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Biomedical subjects

E A Stone

Publications and source records attributed to E A Stone.

At least 73 records · Page 4Linked to original sources
PubMed1985

Potentiation of cold-water swim analgesia by acute, but not chronic desipramine administration.

Like other stress responses, cold-water swim (CWS) analgesia can be altered by changes in norepinephrine (NE) availability. While clonidine pretreatment potentiates CWS analgesia, lesions placed in the noradrenergic locus coeruleus reduce this response. Desipramine (DMI) can alter both the availability and receptor function of catecholamines, particularly NE: while both acute and chronic DMI treatments decrease NE reuptake, subsensitivity of beta-adrenergic receptors occurs only after chronic DMI treatment. The present study examined whether acute and chronic DMI treatments differentially alter CWS analgesia as measured by the jump test, CWS hypothermia and basal jump thresholds. The first experiment determined that pretreatment at either 24, 5 and 1 hr or only at 1 hr with DMI doses of 20 and 5 but not 1 mg/kg potentiated CWS analgesia. The second experiment found that chronic DMI pretreatment at a dose of 10 mg/kg administered twice daily over seven days failed to alter CWS analgesia at 1, 24, 48 or 72 hr thereafter. Neither CWS hypothermia nor basal jump thresholds were affected by the acute or chronic DMI injection regimens. The selective potentiation of CWS analgesia by acute DMI pretreatment is discussed in terms of the differential actions of acute and chronic injection regimens upon NE availability, receptor function, and adaptation processes.

Analgesia↗
PubMed1985

Reduction of the cyclic adenosine 3',5'-monophosphate response to catecholamines in rat brain slices after repeated restraint stress.

Restraint stress reduces the cyclic AMP (cAMP) response to norepinephrine (NE) in slices of the rat cerebral cortex and hypothalamus. This effect is found after repeated but not single exposure to stress and persists for at least 24 hr poststress. The magnitude of the reduction is dose-dependent in that greater decreases are found after higher frequencies and longer durations of restraint as well as after more disturbance during the stress. Analysis of the NE-cAMP dose-response curve indicates that the stress reduces the maximum cAMP response to NE but does not increase the EC50 value of NE. The cAMP response to isoproterenol is only slightly affected by the stress. No effect is observed on specific [3H]dihydroalprenolol binding in either brain region at 24 hr poststress. These results suggest that repeated restraint stress produces a selective persistent reduction of the function of brain non-beta adrenergic receptors. This effect may be mediated by an increased release of adrenocorticotropic hormone as chronic infusion of the latter hormone mimics the action of stress on cAMP responses to catecholamines. An increased release of brain NE may also be involved as repeated administration of the NE-reuptake inhibiting antidepressant, desmethylimipamine, reduces the function of non-beta as well as beta adrenergic receptors as evidenced by reductions of both the NE- and isoproterenol-cAMP responses.

Adrenocorticotropic Hormone↗
PubMed1984

Reduction of the cAMP response to norepinephrine in rat cerebral cortex following repeated restraint stress.

The present studies examined the effect of restraint stress on the sensitivity of the catecholamine-cAMP generating system in the rat cerebral cortex. Restraint was found to cause a persistent reduction in the magnitude of the cAMP response to catecholamines. This effect occurred after repeated but not acute stress and was more marked with twice-daily as compared to once-daily treatment. The reduction in response was more marked with norepinephrine than with isoproterenol, indicating a selective action of stress on the non-beta component of the noradrenergic response. The findings suggest that subsensitivity of the cAMP response to norepinephrine is a general response to chronic stressful stimuli and may be related to the action of certain antidepressant agents.

Animals↗
PubMed1984

The effect of acute and chronic administration of desmethylimipramine on responses to stress in rats.

Rats were given single or repeated injection of desmethylimipramine (DMI) and subjected to a single session of restraint or footshock stress. The degree of anorexia and plasma corticosterone elevation in response to the stress was measured. Repeated but not single injection of DMI was found to reduce the anorectic response to restraint and footshock but not to affect the corticosterone response to restraint. It is concluded that repeated DMI treatment has differential effects on responses to acute stress.

Acute Disease↗
PubMed1983

Massive hematuria of nontraumatic renal origin in dogs.

Massive hematuria of renal origin was diagnosed in 4 dogs. In all dogs, blood and blood clots were clearly visible in the urine. Serum urea nitrogen and urine concentrating ability were normal. All dogs were anemic, and results of coagulation and platelet function tests were within normal limits. Excretory urography indicated hydroureter and hydronephrosis in all dogs, with filling defects in the bladder attributable to large blood clots in 2 dogs. Cystotomy and catheterization of the ureters enabled identification of one kidney as the source of bleeding in 3 dogs. Unilateral nephrectomy and ureterectomy resolved their hematuria. The results of histologic examination were normal in 2 dogs. The 3rd dog had evidence of pyelitis. Cystoscopy of the 4th dog did not reveal hematuria from either ureter. The dog was not operated on and it continued to have intermittent hematuria.

Animals↗
PubMed1983

Reduction in cortical beta adrenergic receptor density after chronic intermittent food deprivation.

The effect of chronic intermittent food deprivation on beta adrenergic receptor binding in the rat brain was studied. Rats subjected to six 48 h fasts given over a period of 3 weeks demonstrated a reduction in the density of beta adrenergic receptors in the cerebral cortex but not in the hypothalamus or lower brainstem. This receptor alteration did not occur after one 48 h fast. This effect of chronic food deprivation is shared by several other forms of repeated stress, suggesting that it is a general mechanism of adaptation.

Adaptation, Physiological↗
PubMed1983

Rapid adaptation of the stimulatory effect of CO2 on brain norepinephrine metabolism.

The present study examined the effects of exposure of rats to elevated environmental levels of CO2 on norepinephrine metabolism in the hypothalamus and other regions of the brain. In confirmation of previous findings by others CO2 at 10 or 15% was found to elevate both dopa accumulation after dopa decarboxylase inhibition and norepinephrine utilization after tyrosine hydroxylase inhibition. These effects however were found to be transient occurring only during the first 30 min of 2.5 h exposure. In this regard CO2 differs from another form of stress, restraint which produces a sustained 2.5 h increase of dopa accumulation and NE accumulation. Restraint was also more effective than CO2 in depleting endogenous stores of hypothalamic NE. The factor responsible for the adaptation of the catecholamine response to CO2 was not identified although it was shown not to be hypothermia and it was reversed by a 2 h CO2-free recovery period.

Animals↗
PubMed1983

Adaptation to stress: tyrosine hydroxylase activity and catecholamine release.

The effects of adaptation to stress and of genetic differences on levels of in vitro tyrosine hydroxylase (TH) activity and in vivo catecholamine (CA) release are reviewed. It is shown that adaptation of animals to a wide variety of stressors including immobilization, electroconvulsive shock, footshock, hemorrhage, exercise and cold exposure results in a reduced CA response in the plasma, brainstem and heart to subsequent exposure to the same stress. Adaptation to many of the latter stressors also produces increased in vitro levels of TH activity. A similar inverse relation between in vitro TH activity and in vivo CA release is described for two inbred rat strains which differ in emotionality (Brown-Norway and Wistar Kyoto). The inverse relationship between TH activity and CA release may reflect different processes of biochemical adaptation utilized either for acclimation to stress, for preparation for emergency reactions or for changes in the metabolic costs of transmitter release. The similarity between environmental and genetic effects on these variables suggests that the above changes have a common adaptive function.

Adaptation, Psychological↗
PubMed1983

Adaptation to stress and brain noradrenergic receptors.

The present paper reviews the effects of stress on noradrenergic receptor function in the brain. Most forms of stress thus far examined have been found to reduce either the magnitude of the cAMP response to stimulation by catecholamines (CAs) and/or the density of beta adrenergic receptors in the brain. These effects (a) generally occur in the cerebral cortex, (b) are more marked after chronic than acute stress, (c) may be the result of excessive release of norepinephrine (NE), ACTH or serotonin (5-HT) and (d) may occur in neurons glia or both. The function of these receptor alterations is not known but is presumed to be related in some manner to adaptation to chronic stress. A review of similar changes occurring in peripheral organs after repeated stress or CA injections reveals that subsensitivity of beta adrenergic receptors can be associated with either decreases or increases in CA-stimulated organ output. The latter findings caution against concluding that there is a decreased postsynaptic noradrenergic function after adaptation to chronic stress. Instead they suggest that it may be more appropriate to view stress-induced receptor subsensitivity as part of a more complex pattern of adaptive changes which includes alterations in the size, number, efficiency and output of CA effector cells.

Adaptation, Psychological↗
PubMed1983

Total hip replacement induces injury to remote veins in a canine model.

The effects of total hip replacement on the condition of the luminal surface of the jugular and femoral veins and the carotid and femoral arteries were studied in healthy dogs. Four hours after the completion of surgery, most of the blood was removed by whole-body perfusion and the vessels were partially fixed in situ by glutaraldehyde perfusion, harvested, and prepared for scanning electron microscopy. In control dogs (held under anesthesia) the luminal surfaces of the veins (including valves and confluences) and arteries were covered by intact endothelium and were free of adhering blood cells. The arteries from dogs that were operated on were also free of damage. In contrast, the veins from dogs that were operated on showed a series of roughly parallel microtears around 70 to 80 per cent of the confluences of the side branches with the jugular or femoral vein. The basement membrane as well as the endothelial sheet was torn, thereby exposing underlying connective-tissue fibers and smooth muscle cells. The endothelium separated along intercellular junctions. The tears were infiltrated with many leukocytes and platelets and some erythrocytes. Subtle endothelial changes and patchy leukocyte adhesion occurred away from the side branches. The mechanism or mechanisms remain to be elucidated.

Animals↗
PubMed1982

Chronic restraint stress elicits a positive antidepressant response on the forced swim test.

The present study investigated behavioral parallels between adaptation to stress and antidepressant treatment using the forced swim test. Restraint stress given repeatedly for 11 days significantly reduced immobility on this test. A single application of stress had no effect. The reduction in immobility produced by repeated restraint was quantitatively similar to that produced by repeated administration of desmethylimipramine. These results confirm previous findings of similarities in the behavioral and neurochemical response to chronic stress and chronic antidepressant treatment.

Animals↗
PubMed1982

Brain adrenergic receptors and resistance to stress.

The relationship between brain beta-adrenergic receptors and adaptation to stress was studied in rats subjected to repeated restraint stress. The stress was found to produce a reduction in the density of these receptors in the hypothalamus, cerebral cortex and brain stem. This change first appeared after 4-7 days and persisted for the duration of the two-week stress. Adaptation, as judged by resistance to the anorexic and gastric lesion-inducing effects of the stress, occurred progressively over the full two-week period. The loss of beta-receptors was found to correlate positively with the degree of adaptation. The relationship was strongest for the hypothalamus but was also apparent in the cortex and brain stem. These findings support the hypothesis that a reduction in the number of brain adrenergic receptors is one of the biochemical factors underlying adaptation to stress.

Adaptation, Psychological↗
PubMed1981

[3H]dihydroalprenolol binding in the rat brainstem.

The binding of [3H]dihydroalprenolol to beta-adrenergic receptors in the rat brainstem was studied. Propranolol inhibited dihydroalprenolol binding to a greater extent than did isoproterenol or epinephrine. Scatchard plots obtained with propranolol were biphasic whereas those obtained with isoproterenol and epinephrine were monophasic. The results indicate that in the brainstem propranolol displaces dihydroalprenolol from sites other than beta-adrenergic receptors. Nonspecific binding of dihydroalprenolol in this tissue therefore cannot be assayed using propranolol but should be measured with isoproterenol or epinephrine.

Adrenergic beta-Agonists↗
PubMed1981

Mechanism of stress-induced subsensitivity to norepinephrine.

Chronic footshock stress in rats produces a persistent reaction in the sensitivity of the norepinephrine (NE)-cAMP generating system in the cerebral cortex, an effect similar to that reported after chronic antidepressant treatment. The present studies show that footshock-induced subsensitivity is not related to changes in either beta or alpha-1 adrenergic receptors, phosphodiesterase or total adenylate cyclase activity. The stress does not induce a small, selective decrease in binding at high affinity alpha-2 receptor sites but this change does not appear to explain the decreased responsiveness to NE. These data and related findings by others using restraint stress indicate that the mechanism of subsensitivity after chronic stress resembles in part that seen after antidepressants but may also involve additional phenomena which may not occur after the latter agents.

Adenylyl Cyclases↗