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PubMed1992

Effect of acupuncture on gastric acid secretion in healthy male volunteers.

Six randomized, placebo controlled studies were performed to investigate the effect of electroacupuncture on gastric acid output in 38 healthy males. Electroacupuncture decreased basal acid output when compared to placebo acupuncture [from 3.50 +/- 0.59 mmol/hr to 2.54 +/- 0.56 mmol/hr (P < 0.05)] as well as sham feeding-stimulated acid output [from 18.52 +/- 2.25 mmol/hr to 5.38 +/- 2.11 mmol/hr (P < 0.005)], but had no effect on the pentagastrin stimulated acid output. The inhibitory effect of acupuncture on sham feeding-stimulated acid output was not affected by local anesthesia of the acupoint, but was prevented by a prior intravenous naloxone injection. Acupuncture did not alter plasma gastrin levels (20.7 +/- 7.6 micrograms/liter, vs control 21.2 +/- 7.2 micrograms/liter) but naloxone increased it (26.1 +/- 14.5 micrograms/liter) (P < 0.05). We conclude that the antisecretory effects of electroacupuncture do not result from decreased gastrin release or decreased parietal cell sensitivity to gastrin, but are mediated through naloxone-sensitive opioid neural pathways and vagal efferent pathways.

Acupuncture Points↗

PubMed1986

Effect of CCK-OP and intraduodenal administration of essential amino acids on intraluminal pressures of sigmoid and rectum in patients with Chagasic megacolon.

The motility of the sigmoid colon and rectum was studied by manometry in patients with Chagasic megacolon and in control individuals using two different experimental procedures: (1) intravenous infusion of saline, followed by intravenous infusion of cholecystokinin octapeptide (OP-CCK) at the dose of 20 ng/kg/hr; and (2) intraduodenal instillation of saline followed by a solution of essential amino acids at a flow of 10 ml/min. CCK-OP induced an increase in motility index in the sigmoid colon (P less than 0.05) and rectum (P less than 0.05) in the controls, whereas intraduodenal infusion of amino acids produced a significant increase in motility index exclusively in the sigmoid colon (P less than 0.005). A significant increase (P less than 0.05) in sigmoid colon motility also occurred in the control group after duodenal saline infusion was interrupted. The release of other substances in addition to CCK must have been responsible for the different behavior of sigmoid colon and rectum in response to the stimuli used. Neither procedure caused significant changes in the motility of the sigmoid colon or the rectum of the Chagasic patients. The extensive intramural denervation occurring in Chagasic megacolon probably destroys the neural pathway through which OP-CCK and the substances released by the duodenum by the infusion of essential amino acids activate the motor cells of the human terminal intestine.

Adult↗

PubMed1990

Idiopathic autonomic denervation in eight patients presenting with functional gastrointestinal disease. A causal association?

Gut dysmotility may result from disease of the extrinsic neural pathways supplying the gut. We report the results of studies on sweating, cardiovascular, and sudomotor reflexes in eight prospectively evaluated patients with apparently functional gastrointestinal disorders. There was no personal or family history of neurologic disease, except for one patient with known atony of the bladder. Motility of the esophagus, stomach, and small intestine were, respectively, abnormal in two, six, and seven patients and showed either uncoordination of contractions between segments or postcibal hypomotility. All had generalized or patchy anhidrosis; quantitative sudomotor axon reflex tests were also abnormal in four patients and borderline in one. Plasma levels of catecholamines were abnormal in one patient. All patients had evidence of sympathetic denervation: preganglionic in two patients, postganglionic in five patients, and mixed in one patient. Three patients also had abnormal heart-rate responses to deep breathing, suggesting parasympathetic dysfunction. No underlying cause for the autonomic dysfunction was identified in any of these patients despite extensive investigations. Thus, these data support the hypothesis that apparently functional gastrointestinal disorders may be due to idiopathic autonomic denervation.

Adolescent↗

PubMed1989

Pain control in breast cancer. A panel discussion.

Pain can be a prominent finding in breast cancer patients. It may occur in the setting of the postmastectomy period, related to the disruption of normal neural pathways or the development of lymphedema. In advanced disease, the management of pain from nerve compression or bone metastases requires special approaches. In this panel discussion, the participating physicians will discuss these topics and provide an up-to-date approach to pain control in breast cancer patients.

Analgesics, Opioid↗

PubMed1994

Sweating and vascular responses in the face: normal regulation and dysfunction in migraine, cluster headache and harlequin syndrome.

At least four neural mechanisms influence facial blood flow. Firstly, sympathetic vasoconstrictor fibres exert a tonic constrictor influence on the vasculature of the ears, lips and nose, and sparsely supply other parts of the face. Secondly, the sympathetic nervous system actively dilates the cutaneous vasculature of the face during heat stress and emotion. Thirdly, parasympathetic vasodilator reflexes in the facial and glossopharyngeal nerves increase blood flow to the exocrine glands and tissues of the eyes, nose and mouth when these tissues are irritated. Fourthly, axon reflexes release vasoactive peptides from sensory fibres, which participate in local inflammatory responses. The sympathetic nervous system normally controls facial sweating. However, after injury to postganglionic sympathetic fibres, parasympathetic fibres sometimes make functional connections with sweat glands, so that parasympathetic reflexes provoke pathological sweating. In this review, new information about the neural pathways and stimuli which influence facial sweating and blood flow is summarized, and this is followed by a discussion of the pathophysiology of extracranial vascular disturbances and facial sweating in migraine, cluster headache and harlequin syndrome.

Blood Vessels↗

PubMed1987

Inhibition of carrageenin-induced pedal oedema in rats by immobilisation stress.

The effect of immobilisation stress on acute pedal inflammation induced by carrageenin, and the mechanism of stress-induced anti-inflammatory effect, were investigated in male Wistar strain albino rats. Carrageenin-induced pedal inflammation oedema was attenuated by immobilisation stress in a time-dependent manner, when the rats were restrained for 30 min, 1 h, and 2 h immediately after the induction of the inflammation. Pentobarbitone exhibited significant anti-inflammatory effect of its own in an anaesthetic dose and also inhibited stress (1 h)-induced attenuation of the inflammation. Likewise, lignocaine, injected behind the knee joint of the inflamed limb, attenuated the inflammation and also inhibited the stress-induced anti-inflammatory effect. These findings indicate the importance of the central nervous system (CNS) and the afferent/efferent neural pathways from and to the inflammatory site, in inflammation and in stress-induced anti-inflammatory effect. Earlier studies from this laboratory have shown that the central noradrenergic, histaminergic, serotonergic and GABA-ergic neurotransmitter systems have a modulatory anti-inflammatory effect on carrageenin-induced pedal oedema. Since all these neurotransmitter systems have been reported to be activated by stress, their role was assessed in the inflammation-attenuation effect of immobilisation stress. The present studies indicate that, of these neurotransmitters, only the central noradrenergic system is involved in the anti-oedema effect of stress. Endogenous opioid peptides may also be involved in the stress-inflammation interaction, since naloxone inhibited the stress effect. Bilateral adrenalectomy and peripheral chemical sympathectomy, induced by i.p. administration of 6-hydroxydopamine, augmented carrageenin oedema and antagonised the stress-induced anti-inflammatory effect. However, metyrapone, an inhibitor of endogenous corticoid synthesis, failed to inhibit the stress effect. These findings indicate that the sympatho-medullary system, which is known to be activated during stress, is responsible for the observed anti-inflammatory effect of immobilisation stress, rather than augmented release of adrenal corticoids. It is suggested that the observed inflammation reducing effect of immobilisation stress is a consequence of increased central noradrenergic and peripheral sympatho-medullary activity.

5,6-Dihydroxytryptamine↗

PubMed1992

Tracheal ciliary beat frequency in baboons: effects of peripheral histamine and capsaicin.

To determine if tracheal ciliary beat frequency (CBFt) in the nonhuman primate could be stimulated indirectly, either by an inhaled irritant or by a mediator potentially released from an inhalation challenge, saline (0.9%), capsaicin (3 x 10(-9) M), or histamine (8 mg/ml) were delivered for three minutes as 100 ml aerosol (0.25 micron MMAD) boluses at the beginning of each breath, followed by 10 sec breath hold. Each of five adult baboons (17-27 kg, Papio cynocephalus) underwent three studies using a randomized block design. The baboons were anesthetized and ventilated eucapnically through an endotracheal tube whose cuff was inflated in the distal trachea. CBFt was measured in the mid-trachea proximal to the cuff at one minute intervals using heterodyne laser light scattering. There was no change in CBFt from a baseline of 7.2 +/- 0.6 Hz (mean +/- SE) following inhalation of saline deposited peripherally. Capsaicin stimulated CBFt for over 80 min reaching a maximum of 14.7 +/- 6.3 Hz 46 min after aerosol delivery. Histamine stimulated CBFt for 90 minutes reaching a maximum of 19.3 +/- 9.9 Hz 67 min after aerosol delivery. The prolonged stimulatory responses of CBFt to peripherally deposited capsaicin and histamine most likely involve both cellular and neural pathways through which the tracheobronchial airways, in response to an alveolar challenge, are cleansed of secretions thus enabling the maintenance of effective gas transport.

Animals↗

PubMed1994

A study of the mechanism of action of the mild analgesic dipyrone.

The mechanism of action for the mild analgesics is controversial. While some have proposed that they inhibit prostaglandin synthesis in the central nervous system to interfere with nociceptive mediators in the brain, others have proposed that they act directly on nociceptive neural pathways to produce analgesia. This class of drugs also possesses antipyretic activity. We examined the antipyretic effect of one such drug, dipyrone, because this might elucidate the mechanism of its analgesic activity. In rats implanted with a femoral vein catheter and a cannula guide tube aimed towards the organum vasculosum laminae terminalis (OVLT) in the brain, an i.v. injection of 2 micrograms/kg interleukin-1 beta (IL-1 beta) produced a fever of 0.38 +/- 0.07 degrees C while an injection of 20 ng prostaglandin E1 (PGE) into the OVLT produced a fever of 1.18 +/- 0.18 degrees C. Dipyrone (25 mg/kg, i.v.) decreased the IL-1 beta fever but had no effect on the PGE fever. After pretreatment with the immunoadjuvant, zymosan, the IL-1 beta fevers were enhanced to equal those induced by PGE. Only 0.1 micrograms/kg, i.v. IL-1 beta raised body temperature by 1.20 +/- 0.10 degrees C. An increased dose of dipyrone (50 mg/kg, i.v.) was required to attenuate this IL-1 beta fever; however, the PGE fever remained unaffected by this treatment with dipyrone. Thus, dipyrone treatment blocks IL-1 beta fever where synthesis of prostaglandin is a crucial step in the febrile process, but it has no effect on PGE fever where synthesis is bypassed. This suggests that dipyrone, probably through its active metabolites, inhibits prostaglandin synthesis to induce antipyresis and, by analogy, analgesia as well.

Animals↗

PubMed1994

Effect of alpha 1-adrenergic blockade on canine ileal water, electrolyte, and glucose absorption.

Meal ingestion stimulates an increase in small intestinal water and electrolyte absorption. Endogenous norepinephrine may at least partially mediate this meal-stimulated proabsorptive response. Luminally administered alpha 1-adrenergic agonists such as norepinephrine and phenylephrine cause significant small bowel absorption, which can be prevented by the selective alpha 1-adrenergic antagonist terazosin. This study tested two hypotheses: (1) a meal stimulates ileal water, electrolyte, and glucose absorption; and (2) meal-stimulated ileal absorption is mediated via alpha 1-adrenergic receptor activation. Absorption studies (N = 27) were performed on dogs with 25-cm ileal Thirty-Vella fistulas (TVF). Perfusion with [14C]PEG was used to calculate absorption of water, electrolytes, and glucose from the TVF. Three groups were randomly studied over 4 hr: (1) terazosin alone, (2) meal alone, and (3) terazosin plus meal. Terazosin (10(-4) M) was administered to the TVF in groups 1 and 3 following the first hour. A 480-kcal mixed canine meal was ingested at the end of the second hour in groups 2 and 3. Ileal water, electrolyte, and glucose absorption increased significantly in response to meal ingestion (P < 0.05). Luminal terazosin did not significantly alter basal or meal-stimulated ileal absorption. In conclusion, meal ingestion stimulates ileal absorption of water, electrolytes, and glucose. Neither basal nor meal-stimulated ileal absorption is altered by alpha 1-adrenergic receptor blockade. These data suggest that nonadrenergic neural pathways or humoral factors are the likely mediators of meal-induced intestinal absorption.

Adrenergic alpha-Antagonists↗

PubMed1994

Effects of jejunoileal autotransplantation on gastrointestinal regulatory peptides.

Plasma gastrointestinal hormones were measured before and during feeding in eight dogs, more than one year after total autotransplant of the entire jejunoileum, and in controls. At sacrifice, tissues were taken from the transplanted segment and intact bowel for measurement of hormone and enteric neuropeptide content. Gastrin levels were reduced in autotransplanted dogs (fasting 63% of control, incremental response 67% of control, both P < 0.05), reflecting the loss of acid inhibitory reflexes. Secretin and cholecystokinin responses were identical between the two groups. Postprandial levels of gastric inhibitory peptide (incremental response 175% of control, P < 0.005), insulin, and peptide YY (158% of control, P < 0.05) were elevated following denervation, the former suggesting more rapid gastric emptying while the latter may reflect malabsorption. The neurotensin meal response was obtunded by denervation (incremental response 43% of control, P < 0.05), providing evidence for a neural pathway for its release. Pancreatic polypeptide responses were identical between the groups, suggesting intact pancreatic innervation. Abnormal hormone secretion may contribute to the impaired fed motor responses seen following extrinsic denervation of the small bowel. In contrast, the neuropeptide content of the autotransplanted small intestine is normal, suggesting that extrinsic denervation has no long-term effects on peptide content of the enteric nervous system.

Animals↗

PubMed1991

Thoughts and feelings and things: a new psychiatric epistemology.

Epistemology--the study of knowledge--is a philosophical discipline with close ties to psychiatry. When epistemologists address specific questions about how knowledge is actually realized by human beings, their philosophy must be informed by empirical studies of the sort psychiatrists now take up in a variety of forms. As this paper describes, psychiatrists can likewise improve their understanding of human psychology through a deeper appreciation of philosophical analysis in epistemology. The aim of this article is to introduce a unifying framework within which the experience from different approaches to psychiatry--(1) the conceptual schemas of cognitive psychiatry, (2) the mental structures of psychoanalytic psychiatry, (3) the categorical forms of existential psychiatry, and (4) the neural pathways of biological psychiatry--can all be applied productively to the central question of epistemology. By establishing a broad understanding of the problem of knowledge, this new view of epistemology is developed within the idiom of each psychiatric approach. In addressing themselves to a unitary problem, these diverse psychiatric approaches are themselves revealed, not as competing points of view, but as complementary views of a single subject. The result is a new epistemology that can not only bring the insights of psychiatry to philosophy, but can also contribute to the care of patients when psychiatrists bring this broader view to their clinical work.

Humans↗

PubMed1994

SDZ 208-911, an amino-ergoline with partial dopamine agonist properties, dose dependently increases cocaine self-administration in the rat.

Brain dopamine neurotransmission appears to be an important component of the neural pathways involved in the maintenance of intravenous (IV) cocaine self-administration in rats. The effects of a novel partial dopamine agonist, SDZ 208-911, on intravenous cocaine self-administration in rats was studied. SDZ 208-911 at a dose range of 0.025-1.6 mg/kg SC dose-dependently increased the number of lever presses and drug intake in rats exposed to limited (3-h) daily access to cocaine on a continuous reinforcement schedule (0.75 mg/kg per injection). This behavioral profile is similar to that observed following administration of dopamine antagonist drugs and has been hypothesized to reflect a compensatory increase in drug intake due to a reduction of the reinforcing efficacy of the drug, probably because of functional antagonism at the receptor site. These results suggest that dopamine partial agonists may act as functional dopamine antagonists in the face of pharmacologically induced activation of brain dopamine function.

Animals↗

PubMed1994

Chronic exposure to noise modifies the anxiogenic response, but not the hypoactivity, detected on withdrawal from chronic ethanol treatment.

Two groups of rats received chronic ethanol treatment in quiet or noisy housing conditions. Animals from both housing conditions were then withdrawn from ethanol for 12 h prior to testing in the social interaction and elevated plus-maze tests of anxiety. Both ethanol withdrawal groups showed marked hypoactivity (decreased motor activity and decreased closed arm entries in the plus-maze), but they differed in their anxiogenic response (decreased social interaction and percentage of time spent on the open arms), with only the group treated in quiet conditions showing a significant response. A similar pattern of results was found in rats tested 18 h after withdrawal and thus it is unlikely that the anxiogenic response was simply delayed in time. It therefore seemed that chronic exposure to noise during the chronic ethanol treatment modifies dependence, but only as assessed by measures reflecting anxiety. This implies that the adaptive changes are suppressed only in the neural pathways mediating anxiety; possible mediating factors are discussed.

Animals↗

PubMed1995

Effects of diphenhydramine on human eye movements.

Peak saccadic eye movement velocity (SEV) and average smooth pursuit gain (SP) are reduced in a dose-dependent manner by diazepam and provide reliable, quantitative measures of benzodiazepine agonist effects. To evaluate the specificity of these eye movement effects for agents acting at the central GABA-benzodiazepine receptor complex and the role of sedation in benzodiazepine effects, we studied eye movement effects of diphenhydramine, a sedating drug which does not act at the GABA-benzodiazepine receptor complex. Ten healthy males, aged 19-28 years, with no history of axis I psychiatric disorders or substance abuse, received 50 mg/70 kg intravenous diphenhydramine or a similar volume of saline on separate days 1 week apart. SEV, saccade latency and accuracy, SP, self-rated sedation, and short-term memory were assessed at baseline and at 5, 15, 30, 45, 60, 90 and 120 min after drug administration. Compared with placebo, diphenhydramine produced significant SEV slowing, and increases in saccade latency and self-rated sedation. There was no significant effect of diphenhydramine on smooth pursuit gain, saccade accuracy, or short-term memory. These results suggest that, like diazepam, diphenhydramine causes sedation, SEV slowing, and an increase in saccade latency. Since the degree of diphenhydramine-induced sedation was not correlated with changes in SEV or saccade latency, slowing of saccadic eye movements is unlikely to be attributable to sedation alone. Unlike diazepam, diphenhydramine does not impair smooth pursuit gain, saccadic accuracy, or memory. Different neurotransmitter systems may influence the neural pathways involved in SEV and smooth pursuit again.

Adult↗

PubMed1998

The sympathetic skin response in peripheral autonomic failure--evaluation in pure failure, pure cholinergic dysautonomia and dopamine-beta-hydroxylase deficiency.

The sympathetic skin response (SSR) detects changes in the electrical potential in the skin in response to physiological and electrical stimuli and, therefore, may indicate the integrity of sympathetic cholinergic neural pathways to sweat glands. This has been evaluated in 21 patients with three forms of peripheral autonomic failure. Of these, 15 had pure autonomic failure (PAF) without additional neurological features; investigations indicated both sympathetic and parasympathetic failure. Four patients had pure cholinergic dysautonomia (PCD), with clinical and laboratory features indicating only cholinergic failure. Two siblings had dopamine-beta-hydroxylase (DBH) deficiency with only sympathetic adrenergic failure. None was on drugs affecting cholinergic function. Ten normal individuals were aged-matched with PAF patients and studied as controls. The SSR was recorded from the palmar hand and plantar foot surfaces, using previously described techniques, in response to physiological (auditory, cough and inspiratory gasp) and electrical stimuli. Nerve conduction studies excluded an associated motor or sensory neuropathy. The SSR was present in all normal individuals, and in both patients with DBH deficiency who had preserved cholinergic and sudomotor function, It was absent in all 15 PAF and all four PCD patients with impaired cholinergic function. Therefore, we conclude that the SSR reflected sympathetic cholinergic function in these three different groups with peripheral autonomic failure.

Adult↗

PubMed1994

Modulation of gastric perception and motility in man. Current concepts and correlation with symptoms.

Gastric function is controlled by central and peripheral modulation. Most often, afferent information from the stomach does not reach conscious level. At extremes of chemical and mechanical stimulation, however, afferent signals are perceived as pain. Whether or not a signal is perceived depends on gating of afferent signals at the levels of both spinal cord and brainstem. Inhibition of gastric tone and peristalsis during perceived discomfort largely results from stimulation via sympathetic neural pathways. These findings may be clinically relevant because upper gastrointestinal symptoms in many dyspeptic patients could be the result of primary afferent neuron dysfunction rather than motor dysfunction.

Afferent Pathways↗

PubMed1991

Effects of the phosphodiesterase inhibitor rolipram on the acoustic startle response in rats.

Systemic administration of the phosphodiesterase inhibitor rolipram (0.05-10.0 mg/kg, IP) produced a rapid and dose-related increase in the amplitude of the acoustic startle response in rats. The (-) isomer was more potent than the (+) isomer in enhancing startle amplitude. Rolipram increased startle responses that were elicited by brief electrical stimulation of the ventral cochlear nucleus or nucleus reticularis pontis caudalis, two brainstem relay nuclei of the startle neural circuit. A low (5 micrograms) dose of rolipram produced an excitatory effect on startle following spinal (lumbar intrathecal) infusion but not following supraspinal (lateral ventricle) infusion. Rolipram (0.5 mg/kg, IP) excitation of startle was not blocked by drugs which differentially disrupt the release of monoamines (DSP4, reserpine + alpha-methyl-para-tyrosine, reserpine + para-chloro-phenylalanine) or by drugs which differentially block monoamine receptors (haloperidol, prazosin, idazoxan, cinanserin, or cyproheptadine). The marked increase in startle seen following systemic rolipram injection is attributable, at least in part, to an action in the lumbar spinal cord that directly or indirectly facilitates neural transmission along the reticulospinal component of the startle reflex neural pathway. The startle reflex should be a useful behavioral test system for studying the mechanism of action of rolipram and related compounds purported to selectively inhibit calmodulin-independent forms of phosphodiesterase.

Acoustic Stimulation↗

PubMed1986

Effects of exogenous and endogenous bombesin on gastrin secretion from rat antral mucosa in tissue culture.

Effects of exogenous and endogenous bombesin on gastrin secretion were examined using rat antral mucosa in tissue culture. Gastrin secretion was significantly stimulated by exogenous bombesin at a dose of 10(-8) M. Atropine 10(-6) M, which abolished the action of the cholinergic agent carbachol to stimulate gastrin secretion, had no effect on bombesin-stimulated gastrin secretion. In addition, gastrin secretion was significantly inhibited by anti-bombesin antiserum used to block the effect of endogenous bombesin by immunoneutralization. These findings suggest that the stimulation of gastrin secretion by bombesin does not involve cholinergic neural pathways and that endogenous bombesin exerts a continuous stimulation on gastrin secretion in the basal state.

Animals↗