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PubMed1997

Capsaicin-evoked release of pituitary adenylate cyclase activating peptide (PACAP) and calcitonin gene-related peptide (CGRP) from rat spinal cord in vivo.

Capsaicin-evoked release of pituitary adenylate cyclase activating peptide (PACAP)-like immunoreactivity (LI) from rat spinal cord was examined in vivo. In anaesthetized rats, a catheter was inserted through the atlanto-occipital membrane into the subarachnoid space at the level of the sacral spinal cord for infusion of artificial cerebrospinal fluid. Another catheter was placed in the cisternal opening for outflow. Blood pressure was monitored and kept stable during the experiment. Perfusion samples were analyzed for PACAP and calcitonin gene-related peptide (CGRP) by radioimmunoassay. The addition of capsaicin (10 microM) to the perfusate elevated the concentrations of PACAP-27-LI in the artificial cerebrospinal fluid by 177%, PACAP-38-LI by 93% and CGRP-LI by 692%. In view of the presence of PACAP-immunoreactive nerve fibres in the superficial layers of the dorsal horn and the expression of PACAP in the small sized neurons in the dorsal root ganglia, the findings suggest that PACAP is released into the artificial cerebrospinal fluid from C-fibres in the spinal cord. PACAP conceivably plays a modulating role in nociception.

Animals↗
PubMed1998

Effect of nimodipine on regression of spinal analgesia.

We have investigated the effect of infusion of nimodipine on the spread of spinal anaesthesia in 50 patients undergoing transurethral procedures. Patients were allocated randomly to receive during operation continuous infusion of nimodipine 10 ml h-1 (group N, n = 25) or normal saline (group C, n = 25) in a double-blind manner. All patients received hyperbaric lidocaine 100 mg (5% in 8% dextrose) intrathecally and were then placed in the lithotomy position. Twenty minutes after intrathecal injection the level of spinal anaesthesia was tested with a pressure palpator and a baseline was established. Assessments were repeated 5, 10 and 15 min thereafter. Five minutes after establishing baseline, mean regression of sensory analgesia did not differ between groups. Analgesia had regressed by 1.3 (SD 1.4) and 1.0 (1.9) cm, respectively. After 10 min, sensory block in group N regressed by 1.7 (1.7) cm and in group C by 1.5 (1.6) cm. After 15 min these values were 1.1 (1.7) cm and 2.2 (1.9) cm, respectively (P < 0.035). Similar results were found after normalizing the changes by dividing the change by patient height.

Aged↗
PubMedDate not supplied

Thermoregulatory response in rats following administration of histamine in different CSF compartments.

Recently histamine is being considered as an important neurotransmitter/neuromodulator in the central nervous system. This has been supported from the present observations with regard to thermoregulatory responses elicited following histamine administration into different CSF compartments. Administration of histamine into the right lateral cerebral ventricle of rats showed a dose dependent fall in rectal temperature. This hypothermic response was evident only at moderately low or at thermoneutral ambient temperature. Administration of histamine into fourth ventricle produced hypothermic response at low ambient temperature and hyperthermia at thermoneutral ambient temperature, which was no longer observed when the ambient temperature remained above the thermoneutral zone. Infusion of histamine into spinal subarachnoid space produced hyperthermia which developed very slowly. However, the infusion of histamine into the subarachnoid space around the brain stem did not exhibit any change in rectal temperature. The significance of these observations has been discussed.

Animals↗
PubMed1990

Sedation during spinal anaesthesia: comparison of propofol and midazolam.

Propofol and midazolam were compared in 40 patients undergoing orthopaedic surgery under spinal anaesthesia. An infusion of either 1% propofol or 0.1% midazolam was given at a rate adjusted to maintain a similar level of sedation. The mean time to reach this required level was similar in both groups. Quality and ease of control of sedation were good in all patients. A mean infusion rate of 3.63 mg kg-1 h-1 was required for propofol and 0.26 mg kg-1 h-1 for midazolam. Immediate recovery, as judged by ability to open eyes and recall date of birth, was significantly more rapid following propofol (P less than 0.001). Similarly, restoration of higher mental function was significantly faster following propofol, measured by choice reaction time and critical flicker fusion threshold. Amnesia for the immediate postoperative period was significantly greater after midazolam (P = 0.0001).

Anesthesia Recovery Period↗
PubMed1981

Effects of propranolol on the cardiovascular and renin-angiotensin systems during hypotension produced by sodium nitroprusside in humans.

The authors examined the effects of controlled hypotension induced with sodium nitroprusside (SNP) with and without propranolol on the cardiovascular, pulmonary, and renin-angiotensin systems in 10 consecutive anesthetized patients with kyphoscoliosis undergoing posterior spinal fusion. SNP infusion (4.1 microgram . kg-1 . min-1) alone decreased mean systemic arterial pressure (SAP) by 25 torr +/- 3 SE (P less than 0.001), systemic vascular resistance index (SVRI) by 1113 dyne . sec. cm-5 . m2 +/- 125 SE (P less than 0.001), mean pulmonary artery pressure (PAP) by 6 torr +/- 2 SE (P less than 0.02), pulmonary capillary wedge pressure (PCWP) by 4 torr +/- 1 SE (P less than 0.01), pulmonary vascular resistance (PVR) by 50 dyne . sec . cm-5 +/- 18 (P less than 0.05), and PaO2 by 16 torr +/- 7 SE (P less than 0.05), whereas cardiac index increased by 1.08 l . min-1 . m2 +/- 0.24 SE (P less than 0.01) and heart rate increased 16 beats/min +/- 5 SE (P less than 0.02). After 40 min of hypotension, 0.03 mg/kg propranolol was injected intravenously while the SNP infusion rate was held constant. Ten min later there was a significant decrease in the heart rate (10 beats/min +/- 4 SE, P less than 0.02) and cardiac index (0.65 l . min-1 . m-2 +/- 0.21, P less than 0.02). Plasma renin activity (PRA) increased from 2.37 ng . ml-1 . h-1 +/- 0.7 SE before anesthesia to 6.50 ng . ml-1 . h-1 +/- 1.45 SE (P less than 0.05) after 40 min of nitroprusside infusion. Forty min after propranolol there was a significant reduction in PRA to 4.07 ng . ml-1 . h-1 +/- 0.73 SE (P less than 0.05). Thus propranolol, when given during SNP hypotension, exhibits an early cardiovascular response manifested as a decrease in cardiac output and heart rate and a delayed action of the kidney resulting in an inhibition of renin release.

Adolescent↗
PubMed1996

Role of GABA receptor subtypes in inhibition of primate spinothalamic tract neurons: difference between spinal and periaqueductal gray inhibition.

1. gamma-Aminobutyric acid (GABA) is thought to inhibit both pre- and postsynaptically the transfer of nociceptive signals from primary afferent fibers to spinal dorsal horn sensory cells, including spinothalamic tract (STT) neurons. The inhibition can be mediated by both GABAA and GABAB receptors. We now attempt to characterize the synaptic inhibition of STT cells by spinal GABAA and GABAB receptors in anesthetized monkeys and to analyze the roles of these two receptor subtypes in the inhibition of STT cellular activity produced by stimulation in the periaqueductal gray (PAG). 2. Iontophoretic release of GABA or muscimol (a selective GABAA receptor agonist) onto STT cells elicited a profound and dose-related inhibition of the responses of all cells tested to noxious cutaneous stimuli. Only four cells (16.7%) were found to be inhibited when baclofen (a selective GABAB receptor agonist) was applied iontophoretically. However, a strong and dose-dependent inhibition of the responses to cutaneous mechanical and thermal stimuli was obtained in all cells examined when baclofen was administered into the dorsal horn through a microdialysis fiber. The inhibitory effects were mainly on nociceptive inputs. 3. The inhibition of cellular activity by GABAA and GABAB agonists could be selectively antagonized by specific antagonists applied through a microdialysis fiber. 4. The excitatory responses evoked by pulsed release of glutamic acid (GLUT) were also inhibited in a dose-related manner by iontophoretic application of GABA and muscimol, but not by baclofen. A high dose of baclofen administered by microdialysis resulted in only a small decrease in GLUT-evoked excitatory responses. 5. Infusion of GABAA and GABAB antagonists into the dorsal horn by microdialysis caused an increase in both background activity and responses to cutaneous stimuli, suggesting that there is a tonic GABAergic inhibition of STT cells. 6. The inhibition of responses to mechanical and thermal stimulation of the cutaneous excitatory receptive field resulting from stimulation in PAG was significantly antagonized in most of the STT cells tested when the GABAA antagonist bicuculline was infused into the spinal dorsal horn through a microdialysis fiber. In contrast, the inhibition produced by PAG stimulation in most of the cells examined was not significantly antagonized by the GABAB antagonists phaclofen or 3-amino-propyl(diethoxymethyl)phophinic acid (CGP35348) administered into the spinal dorsal horn by microdialysis. 7. Our results support the contention that GABAergic mechanisms in the spinal dorsal horn normally exert a tonic modulation of nociceptive inputs through both GABAA and GABAB receptors. The evidence provided here indicates that GABAA receptors located on primate STT neurons contribute to a postsynaptic inhibitory effect on the transmission of peripheral nociceptive inputs. A possible presynaptic GABAA action was not investigated. Our finding of a GABAB-receptor-mediated inhibition is consistent with the view that both pre- and postsynaptic GABAB receptors are involved in inhibitory modulation of spinal nociceptive transmission. Finally, it is suggested from this study that primate spinal GABAA, but not GABAB receptors, are involved in mediating the descending inhibition induced by PAG stimulation.

Animals↗
PubMed1985

Cardiovascular pharmacology of ASL-7022. III. Peripheral vascular adrenergic mechanisms.

The peripheral vascular actions of i.v. administered ASL-7022 were investigated in anesthetized, open-chest dogs and in isolated hindlimbs of normal, acute baroreceptor-denervated and spinal dogs. ASL-7022 decreased diastolic arterial blood pressure in open-chest dogs, an effect which was inhibited by ganglion blockade (hexamethonium bromide, 10 mg/kg i.v.). In hindlimbs from control animals, ASL-7022 produced vasodilation. Propranolol (1.0 mg/kg i.v.) reduced but did not eliminate vasodilation in these preparations but combined beta adrenergic and ganglion blockade converted responses to vasoconstriction. ASL-7022 induced greater vasodilation in hindlimbs from acute baroreceptor-denervated animals than in control animals. In acute baroreceptor-denervated preparations ganglion blockade eliminated vasodilation, propranolol partially blocked vasodilation and combined beta adrenergic and ganglion blockade converted responses to vasoconstriction. In spinal dogs i.v. infusion of low doses of ASL-7022 induced small increases in perfusion pressure; higher doses produced small decreases in perfusion pressure. The compound caused only vasoconstriction in propranolol-pretreated hindlimbs and caused only vasodilation in phentolamine-pretreated hindlimbs. ASL-7022 also dose dependently inhibited vasoconstrictor responses to electrical stimulation of the lumbar sympathetic chain and to exogenously administered norepinephrine. The data suggest that ASL-7022 blocks sympathetic vasoconstriction by either inhibiting the sympathetic nervous system or by inducing postsynaptic alpha adrenoceptor blockade. The compound also produces beta adrenoceptor-mediated vasodilation and, under appropriate pharmacological conditions, can be demonstrated to produce alpha adrenoceptor-mediated vasoconstriction.

Animals↗
PubMed2006

Development of baclofen tolerance in a rat model of chronic spasticity and rigidity.

Systemic or spinal treatment with baclofen has been associated with the development of tolerance in patients with chronic spasticity. In the present study, we used a rat model of spinal ischemia-induced spasticity to characterize the development of baclofen tolerance after chronic intrathecal (i.t.) baclofen infusion. Following the induction of spinal ischemia and the development of behavioral spasticity, animals were implanted with i.t. catheters connected to osmotic pumps to continuously infuse baclofen (1.0 microg/0.5 microl/h). Hindleg peripheral muscle resistance (PMR) was measured periodically after initiation of chronic infusion and after bolus i.t. baclofen injection (1.0 microg). Peripheral muscle resistance was significantly decreased at the onset of baclofen infusion, however, after 5-7 days of infusion a progressive return of spasticity was noted, where baseline PMR values returned to preinfusion levels. At the same time, the efficacy of bolus i.t. baclofen treatment also decreased, where after 5 days of baclofen infusion 1.0 microg (i.t.) baclofen only reduced PMR by 10% (compared to 40-50% preinfusion). Baclofen efficacy progressively returned once continuous infusion was stopped. These data demonstrate that transient spinal ischemia leads to the development of spasticity which is sensitive to spinal baclofen. Chronic i.t. infusion leads to a progressive development of tolerance. This model offers potential to study tolerance mechanisms after spinal injury, and aid in drug discovery for use in baclofen-tolerant patients.

Animals↗
PubMed1997

Activation of the cAMP transduction cascade contributes to the mechanical hyperalgesia and allodynia induced by intradermal injection of capsaicin.

1. The spinal role of the cAMP transduction cascade in nociceptive processing was investigated in awake behaving rats (male, Sprague-Dawley) by activating or inhibiting this pathway spinally. Microdialysis fibres were implanted into the dorsal horn to infuse drugs directly to the spinal cord. 2. Animals, without peripheral tissue injury, were tested for responses to repeated applications (10 trials) of von Frey filaments and threshold to mechanical stimulation before and after infusion of 8-bromo-cAMP. In this group of animals treated spinally with 8-br-cAMP (1-10 mM) a dose-dependent hyperalgesia and allodynia were produced. This was manifested as an increased number of responses to 10 trials of von Frey filaments (10, 50, 150, 250 mN) and a decrease in mechanical threshold. 3. A second series of experiments studied the manipulation of the cAMP pathway spinally in a model of tissue injury induced by intradermal injection of capsaicin. Animals were either pre- or post-treated spinally with the adenylate cyclase inhibitor, tetrahydrofuryl adenine (THFA) or the protein kinase A inhibitor, myrosilated protein kinase (14-22) amide (PKI). Injection of capsaicin resulted in an increased number of responses to repeated applications of von Frey filaments and a decrease in threshold to mechanical stimuli outside the site of injection, secondary mechanical hyperalgesia and allodynia. 4. Pre-treatment with either THFA (1 mM) or PKI (5 mM) had no effect on the capsaicin-evoked secondary hyperalgesia and allodynia. 5. In contrast, post-treatment spinally with THFA (0.01-1 mM) or PKI (0.05-50 mM) dose-dependently reduced the mechanical hyperalgesia and allodynia produced by capsaicin injection. Furthermore, the mechanical hyperalgesia and allodynia blocked by the adenylate cyclase inhibitor, THFA (1 mM), was reversed by infusion of 8-bromo-cAMP (0.01-10 mM) in a dose-dependent manner. 6. Thus, this study demonstrates that activation of the cAMP transduction cascade at the spinal cord level results in mechanical hyperalgesia and allodynia and that the secondary mechanical hyperalgesia and allodynia following intradermal injection of capsaicin is mediated by this same transduction cascade.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1995

Thyrotropin-releasing hormone (TRH) and CNS regulation of anorectal motility in the rat.

The effect of thyrotropin-releasing hormone (TRH) upon anorectal motility was investigated in acute male rat preparations. Micromolar doses of TRH were intrathecally (i.t.) infused at the L6 spinal level at a rate of 1 microliter/min over 8 min. TRH infusions in 1.0-1000 microM concentrations elicited biphasic, dose-dependent anorectal contractions as measured by a rectal manometer. The 100 microM dose yielded the most significant increase in contractions over the greatest period of time. Atropine, administered as a pretreatment (100 micrograms s.c.), blocked contractions normally produced by i.t. infusion of TRH (1000 microM). Intravenous infusions of atropine (10 micrograms) through a jugular catheter immediately blocked anorectal contractions produced by i.t. infusion of 100 microM TRH. Sectioning of the hypogastric nerve, which supplies sympathetic innervation to the colon and internal anal sphincter, did not significantly affect contractions induced by 100 microM TRH applied intrathecally. Disruption of the major pelvic ganglion fibers, however, completely abolished the contractions induced by 100 microM TRH, either through the interruption of preganglionic parasympathetic fibers in the pelvic nerve, or by disrupting postganglionic fibers. These findings extend the role of TRH in the regulation of defecatory behaviors.

Animals↗
PubMed1998

Increased spinal release of excitatory amino acids following intradermal injection of capsaicin is reduced by a protein kinase G inhibitor.

Second messengers have been shown to play a role in the release of neurotransmitters presynaptically in several brain regions and cell types. This study was designed to test the hypothesis that the increased release of aspartate and glutamate that occurs after injection of capsaicin is dependent on activation of the cAMP and the cGMP transduction cascades. A microdialysis fiber was implanted into the dorsal horn of the spinal cord for collection of extracellular fluid and for administration of drugs to the spinal cord. Dialysate samples were collected before and after injection of capsaicin and after infusion of inhibitors of protein kinase G (PKG; KT5823) or protein kinase A (PKA; H89). KT5823, H89, or artificial cerebrospinal fluid (ACSF; control) were administered after injection of capsaicin to reduce the increased release of aspartate and glutamate. At the time of injection of capsaicin, there is an increase in release of aspartate (191+/-21%) and glutamate (194+/-14%). This increased release is maintained through 2.5 h for both glutamate and aspartate at approximately 125% to 150%. The increase in aspartate and glutamate concentrations that occurs after capsaicin injection was reduced back to baseline after spinal infusion of the PKG inhibitor, KT5823. Blockade of PKA had no effect on the increased release of aspartate and glutamate. Thus, the current data support a role for the cGMP-PKG pathway in the control of neurotransmitter release in vivo.

Alkaloids↗
PubMed1996

Rapid and long duration tolerance to the vagal bradycardic effects of 5-HT1A receptor agonists.

Administration of a single dose of the 5-HT1A receptor high intrinsic agonist U-93385E (either 0.3, 1.0 or 3.0 mg/kg, i.v.) results in a 20-30% decrease in heart rate. In contrast, cumulative dosing of U-93385E (0.01-3.0 mg/kg, i.v.) failed to lower heart rate in the spinal cat. Similarly, infusion of 1 mg/kg of U-93385E over a 2 h period failed to lower heart rate and prevented a bradycardic effect of a single bolus dose of U-93385E or flesinoxan. In contrast, the alpha 2-receptor agonist clonidine decreased heart rate in animals receiving the U-93385E infusion. Single bolus doses of flesinoxan or U-93385E failed to decrease heart rate in cats treated for 7 days with U-93385E (3 mg/kg, b.i.d.) and then saline for 3 days. Similarly, U-93385E failed to lower heart rate 12 days following a 14 day infusion of U-93385E (1 mg/kg per day). These data indicate that a rapid and long duration tolerance develops to the vagal bradycardia produced by 5-HT1A receptor agonists.

Animals↗
PubMed1992

Comparison of cerebral blood flow by radionuclide cerebral angiography and by microspheres in cats.

BACKGROUND: Radionuclide cerebral angiography is commonly used as an adjunct to the diagnosis of brain death. Despite its acceptance as a diagnostic tool, it is not clear whether the absence of cerebral blood flow by radionuclide cerebral angiography denotes a complete lack of cerebral blood flow. METHODS: To compare cerebral blood flow estimated by radionuclide cerebral angiography with cerebral blood flow measured by the radiolabeled microsphere technique, we systematically varied cerebral perfusion pressure (mean arterial BP minus intracranial pressure) in anesthetized cats by infusing artificial cerebral spinal fluid into the lateral ventricle to increase intracranial pressure. We measured cerebral blood flow with both techniques as cerebral perfusion pressure was decreased from its baseline of 111 +/- 10 mm Hg to 20, 10, 5, 0, and less than 0 mm Hg, causing a stepwise decrease in cerebral blood flow. RESULTS: We found a correlation by regression analysis (r2 = .47, p less than .05) between radionuclide cerebral angiography and microsphere measurements of cerebral blood flow, when both blood flow measurements were expressed as a percentage of baseline values. However, if 20% of baseline flow was assigned as a cut-off point for critically low cerebral blood flow (based on human studies), radionuclide cerebral angiography was only 33% sensitive to detect critically reduced cerebral blood flow and had a positive predictive accuracy (of low-flow interpretation) of only 60%. Radionuclide cerebral angiography was unable to demonstrate a complete lack of cerebral blood flow, even in two instances when cerebral blood flow by microspheres was less than 0.1% of baseline. CONCLUSIONS: We conclude that the ability of radionuclide cerebral angiography to quantify low cerebral blood flow is poor, and that this technique may not identify severely reduced cerebral blood flow.

Animals↗
PubMed1996

Middle latency auditory evoked potentials during repeated transitions from consciousness to unconsciousness.

We have investigated the relationship between changes in the middle latency auditory evoked potentials during alternating periods of consciousness and unconsciousness produced by propofol infusion combined with spinal anaesthesia for total knee replacement. Eleven patients completed the study, of whom two had recollection of events after the onset of the anaesthetic. There were no significant differences in heart rate or systolic arterial pressure between any conscious and unconscious period. With the first change from consciousness to unconsciousness, latencies of Na, Pa and Nb increased from mean (SD) starting values of 20.0 (1.4), 31.7 (1.0) and 42.8 (1.6) ms to 22.5 (2.0), 39.3 (2.1) and 57.8 (4.4) ms, respectively. During successive transitions from unconsciousness to consciousness, awake latencies were slightly higher than those of baseline awake, whereas anaesthetised latencies were similar to the ones obtained during the first period of unconsciousness. The consistent changes demonstrated, suggest that the auditory evoked potentials could represent a reliable indicator of potential awareness during anaesthesia.

Aged↗
PubMed1985

Effects of some alpha-adrenoceptor antagonists on central cardio-decelerator mechanisms in the rabbit.

Bradycardia was evoked in rabbits anaesthetized with chloralose-urethane by electrical stimulation (200 or 300 microA, 1 ms, 60 s-1 for 9 s, repeated every 5 min) of a selected point in the caudal hypothalamus 1.5 mm from the midline dorsal to the mammillary bodies. Phenoxybenzamine, prazosin and yohimbine solutions were infused intracerebroventricularly at a rate of 20 microliters min-1. Phenoxybenzamine did not cause any effects additional to those attributable to the solvent alone. Prazosin attenuated the evoked bradycardia at all doses (40 to 300 micrograms) and altered resting heart rate (HR) and arterial blood pressure (BP) after the higher doses. Yohimbine (200 + 300 micrograms) attenuated the bradycardia with negligible effects on HR and BP. Prazosin and yohimbine were given intravenously. Both caused dose-related attenuation of evoked bradycardia but prazosin also lowered BP sufficiently for this action alone to account for almost all the loss of bradycardia. The weaker hypotensive action of yohimbine was insufficient to account for the attenuation, a conclusion confirmed in animals whose BP was maintained constant by noradrenaline infusion after cervical spinal transection. In this preparation yohimbine caused dose-related attenuation of the bradycardia. The experiments have shown that yohimbine and probably prazosin also, can prevent hypothalamic stimulation from evoking bradycardia. The results suggest the presence of an alpha-adrenergic pathway from this region of the hypothalamus which projects caudally to increase the gain of the cardio-decelerator baroreceptor reflex in the rabbit.

Adrenergic alpha-Antagonists↗
PubMed2002

[Posterior block of lumbar plexus for postoperative analgesia after hip arthroplasty].

OBJECTIVES: To describe early postoperative analgesic quality from a posterior lumbar plexus block in the psoas compartment, located by neurostimulation. We used a single paramedial puncture at L4, following Chayen's approach, in patients undergoing uncemented hip arthroplasty under subarachnoid anesthesia with 0.5% bupivacaine. MATERIAL AND METHODS: Twenty patients were enrolled. We studied pain intensity on a visual analogical (VAS) scale every hour for the first 12 hours and every 2 hours for the next 12. The need for rescue analgesia, specifically non-steroidal anti-inflammatory drugs (NSAIDs) if pain was over 3 on the VAS and for morphine if analgesia was still insufficient. The patients assessed quality of analgesia received on a verbal scale. Complications were also noted. RESULTS: VAS scores were under 3 throughout the first 11 hours, gradually rising to 4.7 at 24 h. Only 5 patients (2%) needed NSAIDs in the first 12 hours and non needed morphine. Sixteen patients (80%) needed a mean 1.6 doses of NSAIDs and 3 (15%) needed morphine for persistent pain or for pain greater than 5 on the VAS. On the verbal scale, only 10% reported experiencing intense pain during the postoperative period, whereas 90% said they had experienced mild or moderate pain. CONCLUSIONS: A posterior lumbar plexus block using a single shot gives effective analgesia in the first 12 hours after surgery performed with spinal anesthesia. Continuous infusion through a catheter may provide better analgesia than that observed in this study.

Aged↗
PubMed1994

Tolerance development to the vagal-mediated bradycardia produced by 5-HT1A receptor agonists.

The purpose of this study was to characterize the bradycardic effects of 5-hydroxytryptamine (5-HT)1A receptor agonists in the chloralose-anesthetized spinal cat and to determine if tolerance develops to the bradycardia produced by these drugs. 5-HT1A receptor agonists studied included 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), buspirone, gepirone, flesinoxan and U-93385E (cis-(3aR)-(-)-2,3,3a,4,5,9b-hexahydro-3-propyl-1H-benz[e]indole-9 - carboxamide). These compounds reduced heart rate by 20 to 30% in the spinal cat and lowered arterial blood pressure. The hypotension resulted from a decrease in cardiac output. Atropine reversed and vagotomy prevented the bradycardia produced by a single dose of U-93385E. The decrease in heart rate produced by i.v. bolus doses of flesinoxan or U-93385 was reversed by administration of the 5-HT1A receptor antagonists spiperone or WAY 100135. Administration of a single dose of U-93385E (either 0.3, 1.0 or 3.0 mg/kg i.v.) resulted in a 20 to 30% decrease in heart rate. In contrast, cumulative dosing of U-93385E (0.01-3.0 mg/kg i.v.) failed to lower heart rate in the spinal cat. Similarly, infusion of 1 mg/kg of U-93385E over a 2-hr period failed to lower heart rate and prevented a bradycardic effect of a single bolus dose of U-93385E or flesinoxan. In contrast, the alpha-2 receptor agonist clonidine decreased heart rate in animals receiving the U-93385E infusion. Finally, single bolus doses of flesinoxan or U-93385E failed to decrease heart rate in cats treated for 7 days with U-93385E and then saline for 3 days.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗