventilated mechanically after a tracheostomy and paralyzed with gallamine triethiodide. Heart rate (HR), mean blood pressure (MBP) and central venous pressure (CVP) were measured simultaneously with RNA. The animals were divided into the following four groups: (1) animals with intact baroreceptors that received HTS (intact HTS group, N = 5); (2) those with intact baroreceptors that received normal saline (intact NS group, N = 5); (3) those that underwent selective cervical vagotomy (vagotomy group, N = 5); (4) those with sino-aortic denervation (SAD group, N = 5). The last two groups were given HTS only. After inducing hemorrhagic hypotension to 40 mmHg over 10 min, 3.5% HTS at half the volume of shed blood was infused over approximately 120 s. In the intact HTS group, sympathetic activation, associated with tachycardia and pressor effects, developed. This enhancement of RNA was followed by a return to the pre-infusion level, but the increased blood pressure and tachycardia lasted until the end of the experiment. These levels of MBP and HR were significantly higher than those of the intact NS group. In the vagotomized animals, HTS resuscitation also increased RNA and systemic blood pressure. In contrast, in the SAD group, neither sympathetic activation nor an early phase increase in systemic blood pressure occurred. These results indicate that in hemorrhaged rabbits, 3.5% HTS produces sympathetic activation along with an acute pressor effect and that this is likely to be mediated through the sino-aortic nerves, possibly the peripheral chemoreceptors, but not through the vagal nerves.

Animals↗