Free and forced diving in birds.

Heart rates were measured during free and forced diving on each of two species of aquatic birds: the double-crested cormorant (Phalacrocorax auritus), a true diver, and the Canada goose (Branta candensis), a bottom feeder in shallow water. When they immersed voluntarily they showed no bradycardia, but when the same birds were forcibly held under water there was a rapid drop in heart rate to well below that at rest. This decrease indicates that ther may be a large component of emotional stress in the heart rate records from previous diving studies where restrained animals were forcibly submerged.

Genetic predisposition and stress-induced hypertension.

When chronically exposed to an approach-avoidance conflict, rats with a genetic susceptibility to hypertension showed persisten elevations in systolic blood pressure, but rats with a genetic resistance to hypertension did not. Hence, psychic stress is selectively efficacious in producing hypertensive effects depending on genetic predisposition of the animal.

Early maternal separation increases gastric ulcer risk in rats by producing a latent thermoregulatory disturbance.

Rat pups that are separated early from their mothers, at postnatal day 15, become hypothermic when subjected to physical restraint on postnatal day 30. Restraint of separated pups also elicits an unusually high incidence of gastric erosions, as well as insomnia and an increase in quiet wakefulness. If hypothermia during restraint is prevented, neither the erosions nor the behavioral responses occur. Rat pups separated at the customary age (postnatal day 22) do not become hypothermic during restraint, and the restraint of such pups is not associated with either gastric erosion or insomnia.

Stress-induced modulation of the immune response.

After mice were exposed to a daily auditory stressor for varying lengths of time, the responses of their splenic lymphoid cells in vitro were assessed. Both the blastogenic activity of concanavalin A or lipopolysaccharide and the ability of immune lymphocytes to lyse P815 target cells showed the same patterns of immunosuppression and enhancement.

Lesch-Nyhan syndrome: low dopamine-beta-hydroxylase activity and diminished sympathetic response to stress and posture.

Patients with Lesch-Nyhan syndrome with virtually no hypoxanthine phosphoribosyltransferase activity demonstrate significantly low plasma activity of dopamine-beta-hydroxylase but normal basal levels of norepinephrine. Under conditions of emotional or postural stress the plasma concentrations of norepinephrine in Lesch-Nyhan patients increased less than in a normal population.

Meprobamate reduces accuracy of physiological detection of deception.

Normal male subjects attempted to deceive an experimenter recording electrodermal, respiratory, an cardiovascular activity. Those who had ingested a placebo or nothing were detected with statistically significant frequency on the basis of their phasic electrodermal responses, which clearly distinguished them from truthful suspects. That was not the case with deceptive subjects who had ingested 400 milligrams of meprobamate, nor did the examiner detect which subjects had received the drug.

Pheromonally induced sexual maturation in females: regulation by the social environment of the male.

Social subordination, which suppresses gonadal function in juvenile and adult male house mice, also suppresses the activity of an androgen-dependent urinary pheromone that accelerates the rate of sexual maturation in juvenile females. Pheromone production may also be suppressed by the presence of pregnant or lactating females. This suggests that the social environment may influence the fertility of population females by altering urinary pheromone activity in the male.

Cardiovascular reflex responses to apnoeic face immersion and mental stress in diabetic subjects.

The cardiovascular reflex responses to apnoea accompanied by immersion of the face in water and to mental stress, have been investigated in 21 diabetic subjects. Apnoeic face immersion caused bradycardia and forearm vasoconstriction (in seven subjects), bradycardia and forearm vasodilation (three subjects), tachycardia and forearm vasoconstriction (three subjects), or tachycardia and forearm vasodilatation (eight subjects). Mental stress evoked a tachycardia and forearm vasodilatation in all subjects. The abnormalities in the responses to apnoeic face immersion are most readily accounted for by loss of vagal and/or vasoconstrictor function.

The role of endorphins in stress: evidence and speculations.

Several lines of evidence suggest that the endogenous opioid peptides endorphins may play a role in the defensive response of the organism to stress. The present paper summarizes these findings as well as evidence linking endorphins to the anterior pituitary polypeptide hormone adrenocorticotropin (ACTH). Evidence is presented that endorphins may function as trophic hormones in peripheral target organs such as the adrenal medulla and the pancreas. As such they may be part of the physiological mechanisms that mediate adrenaline and glucagon release in response to stress. Endorphins (enkephalins) are also suggested to play a role in the control of the pituitary gland during stress. In such capacity they may act as hormone-releasing or inhibiting factors. Finally, endorphins appear to play a role in the behavioral concomitants of stress. In such capacity endorphins are suggested to function as modulators of neural systems that mediate the elaboration and expression of the reactive/affective components of stress. Speculations on the mode of interaction between endorphins and ACTH in the global response to stress are discussed.

Prolactin and growth hormone responses to psychological stress in normal and neurotic subjects.

In order to study the response of plasma prolactin (PRL) to acute psychological stress and to compare it with that of growth hormone (GH), the mirror drawing test (MDT) was performed in 20 normal controls (11 male, 9 female) and 22 neurotic patients (12 male, 10 female). Plasma PRL and GH were measured serially before, during and after the test. In controls, the test caused no significant change in plasma levels of either hormone. In neurotic males, the response of PRL to the test was not consistent, whereas, in neurotic females, plasma PRL level rose significantly following the test. Increase of GH, on the other hand, was apparent in the neurotics of both sexes. The correlation between the responses of the two hormones in the neurotics was low and non-significant. The results indicate that although the psychoendocrine coping mechanism in the neurotics works less effectively for both PRL and GH, the two hormones may have different psychological correlates.

Coping with stress: parallelism between the effects of septal lesions on growth hormone and corticosterone levels.

In order to characterize the effects of a septal lesion on plasma growth hormone levels, blood samples were taken from normal and sham-operated rats and rats with a bilateral septal lesion under conditions of rest and following stressful stimulation. Nonlesioned control rats evidenced a significant base line diurnal rhythm in plasma growth hormone levels which was unaffected by a septal lesion. In response to stress, plasma growth hormone levels evidenced a significant drop. Minimum levels were reached 15 min after stimulation and remained depressed during 1 hr of observation after stimulation. Rats with a septal lesion evidenced the same pattern of growth hormone response to stressful stimulation as nonlesioned rats, however the magnitude of response was potentiated in septal rats. The present data were compared to the previously published corticosterone data from the same animals. A septal lesion has similar effects on boting 24-hour rhythm of either of these hormones but potentiated the response of both corticosterone and growth hormone to stress even though the direction of response is opposite. The results are interpreted as suggesting the septum is an element in some central coping mechanism which is involved when an organism reacts to environmental demands. Preliminary data further suggest that the same central coping mechanism is involved in both the behavioral and hormonal responses to stress.

Cortisol, growth hormone, free fatty acids, and experimentally evoked affective arousal.

Eight male volunteers who viewed selected control, suspense, and erotic films experienced significant changes in affect that were limited to fatigue, anxiety, and sexual arousal, respectively. All subjects showed free fatty acid elevations with the suspense and erotic films and those subjects with the most anxiety and sexual arousal showed cortisol elevation with the suspense and erotic films, respectively. Growth hormone elevations occurred independently of cortisol elevations and were not clearly related to film or affect. Thus, activation of the pituitary-adrenocortical and sympathetic nervous systems appears to occur not in relation to a specific dysphoric state but rather with nonspecific affective arousal.

Beta-adrenoreceptor blockade in hypertension.

There is good evidence from many sources that beta-adrenoreceptor blockade is an effective form of therapy in mild, moderate and severe hypertension either alone or in combination with other antihypertensive agents. Although a number os such beta blocking compounds are now available, they appear to have a hypotensive effect of approximately equal magnitude. This hypotensive effect is obtained in both the supine and standing positions thus avoiding postural hypotension. The maximum hypotensive effect may take some time to become apparent. Despite considerable work the mode of action remains uncertain, reduction in cardiac output, resetting of baroreceptors, reduction in plasma renin and a central nervous system effect have been suggested but remain unproved. There is evidence to suggest that these compounds can control, to some degree, the surges in blood pressure resulting from either mental or physical stress. A low incidence of serious side effects has been reported by many workers. Only the long-term use of these compounds in comparison with other antihypertensive agents will determine their place in the management of hypertension.

Adrenoceptors on blood cells in patients with essential hypertension before and after mental stress.

The effect of mental arithmetic (MA) on alpha 2- and beta 2-adrenoceptors on platelets and lymphocytes, respectively, and on plasma catecholamines was studied in normotensive (NT) and essential hypertensive (HT) subjects. There were no significant differences in responses of blood pressure, forearm blood flow (FBF) and heart rate to MA between the two groups. Baseline values and changes in adrenaline and noradrenaline levels during MA were similar in NT and HT. Alpha 2-adrenoceptor density and antagonist affinity did not differ between NT and HT and was not influenced by MA. Baseline values of beta 2-adrenoceptor density also did not differ between NT and HT and increased similarly after MA in both groups. Antagonist affinity to the beta 2-adrenoceptors under baseline conditions was lower in HT and did not change during MA in either group. Our results indicate that there are no differences between NT and HT in alpha 2- and beta 2-adrenoceptor density, either under baseline conditions or after mental stress.

Neural and psychologic mechanisms and the problem of sudden cardiac death.

Brain stimulation can provoke a variety of arrhythmias and lower the ventricular vulnerable threshold. In the animal with acute myocardial ischemia such stimuli suffice to provoke ventricular fibrillation. Vagal neural traffic or adrenal catecholamines are not the conduits for this brain-heart linkage. Accompanying increases in heart rate or blood pressure are not prerequisites for the changes in cardiac excitability. Increased sympathetic activity, whether induced by neural or neurohumoral action, predisposes the heart to ventricular fibrillation. Protection can be achieved with surgical and pharmacologic denervation or reflex reduction in sympathetic tone. With acute myocardial ischemia, augmented sympathetic activity accounts for the early surge of ectopic activity frequently precipitating ventricular fibrillation. Asymmetries in sympathetic neural discharge may also contribute to the genesis of serious arrhythmias. The vagus nerve, through its muscarinic action, exerts an indirect effect on cardiac vulnerability, the consequence of annulment of concomitant adrenergic influence, rather than of any direct cholinergic action on the ventricles. There exist anatomic, physiologic as well as molecular bases for such interactions. Available experimental evidence indicates that environmental stresses of diverse types can injure the heart, lower the threshold of cardiac vulnerability to ventricular fibrillation and, in the animal with coronary occlusion, provoke potentially malignant ventricular arrhythmias. Available evidence indicates that in man, as in the experimental animal, administration of catecholamines can induce ventricular arrhythmia, whereas vagal activity exerts an opposite effect. Furthermore, in certain subjects diverse stresses and various psychologic states provoke ventricular ectopic activity.

Effect of emotional stress on platelet aggregation in humans.

In 16 young house physicians, each of whom presented a case at grand rounds, the effect on platelet function of the emotional stress involved in presenting the case was determined. Platelet-aggregation curves, using adenosine diphosphate and epinephrine, were determined immediately before, immediately after, and seven days after stress. Platelet aggregation was diminished during the stress period in 15 of the subjects. These findings may possibly be of importance in the relationship between stress and myocardial infarction; they also suggest that the emotional state of the patient must be considered when interpreting platelet-aggregation curves.

Continuous social defeat induces an increase of endogenous opioids in discrete brain areas of the mongolian gerbil.

Dyads of a victor and a loser of mongolian gerbils (Meriones unguiculatus) coexisted for seven days; isolated animals served as a further experimental group. beta-Endorphin, Met-enkephalin and dynorphin were measured in several brain areas and in the anterior and neurointermediate pituitary. beta-Endorphin and Met-enkephalin were increased in the amygdala of defeated as compared to victorious animals. Met-enkephalin in the hypothalamus and in the striatum were lower in isolated than in coexisting gerbils. Coexistence decreased beta-endorphin in the amygdala and in the hypothalamus as compared to isolation. The results provide biochemical evidence for the role of central endogenous opioid-peptide systems in the physiology of victory and defeat. Dynorphin showed no variation with social conflict and social status.

Abolition of plasma growth hormone response to stress and of the circadian rhythm in pituitary-adrenal function in female rats with preoptic-anterior hypothalamic lesions.

The chronic effects of lesions placed in the medial or lateral preoptic-anterior hypothalamic area (PO-AHA) on plasma growth hormone (GH) and corticosterone (cpd B) responses to stress, non-stress levels of these hormones and somatic growth were studied in adult female rats. Responses to 3-min immobilization--blood withdrawal stress uere tested at 2 and 11 weeks and to 3-min ether--blood withdrawal at 5 weeks after surgery. Non-stress plasma GH levels were further assessed in serial blood samples collected at 4-h intervals during a 24-h period at 15 weeks, and cpd B levels were studied similarly for a 44-h period at 22 weeks. Rats with lateral PO-AHA lesions showed normal GH suppression and cpd B elevation in response to both stress procedures. In contrast, neither stressor suppressed plasma GH levels in rats with medial PO-AHA lesions, but both produced normal increments in cpd B. The 24-h mean non-stress level of plasma GH in the group with medial lesions was higher and that of the group with lateral lesions was lower than those of controls. Cpd B levels were reduced during the 44-h study, and circadian rhythmicity was abolished in rats with medial lesions. The group with lateral lesions showed normal rhythmicity in plasma cpd B levels, Linear growth was not affected in either lesioned group. The GH findings suggest that the medial but not lateral PO-AHA is essential for stress-induced inhibition of GH secretion and that this region may exert a tonic inhibitory influence on non-stress GH secretion. The data also suggest that the medial PO-AHA is importantly involved in producing the circadian rhythm in pituitary-adrenal function.

Absence of glucoprivic feeding after stress suggest impairment of noradrenergic neuron function.

Feeding in response to 2-deoxy-D-glucose (2DG), a quantifiable behavior which appears to depend on noradrenergic (NE) neuron function, was used in these experiments to evaluate the functional capabilities of NE neurons after stress exposure. Depletion of hypothalamic NE after footshock or hypothermic stress was directly correlated with impairment of glucoprivic feeding. When NE depletion was prevented by prior exposure to chronic stress, no impairment of feeding was observed. After hypothermic stress, repletion of NE proceeded more rapidly in the telencephalon than in the hypothalamus and reappearance of a normal feeding response precisely paralleled the time course of repletion in the hypothalamus. Drinking in response to cell dehydration, a behavior not directly dependent on brain catecholamines, was not impaired after either footshock or hypothermic stress, despite similar NE depletions. Presence of a normal drinking response assured that deficits observed in the 2DG test were not due to nonspecific behavioral suppression resulting from stress. These data suggest that NE neuron function may be impaired or temporarily abolished after severe stress exposure. In addition, these results demonstrate that behavioral pathology need not be the result of massive neurotransmitter depletion but may result from relatively subtle alterations of specific neurotransmitter pools.