Period Of Immobilization Stress Research Articles

The levels of oxidative stress in a combination of stress factors.

We studied the effect of the combined action of ionizing radiation and induced immobilization stress on the lipid peroxidation process and antioxidant protection of organs (mesenteric lymph nodes, spleen, adrenal glands, thymus, and liver) and immune cels - the blood lymphocytes. Results were obtained on the role of free-radical oxidation in combination with exposure to ionizing radiation and immobilization stress at an early stage in the experiment. Gamma radiation in the acute period resulted in significant changes in lipoperoxidation and antioxidant systems. The first period of immobilization stress was marked by the imbalance of LPO-AOS systems disturbance with an accumulation of toxic compounds in tissues which had affected their function. The combined sublethal gamma radiation and immobilization stress disturbed the functional activity of adaptive systems of the body in the early stage of adaptation syndrome. Furthermore, the results show the dominant role of ionizing radiation in it.

Deranged Spermatogenesis of Adult Swiss Albino Mice as Effect of Immobilization Stress -Histological Study.

As the stress is increasing in our life day by day, so we decided to study weather increased stress is one of the causes of infertility. We used immobilisation as stress inducer in our study. Immobilization is mixed type of stress. It acts as physical and psychological stress. The aim of study was to study effect of immobilization stress on spermatogenesis of mice. The present study was performed on 40 adult male Swiss albino mice, out of which 20 served as control and 20 were exposed to immobilization stress .Experimental mice were immobilized by keeping in white transparent plastic jar with 5 holes for 4 hrs a day for 60 days .Food and water provided ad libitum during period of immobilization stress. After two months of immobilization stress mice of both control and experimental group were sacrificed by giving thiopentone anaeshthesia. Testes were removed and labelled. Histological processing of testis tissues was done. Morphological, histological and histomorphometric study of testes revealed suppression of spermatogenesis.

Chewing reduces sympathetic nervous response to stress and prevents poststress arrhythmias in rats

Reducing stress is important in preventing sudden death in patients with cardiovascular disease, as stressful events may cause autonomic imbalance and trigger fatal arrhythmias. Since chewing has been shown to inhibit stress-induced neuronal responses in the hypothalamus, we hypothesized that chewing could ameliorate stress-induced autonomic imbalance and prevent arrhythmias. To test this hypothesis, we analyzed changes in radiotelemetered electrocardiograms in rats that were allowed to chew a wooden stick during a 1-h period of immobilization stress. Chewing significantly reduced the occurrence of ventricular premature beats (VPBs) and complex ventricular ectopy after immobilization and prevented stress-induced prolongation of the QT interval of VPBs throughout the 10-h experimental period. It also prevented prolongation of the QRS complex and fluctuations in the QT interval in normal sinus rhythm beats preceding VPBs during both immobilization and in the poststress period. Fast Fourier transform-based spectral analysis of heart-rate variability further showed that chewing significantly inhibited the stress-induced increase in the power ratio of low-to-high frequency activity (LF/HF: a marker of sympathetic activity) during immobilization and in addition was associated with blunting of the stress-induced increase in plasma noradrenaline observed at the termination of immobilization. Similar suppressive effects on the occurrence of VPBs and the LF/HF were observed in rats that were administered the β-adrenergic blocker propranolol before immobilization. These results indicate that chewing can ameliorate sympathetic hyperactivity during stress and prevent poststress arrhythmias and suggest that chewing may provide a nonpharmacological and cost-effective treatment option for patients with a high risk of stress-induced fatal arrhythmia.

Ultrastructure of rabbit myocardium in the late period of immobilization stress.

Ultrastructure of working myocardium was studied in rabbits subjected to 70-day immobilization in narrow cages excluding active movements. The structure of working cardiomyocytes, nervous apparatus, and microvascular bed in auricles were studied. Particular attention was focused on intercalated disks in muscle fibers, where separation of fasciae adherents was observed, while desmosomes in the lateral area of these contacts were preserved. The role of these findings in triggering of discoordinated contractions of rabbit auricular cardiomyocytes is discussed.

Effect of immobilization stress on testicular germ cell apoptosis in rats.

The influence of immobilization stress on testicular germ cell apoptosis was investigated in rats. A transient increase in serum corticosterone and a transient decrease in serum testosterone were observed during each period of immobilization stress. Twenty-four hours after the last immobilization session, the testicular weight and serum concentrations of corticosterone and testosterone were the same between the immobilization stress and control groups. However, the percentages of apoptotic tubules and apoptotic cells in the stress group were significantly higher than those in controls (P < 0.001). These facts suggest that immobilization stress can enhance testicular germ cell apoptosis in rats.

Quantitative analysis of cutaneous calcitonin gene-related peptide content in response to acute cutaneous mechanical or thermal stimuli and immobilization-induced stress in rats

The effects of various stimuli on restricted skin areas or immobilization-induced stress on the calcitonin gene-related peptide (CGRP) content in rat skin were examined by radioimmunoassay (RIA) and immunohistochemistry. Various stimuli were delivered to the shaven skin of the medial thigh by pinching, brushing, or contact with a glass tube containing hot (50°C) or ice-water for 2 min. To induce immobilization stress, animals were placed in the prone position and wrapped with flexible wire gauze at room temperature. The cutaneous CGRP content determined by RIA as well as the number of CGRP-immunoreactive nerve fibers of the skin were significantly higher at sites stimulated by pinching or ice-water compared to non-stimulated areas within the same animals. However, after brushing, hot water stimulation or any period (2 min, 30 min, 2 h, 6 h, or 3 days × 6 h) of immobilization stress, no differences in cutaneous CGRP content were observed. Plasma corticosterone levels increased after immobilization stress of 30 min or greater, but plasma CGRP level did not change after any period of immobilization stress. These data suggest that some forms of cutaneous stimulation cause a rapid rise in CGRP content in the skin, while emotional stress does not influence the cutaneous CGRP content.

Adrenalectomy attenuates stress-induced elevations in extracellular glutamate concentrations in the hippocampus.

Glucocorticoids and stress have deleterious effects on hippocampal cell morphology and survival. It has been hypothesized that these effects are mediated via an excitatory amino acid mechanism. The present study was designed to evaluate the effects of acute stress on the extracellular levels of glutamate in the hippocampus and to determine if adrenalectomy modifies this response. Rats were adrenalectomized or sham-adrenalectomized and implanted with microdialysis probes in the CA3 region of the hippocampus. Three days later rats were subjected to an acute 1-h period of immobilization stress. Stress significantly increased extracellular glutamate levels in the sham-operated rats, which peaked at 20 min following the initiation of stress. Extracellular glutamate levels also increased immediately following the termination of stress. In the adrenalectomized rats there was a 30% decrease in basal extracellular concentrations of glutamate and a marked attenuation (-70%) of the stress-induced increase in extracellular glutamate levels. Extracellular concentrations of taurine were not modified by adrenalectomy and did not change in response to stress. These results suggest that glucocorticoid-induced elevations in extracellular glutamate concentrations may contribute to the deleterious effects of stress on hippocampal neurons.

Postreceptorial refractoriness of prolactin release mechanisms.

While a first injection of the antidopaminergic benzamide drug, sulpiride, induced a large rise in plasma prolactin (PRL) levels in chronically cannulated adult male rats, a second injection given 2 h later was totally inactive although the pituitary content of the hormone was still 76% of the initial value. When the second injection was given 8 h after the first it was slightly effective, but when administered 24 h later it was as effective as the first. The second of two consecutive injections of haloperidol given at 2-h intervals, or an injection of morphine given 2 h after sulpiride, were incapable of inducing a release of PRL. Two hours after an injection of sulpiride, a 30-min period of immobilization stress induced a significant rise in plasma PRL levels. A significant rise in plasma PRL levels was also observed when larger doses of sulpiride were given 2 h after a first injection of the drug. Apomorphine was at least as effective an inhibitor of PRL secretion when given 2 h after sulpiride than when injected after saline. In vitro studies of dopaminergic binding sites revealed the presence, in pituitary glands of sulpiride-treated rats, of receptors not modified by the drug. These data suggest that the only plausible explanation for the ineffectiveness of the second of two consecutive injections of sulpiride is the development of a state of refractoriness of the mechanisms that subserve the release of PRL induced by suppression of the inhibitory dopaminergic tonus.

Sympatho-adrenal responses of spontaneously hypertensive rats to immobilization stress

Blood pressure, heart rate, and circulating levels of norepinephrine, epinephrine, and corticosterone were measured before and during the first or seventh period of immobilization stress (150 min per day) in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive male rats. A catheter was inserted into the tail artery of each rat to permit direct measurement of blood pressure and heart rate and serial sampling of blood in conscious, unhandled animals. During the first immobilization, SHR rats had significantly higher circulating levels of norepinephrine, epinephrine, and corticosterone than did WKY rats. One day after the sixth immobilization, basal levels of norepinephrine and epinephrine were significantly higher and mean blood pressure was significantly lower in repeatedly stressed SHRs compared to unstressed SHRs. In addition, adaptation to the repeated stress in SHRs was attended by reduced adrenomedullary secretion and an increased blood pressure response. These results demonstrate that adaptive changes in the cardiovascular and sympatho-adrenal medullary systems of repeatedly immobilized rats are greater in SHR than in WKY rats.

Sympatho-adrenal activity of SHR and WKY rats during recovery from forced immobilization

Circulating levels of norepinephrine (NE), epinephrine (EPI), dopamine-β-hydroxylase (DBH), and corticosterone were compared in spontaneously hypertensive (SHR) and Wistar-Kyoto normotensive (WKY) rats during recovery from a 2-hr period of immobilization stress. On the day before the experiments, a catheter was inserted into the ventral caudal artery of each rat to measure directly blood pressure and heart rate and to obtain samples of blood from conscious, unhandled rats. Immediately prior to the period of forced immobilization, while animals were at rest in their home cages, plasma levels of NE and EPI did not differ between rats of the 2 strains. After 2 hr of immobilization, circulating levels of NE, EPI, and DBH were significantly higher in SHR rats than in WKY rats. In contrast, increments in mean blood pressure after 2 hr of stress were greater in WKY rats. When compared to WKY rats, SHR rats had significantly higher circulating levels of NE, EPI, and DBH for up to 4 hr after the period of immobilization. These results are consistent with the view that the sympatho-adrenal medullary system of SHR rats is more responsive than WKY rats to immobilization stress. In addition, in SHR rats, the sympatho-adrenal system remains in a heightened state of activity for a longer period of time following stressful stimulation. The excessive and prolonged discharge of catecholamines into the circulation during stress may be an important factor in the etiology of this form of experimental hypertension.