Biomedical subjects

P Lenzi

Publications and source records attributed to P Lenzi.

At least 37 records · Page 2Linked to original sources

PubMed2001

Time-dependent changes in adrenal cortex ultrastructure and corticosterone levels after noise exposure in male rats.

In response to a stressful stimulus, there is a marked activation of the hypothalamic-pituitary-adrenal axis leading to a release of adrenocorticotropic hormone. This, in turn, acts on the zona fasciculata of the adrenal cortex to increase corticosterone plasma levels. Given the frequency of chronic intermittent noise exposure in man, we selected loud noise to evaluate concomitant changes in the ultrastructure of the adrenal cortex and corticosterone release. Following chronic (21 days, 6 h per day) loud white noise exposure (100 dBA, 0-26 KHz), we found the zona fasciculata to be most sensitive to time-dependent ultrastructural changes. These consisted of modifications in cell compartments involved in hormone synthesis and release. On the other hand, we found a progressive increase in corticosterone plasma levels which reached a plateau 9 days after noise exposure. The significance of these changes, in relation to phenomena like sensitization to repetitive stress, are discussed. Furthermore, the present data suggest that chronic loud noise exposure might potentially lead to endocrine dysfunctions.

Adrenal Cortex↗

PubMed2000

Density of perfused brain capillaries in the aged rat during the wake-sleep cycle.

Structural and functional age-related changes in brain vasculature might affect the cerebral microcirculation. The present study evaluated the density of perfused brain capillaries and the perfusion fraction (perfused/existing capillaries) in aged rats (24 months) during the states of the wake-sleep cycle (quiet wakefulness, quiet sleep, active sleep) characterized by different levels of brain activation. The number of perfused capillaries was determined by intravascular injection of the fluorescent marker Evans Blue; histochemical staining of the capillary endothelium identified the alkaline-phosphatase (AP) reactive quota of the anatomical population. No sleep-related changes in perfused capillary density were found, and the perfusion fraction in the AP-stained sub-population was high and stable (95%) across the sleep-wake cycle: changing levels of brain activation during sleep do not affect functional capillary density in aged rats.

Aging↗

PubMed2000

Interindividual differences in the thermoregulatory response to cool exposure in sleeping neonates.

The responses of the thermoregulatory effectors vary greatly among neonates. Therefore, we assume that a small decrease in air temperature from thermoneutrality induces various thermoregulatory responses within neonates that represent an energy cost due to the cold defence processes. To determine the importance of this variability in nursing, 26 neonates were explored at thermoneutrality and in a cool environment (-1.5 degrees C from thermoneutrality) similar to that which occurs currently in clinical procedure. Oxygen consumption (VO2), oesophageal and skin temperatures, as well as sleep parameters were recorded continuously in both conditions. Analysis of all of the data from all of the neonates revealed that the cool exposure induced thermal and sleep disturbances, but VO2 did not increase and was not negatively correlated to body temperature (as might be expected). Analyses of individual data showed large variability in body temperature regulation: the neonates could be assigned to one of three groups according to the direction of the individual slopes of VO2 versus oesophageal or skin temperature. The groups also differed according to the sleep changes recorded in the cool condition. The results show that the definition of thermoneutrality should be revised by incorporating non only changes in the body temperature, but also the sleep disturbances (increased wakefulness and active sleep, decreased quiet sleep), which are criteria that are more sensitive to mild cool exposure. Thermoneutrality should be defined for each individual, since the results stress that the variability does not help to predict a general pattern of thermoregulatory responses in cool-exposed neonates.

Body Temperature↗

PubMed2000

Effects of newly-developed benzodiazepine ligands on noise-induced mitochondrial damage in the rat.

In this study we measured the ability of three newly-synthesized N-arylalkylindol-3-ylglyoxylylamide derivatives, which have recently been characterized as partial agonists at central benzodiazepine binding sites, to prevent the rat cardiac mitochondrial alterations resulting from acute loud noise exposure. In particular, we evaluated the effects of these new compounds on the ultrastructural damage induced by noise stress on the right atrium and ventricle after 6 and 12 hr of loud noise exposure. In parallel experiments, we measured the affinity of these compounds for peripheral benzodiazepine binding sites. Following a single injection of the test products, we observed a cardioprotective effect which was more marked after 6 hr compared with 12 hr of noise exposure. Confirming our recent data showing that full agonists at benzodiazepine receptors produce cardioprotection, we demonstrate in this study that partial agonists, like indolylglyoxylylamides, can also produce a cardioprotective effect. Based on their greater affinity in binding studies, the protective activity seems to be related more to their action at central than at peripheral benzodiazepine receptors.

Animals↗

PubMed2000

Renal synthesis of prostacyclin and thromboxane in healthy women: differential effects of a short-term saline loading.

It is accepted that the urinary excretions of the stable metabolites of prostaglandin (PG)I2 and thromboxane(Tx) A2, 6-keto-PGF1alpha (6KPGF) and TxB2 respectively, provide an accurate estimate of both basal and stimulated renal synthesis of their precursors. The excretory profile of these metabolites has been evaluated in healthy women submitted to a short-term expansion in extracellular fluid volume. Salt retention (SR group, n=6) was induced by physiological saline (0.9% NaCl) i.v. infusions (2 L per day) over a period of 2 days. On the third day the increase in body weight was 0.92 +/- 0.27 kg (P<0.05). The results of the study have been compared to those previously obtained in normal balance of sodium and potassium (N group, n=20) and in induced salt depletion (SD group, n=14). A common study protocol was used. Basal values of plasma renin activity (PRA) and urinary aldosterone excretion were determined. Renal functional exploration [clearance (cl.) method] was performed during hypotonic polyuria (induced by oral water load) and subsequent moderate antidiuresis (induced by low-dose infusion of an antidiuretic hormone analogue). Urinary 6KPGF and TxB2 concentrations were estimated by RIA method and their urinary excretions were determined at both high and low urinary flow rates. The linear regressions of the urinary metabolite excretions vs. urinary flow rate were estimated by using the data obtained in both hypotonic polyuria and antidiuresis. Salt retention (SR vs. N group) was effective in decreasing the basal values of plasma renin activity and urinary aldosterone excretion. Moreover, during hypotonic polyuria it was effective in increasing the absolute and fractional excretions of sodium and chloride, in the absence of significant variations in mean arterial pressure and creatinine cl. Regarding urinary prostanoid excretions the following results were obtained. 1. Comparative data for hypotonic polyuria. In the SR vs. N group, the urinary excretion of 6KPGF was significantly higher, whereas that of TxB2 was not significantly different. In the SR vs. SD group, the urinary excretion of 6KPGF was not significantly different, whereas that of TxB2 was significantly lower. 2. Comparative data for the regression lines of the urinary prostanoid excretions vs. diuresis. In the SR vs. N group, the regression line slope for 6KPGF excretion was significantly higher, whereas that for TxB2 excretion was not significantly different. In the SR vs. SD group, the regression line slope for 6KPGF excretion was not significantly different, whereas that for TxB2 excretion was significantly lower. 3. Correlative data in the SR group during hypotonic polyuria. The plasma chloride concentration was positively correlated with urinary flow rate, absolute and fractional chloride excretions, and 6KPGF excretion but not with TxB2 excretion. In conclusion, functionally effective salt retention in healthy women induces a selective stimulation of renal synthesis of prostacyclin, unlike salt depletion, in which the synthesis of both PGI2 and TxA2 is upregulated.

6-Ketoprostaglandin F1 alpha↗

PubMed2000

Ultrastructural localization of calcium deposits in rat myocardium after loud noise exposure.

In previous studies we demonstrated that loud noise exposure induces ultrastructural alterations in the rat myocardium together with an increase in noradrenergic activity and in mitochondrial calcium influx. To verify the causal relationship between myocardial calcium entry and ultrastructural alterations induced by loud noise, in the present study we coupled routine electron microscopy with cytochemistry specifically dedicated to visualize calcium accumulation (revealed as antimonate deposits). We observed that the ultrastructural alterations occurring in both atrium and ventricle after 12 h of noise exposure, were densely packed with antimonate deposits. In particular, enlargements of the sarcoplasmic reticulum and dilution of the mitochondrial matrix, observed during routine electron microscopy, were markedly positive for calcium accumulation when observed by using antimonate. The present data strongly suggest that calcium entry results in accumulation of this ion at myocardial subcellular level. Moreover, the present results joined with previous evidence indicate that calcium accumulation is the final common pathway responsible for noise-induced myocardial morphological alterations.

Animals↗

PubMed2000

Cerebral circulation in REM sleep: is oxygen a main regulating factor?

In the transition from NREM to REM sleep, as in other instances of brain activation, a marked increase in cerebral blood flow and glucose uptake is observed, together with a lesser increase in O2 uptake. Brain activation also entails an increase in capillary PO2 and lactate production. The hypothesis of saturation of the oxidative machinery was advanced to explain anaerobic glycolysis and lactate production in the presence of high PO2, but data are available that cannot be explained by this hypothesis: hypoxic spots exist in the brain, augmenting in arterial hypoxia and disappearing in arterial hyperoxia, while tissue [H+] lowers as arterial PO2 increases beyond 100 mmHg. Additional hypotheses are thus required. We suggest that O2 diffusion limitation exists in the brain: microregions lying at mid-distance between capillaries may become hypoxic and partly resort to anaerobic glycolysis. These microregions are thought to enlarge with increasing metabolic rate or arterial hypoxia and give rise to vasodilatatory signals regulating local blood flow. REM sleep time is strongly reduced by hypoxic and increased by hyperoxic atmosphere, in accordance with the existence of an O2 diffusion limitation. Any pathological decrease in arterial PO2 and/or O2 delivery creates a specific risk in REM sleep.

Animals↗

PubMed1999

Central and peripheral benzodiazepine ligands prevent mitochondrial damage induced by noise exposure in the rat myocardium: an ultrastructural study.

Noise represents an environmental stress factor affecting several organs and apparatuses, including the cardiovascular system. In experimental animals undergoing noise exposure, subcellular myocardial changes have been reported, especially at the mitochondrial level. In previous studies we found that diazepam, acting at both central and peripheral benzodiazepine receptors, prevented the onset of this myocardial damage. In the present study, we investigated the specific role played by central and/or peripheral benzodiazepine receptors in preventing noise-induced myocardial alterations. In particular, the effect of clonazepam as a selective ligand for central sites, in comparison with the efficacy of ligands selective for peripheral sites, such as Ro 5-4864 and PK-11195, was evaluated. Rats were pretreated with the test drugs 30 min before exposure to noise for 6 or 12 hr and then sacrificed. After fixing, samples of right atrium and ventricle were taken and processed for either transmission or scanning electron microscopy. After 6 hr of noise exposure, only the atrium exhibited significant mitochondrial alterations, whereas after 12 hr both atrium and ventricle were damaged. As expected, diazepam prevented noise-induced mitochondrial injury at both 6 and 12 hr. By contrast, clonazepam was effective only after 6 hr. The peripheral ligand PK-11195 attenuated mitochondrial damage at both 6 and 12 hr, whereas Ro 5-4864 was effective only after 12 hr. In the present study, we confirm that noise exposure induces mitochondrial damage in the rat myocardium. Drugs acting at both central and peripheral benzodiazepine receptors significantly prevent this damage. Differences in the amount and in the duration of the protective effect might depend on variability in the potency and in the pharmacokinetics of the specific drugs.

Animals↗

PubMed1999

Bilateral dimorphism of Loewenthal's gland in young male albino rats: an ultrastructural investigation.

This study represents a further contribution to our knowledge about the structure of Loewenthal's gland. There are several divergences in the available literature on the topic, concerning both the histological and ultrastructural findings. However, in these studies, the authors did not take into account the potential influence of a putative side-dependent dimorphism previously reported by us. We therefore carried out histological and electronmicroscopic observations specifically aimed at evaluating the importance of the gland shape for its structure. In particular, in male albino rats aged 70-120 days, we compared the structure of the left and right glands. Depending on the side undergoing morphological investigation, we observed differences in the acini, cells, nuclei, endoplasmic reticulum, Golgi apparatus and granular content. Apart from slight individual differences, we found that structural variations were most frequently observed in glands displaying a more evident macroscopic side-specific dimorphism. Our findings demonstrate that several conflicting data in the literature dealing with the structure of Loewenthal's glands might be explained by the morphofunctional side-dependent dimorphism of the organ.

Aging↗

PubMed1999

Renal prostanoids: physiological relevance in healthy salt-depleted women.

The effective role played by prostanoids in the control of renal function has been investigated in healthy women with salt depletion. Salt depletion (SD2 group, n = 6) was induced by low sodium chloride dietary intake (< or = 60 mmol per day) and combined treatment with natriuretic and potassium-sparing drugs. At the end of the depletive treatment, the cumulative sodium deficit was 513 +/- 56 mmol. The renal function and urinary excretions of prostaglandin (PG) E2, 6-keto-PGF1 alpha (6KPGF) and thromboxane (Tx) B2 were evaluated during hypotonic polyuria. The basal values of plasma sodium and potassium concentrations, plasma renin activity (PRA) and urinary aldosterone excretion were determined before the induction of hypotonic polyuria. Paired studies were performed in the absence (control) and presence of indomethacin both in the SD2 group and in a previously studied group (N2, n = 6) of healthy women in normal sodium and potassium balance. Women in normal balance received 100 mg i.m. of indomethacin, salt-depleted women received only 50 mg (because 100 mg of the drug produced a prolonged anuria). In the SD2 vs. N2 group in the absence of treatment the following significant differences were found: (a) higher basal values of PRA and urinary aldosterone excretion; (b) higher urinary excretions of 6KPGF and TxB2 but not of PGE2; (c) lower values of urinary flow rate, creatinine clearance, absolute and fractional excretions of sodium and chloride, plasma osmolality and plasma electrolyte concentrations. The effects of the indomethacin have been assessed as percentage variations by using paired data for each experimental group. In the SD2 vs. N2 group the reduction in urinary excretions of 6KPGF, TxB2 and potassium as well as in creatinine clearance were not significantly different. On the other hand, the following were significantly different: (a) the lower reduction in PGE2 excretion; (b) the higher reduction in urinary flow rate and in CH2O; (c) the reductions in absolute and fractional excretions of sodium and chloride, and the increase in plasma potassium concentration, significant in the SD2 group but not in the N2 group. The data suggest that: (1) when stimulated by salt depletion the renal biosynthetic pathways of PGI2 and TxA2 showed greater sensitivity to indomethacin inhibition; (2) the effects of the neurohormonal systems activated by salt depletion were either modulated or mediated by renal prostanoids.

Adult↗

PubMed1999

Role of peptidase and cyclooxygenase inhibitors in the guinea-pig bronchial response to the synthetic endothelin ET(B) agonist IRL 1620 and antagonist BQ-788.

In isolated guinea-pig bronchial preparations the selective endothelin ETB agonist, IRL 1620 caused a concentration-dependent contraction. The pD2 value (7.16 +/- 0.09, n = 6) was significantly increased in the presence of peptidase inhibitors (thiorfan 1 microM, captopril 1 microM, bestatin 1 microM) (pD2 = 7.75 +/- 0.09, n = 6). Indomethacin (5 microM) did not appear to influence the ETB-agonist pD2 value (6.92 + 0.11, n = 6) but potentiated its maximal response significantly (67.23 +/- 4.81% vs. 53.37 +/- 4.80%). The concentration-response curve for the contractile response to IRL 1620 (pD2=7.83 +/- 0.01, n=16); was reproducible, although not completely, since the second curve to this selective ETB agonist was shifted significantly to the right (pD2 = 7.34 +/- 0.09, n = 16) and a decrease in the maximal response was observed (20.0 +/- 2.0%). BQ 788, a selective antagonist for ETB receptors, employed in concentrations ranging from 1.5 to 150 nM, caused a dose-dependent shift to the right of the concentration-response curve to IRL 1620, with a pIC50 value of 8.11 +/- 0.03; this action was not influenced by adding enzyme inhibitors (pIC50 = 8.17 +/- 0.29). Our data show that IRL 1620 undergoes a hydrolytic metabolism in guinea-pig bronchial preparations, which could influence the calculation of the pD2. Pretreatment of the tissue with peptidase inhibitors and indomethacin is consequently significant in the evaluation of IRL 1620 activity, while it does not influence the action of the antagonist, BQ 788.

Animals↗

PubMed1999

Renal function and urinary prostanoid excretions in salt-depleted women: comparative effects of enalapril and indomethacin treatments.

The acute effects on urinary prostanoid excretion and on renal function induced by pharmacological inhibition of either the angiotensin-converting enzyme or of the cyclooxygenase system, respectively, have been studied in healthy salt-depleted women. Two experimental groups were studied during salt depletion, SD1 (n=8) and SD2 (n=6). Salt depletion was obtained by combining a low sodium chloride dietary intake (< or =60 mmol per day) with natriuretic and potassium sparing treatment. Paired studies were performed in the absence and in the presence of enalapril (SD1 group) or indomethacin (SD2 group). In both paired studies renal function was estimated by the clearance (cl.) method and the urinary concentrations of PGE2, 6-keto-PGF1alpha and TXB2 were estimated by RIA during sustained hypotonic polyuria (induced by oral water load). Enalapril did not influence urinary excretion of prostanoids. Its main significant effects were: (a) a reduction in mean arterial pressure (MAP); (b) an increase in free-water cl. (C(H2O)) and a reduction in osmolar cl. (Cosm); (c) a reduction in the absolute and fractional urinary excretions of sodium and chloride; and (d) a reduction in both the plasma concentration and urinary excretion of potassium. The urinary flow rate and the creatinine cl. were not significantly affected. Indomethacin reduced urinary excretion of prostanoids and in addition it produced the following significant effects: (a) a reduction in urinary flow rate, C(H2O) and Cosm values, and in absolute and fractional urinary excretions of sodium and chloride; and (b) an increase in plasma potassium concentration. MAP, creatinine cl. and urinary potassium excretion were not significantly affected. With regard to the main parameters, both enalapril and indomethacin exerted similar effects on urinary sodium and chloride excretion but opposite effects on C(H2O) and plasma potassium concentration. In conclusion, after enalapril in a salt-depleted state, the functional expression of acute angiotensin II deprivation was partially masked by the activation of a homeostatic system responsible both for improvement in renal salt conservation and for facilitated cellular potassium uptake. After indomethacin in the same setting, the results were consistent with a differential role of prostanoids in modulating or mediating the activities of neuro-hormonal agonists.

6-Ketoprostaglandin F1 alpha↗

PubMed1999

Cerebral blood flow regulation in REM sleep: a model for flow-metabolism coupling.

The pattern of metabolic and circulatory changes occurring during REM sleep in the whole brain is also observed at a regional level in different instances of functional activation. This pattern is characterized by an increase in metabolic rate, blood flow, glucose and oxygen uptake, the increase in glucose uptake generally exceeding oxygen uptake. A model of interpretation is presented, based on the assumption that substantial limitation to oxygen diffusion exists in the brain. According to the model, microregions lying at mid-distance between capillaries may become hypoxic, depending on metabolic rate and blood-cell PO2 difference. At increasing metabolic rates, O2 consumption in pericapillary microregions increases and the PO2 drop becomes steeper. As a consequence, in microregions far from capillaries a decrease in O2 availability occurs, in concomitance with the increase in metabolic rate, so that non-oxidative glucose metabolism develops locally. A similar spatial PO2 pattern forms in the case of arterial hypoxia, when capillary PO2, and then blood-cell PO2 difference, is reduced. The hypoxic microregions are the source of vasodilatatory messages, the consequent vasodilatation increasing average capillary PO2 and then favoring O2 diffusion to the tissue. Oxygen thus appears to be a better candidate than glucose as a mediator of blood flow-metabolism coupling. This is supported by its higher extraction fraction and by the fact that, in physiologic conditions, arterial hypoxia (and not hypoglycemia) acts on cerebral blood flow. Moreover, the diffusion capacity of glucose in the brain is higher than that of oxygen, so that diffusion limitation is more likely to occur for oxygen. The present model allows consistent organization of the stereotyped changes in cerebral blood flow and glucose and oxygen uptake occurring both in REM sleep and in other instances of brain activation.

Animals↗

PubMed1999

Long-term exposure to noise modifies rat adrenal cortex ultrastructure and corticosterone plasma levels.

Female rats were exposed to noise 6 h daily for 7 or 21 days running. The effects of stress were evaluated both on adrenal cortex ultrastructure and on plasma corticosterone levels. Subcellular examination showed a marked involvement of each zona of the adrenal cortex. In particular, we observed various alterations, the most frequent consisting of diluted matrix and cristolysis of mitochondria and swelling of smooth endoplasmic reticulum membranes. These morphological changes were most prominent after longer exposure to noise. Similarly, corticosterone plasma levels significantly increased over the time of application of noise stimulus. The present findings indicate that prolonged exposure to loud noise induced structural and functional modifications in the adrenal gland. These data might be potentially relevant in contributing to explain the effects induced in humans exposed to loud noise in a variety of environmental conditions.

Adrenal Cortex↗

PubMed1998

Effects of experimental salt depletion on urinary prostanoid excretions in normal women.

The effects of moderate salt depletion on urinary excretions of prostanoids (PG)E2, 6-keto-PGF1alpha (6KPGF) and thromboxane (TX)B2 have been investigated in healthy women (SD group, n = 14). Salt depletion was obtained by combining a low sodium chloride dietary intake (< 60 mmol per day) with natriuretic and potassium sparing treatment. At the end of the treatment, the cumulative sodium deficit was 438 +/- 42 mmol (mean +/- SEM). Plasma renin activity (PRA) and urinary aldosterone excretion were determined in basal conditions. Renal functional exploration was performed during hypotonic polyuria (by oral water load) and subsequent moderate antidiuresis (by low dose infusion of an antidiuretic hormone analogue). In both phases, renal function was estimated by the clearance (cl.) method and the urinary concentrations of PGE2, 6KPGF and TXB2 by RIA method. The control group was composed of 20 healthy women in normal sodium and potassium balance (N group). Salt depletion was effective in increasing the basal values of plasma renin activity (PRA) and urinary aldosterone excretion. Moreover, it was effective in inducing the following during polyuria: (a) a depression of the diuretic response to water load in presence of a reduction in plasma osmolality; (b) a reduction in creatinine cl. in the absence of significant changes in mean arterial pressure; (c) an increase in the fractional reabsorption of sodium and chloride, in particular at the level of the diluting segments. Both in polyuria and in antidiuresis, the excretions of 6KPGF and TXB2 were higher in the SD vs. N group, while the excretion of PGE2 was not significantly different. In SD and N pooled groups, significant positive correlations were shown between basal PRA and urinary excretions during polyuria of 6KGPF and TXB2, (but not of PGE2) as well as between the excretions of the two metabolites. In conclusion, functionally effective salt depletion induces in healthy women a stimulation of renal synthesis of both prostacyclin and thromboxane. The excretory data do not give evidence of a similar effect on PGE2 synthesis.

6-Ketoprostaglandin F1 alpha↗

PubMed1998

Ultrastructure of rat atrial tissue after either perfusion-or immersion-fixation both in vivo and in vitro study: comparison of methodological reliability.

The present study compares, from a morphological point of view, the possible differences between perfusion- and immersion-fixation techniques performed on rat myocardium in order to evaluate their reliability. The data we obtained showed that when the two techniques are carried out with particular care, they do not present significant differences in tissue preservation. Furthermore, we also evaluated the ultrastructural of rat myocardium at the end of in vitro experiments. In this case, signs of subcellular changes, such as vacuolar degeneration, swollen mitochondria, intermyofibrillar myelin-like figures and enlargements of non specialized junctions of the intercalated discs can frequently occur. So, our results indicate that the morphological integrity of myocardium is not completely preserved during in vitro investigations.

Animals↗

PubMed1998

Diazepam reduces ultrastructural changes induced by noise stress in rat adrenal gland.

Male rats were exposed to noise for 6 running hours and the effects of pretreatment with the benzodiazepine diazepam on the adrenal gland were evaluated. Ultrastructural examination showed that, after noise exposure, zona reticularis cells resulted the more affected, exhibiting areas of diluted cytoplasm, disarranged endoplasmic reticulum, membrane vestigia and some altered mitochondria; diluted cytoplasmic areas appeared in noradrenaline-storing cells, too. On the contrary, zona reticularis cells from diazepam-pretreated and noise-exposed rats resulted significantly less altered, as well as the noradrenaline-storing cells. The present findings indicate that diazepam is able to exert some protective action on adrenal gland alterations due to noise exposure.

Adrenal Cortex↗

PubMed1997

SEM/TEM investigation of rat cardiac subcellular alterations induced by changing duration of noise stress.

BACKGROUND: Many studies have shown that loud noise is an environmental stressor. Noise exposure causes changes at different levels in living beings; the cardiovascular system, considered to be the most affected apparatus, has received much attention in both animals and humans. The present study investigated the effect of changing duration of noise stimulation on rat myocardium to determine whether the responses could be related to time. METHODS: The study was performed on young albino male rats. Three groups of animals were exposed to white noise (100 dBA) for 1, 6, and 12 hr, respectively, and samples of right atrium and ventricle were processed for ultrastructural examination. The subcellular organization of cardiomyocytes was examined by transmission and scanning electron microscopy, the latter being carried out with the modified osmium maceration method. RESULTS: After 1 hr of noise exposure, atrial and ventricular cardiomyocytes did not present significant alterations. After 6 hr, changes were observed in atrial tissue at the mitochondrial level, whereas the ventricular structure appeared unaffected. After 12 hr of treatment, in addition to the mitochondrial alterations, changes in atrial and ventricular myocardium, consisting of areas of enlargement in intercalated disc membranes and decreased density in sarcoplasm, were detected. CONCLUSIONS: The methods we applied for the visualization of cellular organelles allowed us to demonstrate that atrial tissue is primarily involved in stress response, especially at the mitochondrial level; a more prolonged time of exposure seems to be necessary for ventricular involvement.

Animals↗