Magnetic interactions in graphene decorated with iron oxide nanoparticles.

We present the studies of structural and magnetic properties of graphene composites prepared with several quantities ofα-Fe2O3dopant of 5%, 25% and 50% made with either ethanol or acetone. Our studies showed the presence of a weak magnetic order up to room temperature and saturation magnetization close to 0.2 emu g-1in pure commercial graphene. With regard to magnetic properties of our graphene + iron oxide samples, the solvent used during the preparation of the composite had a significant influence on them. For graphene + Fe2O3samples made with acetone the magnetic properties of pure graphene played a major role in the overall magnetic susceptibility and magnetization. On the other hand, for graphene + iron oxide samples made with ethanol we observed the presence of superparamagnetic blocking atT < 110 K which was due to the additional appearance ofγ-Fe3O4nanoparticles. Changes in the synthesis solvent played a major role in the magnetic properties of our graphene + Fe2O3nanocomposite samples resulting in much higher saturation magnetization for the samples made with ethanol. Both the shape and the parameters characterizing magnetization hysteresis loops depend strongly on the amount of iron oxide and changes in the preparation method.

The role of oxytocin and vasopressin in the pathophysiology of heart failure in pregnancy and in fetal and neonatal life.

Pregnancy and early life create specific psychosomatic challenges for the mother and child, such as changes in hemodynamics, resetting of the water-electrolyte balance, hypoxia, pain, and stress, that all play an important role in the regulation of the release of oxytocin and vasopressin. Both of these hormones regulate the water-electrolyte balance and cardiovascular functions, maturation of the cardiovascular system, and cardiovascular responses to stress. These aspects may be of particular importance in a state of emergency, such as hypertension in the mother or severe heart failure in the child. In this review, we draw attention to a broad spectrum of actions exerted by oxytocin and vasopressin in the pregnant mother and the offspring during early life. To this end, we discuss the following topics: 1) regulation of the secretion of oxytocin and vasopressin and expression of their receptors in the pregnant mother and child, 2) direct and indirect effects of oxytocin and vasopressin on the cardiovascular system in the healthy mother and fetus, and 3) positive and negative consequences of altered secretion of oxytocin and vasopressin in the mother with cardiovascular pathology and in the progeny with heart failure. The present survey provides evidence that moderate stimulation of the oxytocin and vasopressin receptors plays a beneficial role in the healthy pregnant mother and fetus; however, under pathophysiological conditions the inappropriate action of these hormones exerts several negative effects on the cardiovascular system of the mother and progeny and may potentially contribute to the pathophysiology of heart failure in early life.

Impaired hypotensive effects of centrally acting oxytocin in SHR and WKY rats exposed to chronic mild stress.

The present study was designed to determine the role of centrally acting oxytocin (OT) in the regulation of blood pressure during chronic mild stress (CMS) in spontaneously hypertensive (SHR; n = 36) and normotensive Wistar-Kyoto (WKY; n = 38) rats. The rats were implanted with osmotic minipumps for intracerebroventricular infusions of 0.9% NaCl, OT, and oxytocin receptor antagonist (OTANT) and divided into two groups: SHR and WKY 1) exposed to 4-wk CMS and 2) not exposed to stress (controls). After 4 wk, hemodynamic parameters were recorded at rest and after an application of acute stressor [air-jet stress (AJS)]. Resting mean arterial blood pressure (MAP) was significantly lower in CMS-exposed SHR and WKY infused with OT than in the corresponding groups receiving saline. Exposure to CMS exaggerated the AJS-dependent pressor response in WKY receiving saline but not in the corresponding group of SHR. OT infusion reduced the AJS-dependent pressor response in both CMS-exposed and not exposed SHR and in CMS-exposed WKY. Intracerebroventricular infusion of OTANT potentiated the AJS-dependent pressor response in both stressed and not stressed WKY rats but not in SHR. The results show that centrally delivered OT decreases resting MAP during CMS in both SHR and WKY rats and that in SHR it reduces pressor responses to AJS under control and CMS conditions, whereas in WKY this effect is significant only after CMS exposure. The study indicates that endogenous centrally acting OT may play an essential role in buffering pressor responses to AJS in CMS-exposed and not exposed WKY rats and that this function is significantly impaired in SHR.

Efficacy of perilesional and intralesional triamcinolone acetonide injections in pemphigus vulgaris lesions of the scalp: an effective therapeutic option.

The scalp is a common location for pemphigus vulgaris (PV), and scalp lesions may be resistant to standard treatment. Perilesional/intralesional triamcinolone acetonide (TA) injections have been used successfully to treat oropharyngeal and ocular involvement in PV. Data on the efficacy of perilesional and intralesional triamcinolone acetonide injections in scalp lesions in PV are lacking. We report two patients with immunopathologically and histopathologically confirmed PV and residual scalp lesions resistant to standard treatment, who were treated with perilesional and intralesional injections of TA 10 mg/mL. Clearance of scalp lesions was achieved after one after, respectively, one and two perilesional and intralesional injections. Perilesional and intralesional TA injections may serve as an effective and safe treatment for recalcitrant scalp lesions in pemphigus.

Oxytocin differently regulates pressor responses to stress in WKY and SHR rats: the role of central oxytocin and V1a receptors.

The role of central oxytocin in the regulation of cardiovascular parameters under resting conditions and during acute stress was investigated in male normotensive Wistar-Kyoto (WKY; n = 40) and spontaneously hypertensive rats (SHR; n = 28). In Experiment 1, mean arterial blood pressure (MABP) and heart rate (HR) were recorded in WKY and SHR rats at rest and after an air-jet stressor during intracerebroventricular (ICV) infusions of vehicle, oxytocin or oxytocin receptor (OTR) antagonist. In Experiment 2, the effects of vehicle, oxytocin and OTR antagonist were determined in WKY rats after prior administration of a V1a vasopressin receptor (V1aR) antagonist. Resting MABP and HR were not affected by any of the ICV infusions either in WKY or in SHR rats. In control experiments (vehicle), the pressor response to stress was significantly higher in SHR. Oxytocin enhanced the pressor response to stress in the WKY rats but reduced it in SHR. During V1aR blockade, oxytocin infusion entirely abolished the pressor response to stress in WKY rats. Combined blockade of V1aR and OTR elicited a significantly greater MABP response to stress than infusion of V1a antagonist and vehicle. This study reveals significant differences in the regulation of blood pressure in WKY and SHR rats during alarming stress. Specifically, the augmentation of the pressor response to stress by exogenous oxytocin in WKY rats is caused by its interaction with V1aR, and endogenous oxytocin regulates the magnitude of the pressor response to stress in WKY rats by simultaneous interaction with OTR and V1aR.

Angiotensin-(1-7) can promote cell migration and tumor growth of clear cell renal cell carcinoma.

Renal cell carcinoma (RCC) is the most common kidney malignancy, accounting for 3% of all cancers. Despite significant advances in targeted therapies and immunotherapy, many patients with RCC develop resistance to available drugs. Angiotensin-(1-7) (Ang-(1-7)) is a heptapeptide and a member of the renin-angiotensin system which regulates the cardiovascular and the renal system. It has been proposed as a potential anticancer agent for the treatment of various types of cancers, but data regarding its efficiency against RCC are conflicting. The aim of our study was to evaluate the effects of Ang-(1-7) in RCC models in vitro and in vivo. We performed a series of in vitro experiments investigating the effects of Ang-(1-7) on cell viability and migration in Caki-1 and Caki-2 cell lines. In addition, we carried out an in vivo study in xenografts of Caki-1 cells in nude mice. In results: Ang-(1-7) or A779, an antagonist of its receptor MasR (Mas receptor), showed no effect on cell viability. Ang-(1-7) promoted cell migration in a dose-dependent manner by inducing the activation of MasR. It also promoted tumor growth in vivo, and this effect was not inhibited by the blockade of MasR. No effects on cell proliferation or tumor vessel density were observed. The results suggest that Ang-(1-7) can exert protumorigenic activity in RCC, however, further research on other RCC models is needed to better recapitulate the heterogeneity of the disease.

Reperfusion injury as a target for diminishing infarct size.

Therapies for preventing reperfusion injury (RI) have been widely studied. However, the attempts to transfer cardioprotective therapies for reducing RI from experiments into clinical practice have been so far unsuccessful. Pathophysiological mechanisms of RI are complicated and compose of many pathways e.g. hypercontracture-mediated sarcolemma rupture, mitochondrial permeability transition pore persistent opening, reactive oxygen species formation, inflammation and no-reflow phenomenon. Based on research, it cannot be determined which mechanism dominates, probably they cooperate with a domination of one or another in different clinical circumstances. Our hypothesis is, that only intervention that at the same time interferes with different (all?) pathways of RI may turn out to be effective in decreasing the final area of infarction.

Early-life inflammation pathways trigger a cascade leading to development of atherosclerotic plaque through the "butterfly effect" - An hypothesis.

Atherosclerosis is a common disease whose complications, such as myocardial infarction, are a leading cause of mortality worldwide. Therefore, ideas which try to explain the circumstances of atherosclerotic plaque initiation and progression are warranted. We hypothesize that low-grade inflammation in early life (especially an imbalance between pro- and anti-inflammatory macrophages) triggers a "butterfly effect" within the arterial wall by initiating a sequence of processes that finally leads to atherosclerotic plaque development and progression. Therefore, pharmacological and non-pharmacological interventions aimed to prevent atherosclerosis development should be applied not only in the adult population over 40 years old (according to current American and European guidelines) but should start in early life.

Aldosterone and mineralocorticoid receptors in regulation of the cardiovascular system and pathological remodelling of the heart and arteries.

In the review we discuss the role of mineralocorticoid receptors (MRs) in regulation and pathological remodelling of the cardiovascular system and the therapeutic potential of pharmacological targeting of MRs in cardiovascular diseases. MRs are expressed in organs involved in cardiovascular homeostasis: brain, heart, kidneys and vessels. The excessive activation of MRs has deleterious effects on the cardiovascular system through sympatho-excitation, elevated salt appetite, and renal retention of salt with consequent positive sodium balance, fibrosis and remodelling of the heart and arteries, and with propensity for atrial and ventricular arrhythmias. Hence, it provides basis for a common pathophysiological milieu of hypertension and heart failure. Furthermore, MR-mediated changes in the cardiovascular system are potentiated by renin-angiotensin system and activation of angiotensin type 1 receptors. Due to low selectivity, MRs bind both aldosterone and GCs - cortisol in humans and corticosterone in laboratory rodents. The binding of GCs to MRs is determined by availability of tissue specific 11ß-hydroxysteroid dehydrogenase of type 1 (11ß-HSD1) or type 2 (11ß-HSD2). 11ß-HSD1 metabolizes GCs to either active or inactive metabolites depending on the presence of special cofactors, whereas 11ß-HSD2 transforms GCs only into inactive metabolites allowing for selective stimulation of MRs by aldosterone. 11ß-HSD2 is expressed in the vascular wall, renal epithelium and some groups of cardiovascular neurons in the brain. In contrast, cardiac expression of 11ß-HSD2 is low, thus, both aldosterone and GCs interact with cardiac MRs. The importance of MRs in the cardiovascular pathology is reflected in clinical guidelines that recommend use of MR blockers, spironolactone and eplerenone, in the treatment of heart failure, myocardial infarction and hypertension. Furthermore, new MR blockers and selective inhibitors of 11ß-HSD1 have been developed and are currently tested in clinical trials.

Upregulation of angiotensin AT1a receptors mRNA in the heart and renal medulla after myocardial infarction in rats.

The myocardial infarct causes prolonged activation of the renin-angiotensin system and profoundly influences cardiac performance and renal excretory capabilities. The aim of the present study was to determine whether the myocardial infarct is also associated with an altered expression of AT1a receptors (AT1aR) mRNA in the heart and the kidney. To this end male Sprague-Dawley rats were subjected either to the left coronary artery ligation or to the sham surgery. Four weeks after the surgery the animals were sacrificed. In 11 infarcted and 10 sham-operated rats expression of AT1aR mRNA in the walls of the left and right ventricle of the heart, and in the renal cortex and renal medulla was determined by semiquantitative PCR method. In another group of 10 infarcted and 14 sham-operated rats the diameter of cardiomyocytes in the left and right cardiac ventricle was determined. The size of the infarct in the rats used for mRNA determination and for morphometric measurements was equal to 29.4 +/- 1.8% and to 31.0 +/- 1.2 % of the left ventricular wall, respectively. Expression of AT1aR mRNA was significantly greater in the left (P< 0.01) and right ventricle (P<0.03) of the heart in the infarcted than in the sham operated rats. AT1aR mRNA expression was also significantly greater (P<0.02) in the renal medulla of the infarcted rats than in the renal medulla of the sham operated rats whereas no significant difference was found in the renal cortex. The myocardial infarct was associated with a significant increase of diameter of cardiomyocytes of the left ventricle of the heart (P< 0.0001), however there was no significant correlation between changes in AT1aR mRNA expression and diameter of cardiomyocytes. The results provide evidence that the myocardial infarct results in significant and prolonged upregulation of AT1a receptors mRNA expression in the heart and in the medullary region of the kidney.

Fluid consumption, electrolyte excretion and heart remodeling in rats with myocardial infarct maintained on regular and high sodium intake.

The purpose of the study was to determine effect of high sodium intake on fluid and electrolyte turnover and heart remodeling in the cardiac failure elicited by myocardial infarction (MI). The experiments were performed on four groups of Sprague Dawley rats maintained on food containing 0.45% NaCl and drinking either water (groups 1, 2) or 1% NaCl (groups 3, 4). Groups 1 and 3 were sham-operated while in groups 2 and 4 MI was produced by the coronary artery ligation. In each group food and fluid as well as sodium intake, urine (Vu), sodium (UNaV), potassium (UKV) and solutes (UosmV) excretion were determined before and four weeks after the surgery. Size of the infarct, left ventricle (LV) weight and diameter of LV and right ventricle (RV) myocytes were determined during post-mortem examination. Before the surgery groups 3 and 4 ingested significantly more fluid and sodium, had higher Vu, UNaV, UKV and UosmV than the respective groups 1 and 2. In groups 2 and 4 MI resulted in significant decrease in Vu, UNaV and UosmV in comparison to the pre-surgical level. In Group 4 MI resulted also in a significant decrease of food and sodium intake. The MI size did not differ in groups 2 and 4 while diameter of LV myocytes was significantly greater in groups 2 and 4 than in groups 1 and 3, and in group 4 than in group 2. The study reveals that prolonged high sodium consumption increases fluid and electrolyte turnover both in the sham and in the MI rats and that the MI causes decrease in food and sodium intake in rats on high but not on regular sodium intake. In addition high sodium diet promotes development of greater post-MI hypertrophy of the LV myocytes.

Simultaneous labeling of vagal innervation of the gut and afferent projections from the visceral forebrain with dil injected into the dorsal vagal complex in the rat.

The vagal innervation of the different layers of the rat gastrointestinal wall was identified with the fluorescent carbocyanine dye Dil, injected into the dorsal motor nucleus of the vagus (dmnX). Multiple, bilateral injections were used to label all dmnX preganglionic motoneurons, and as a consequence, most of the vagal primary afferents that terminate in the adjacent nucleus of the solitary tract (nts) were also retrogradely and transganglionically labeled. With Fluorogold used to label the enteric nervous system completely and specifically, the Dil-labeled vagal profiles could be visualized and quantified in their anatomical relation to the neurons of the myenteric and submucous ganglia. In the myenteric plexus, vagal fibers and terminals were found throughout the gastrointestinal tract as far caudal as the descending colon, but there was a general decreasing proximodistal gradient in the density of vagal innervation. All parts of the gastric myenteric plexus (fundus, corpus, antrum), as well as the proximal duodenum, were extremely densely innervated, with vagal fibers and terminals in virtually every ganglion and connective. Further caudally, both the percentage of innervated myenteric ganglia and the average density of label within the ganglia rapidly decreased, with the exception of the cecum and proximal colon, where up to 65% of the ganglia were innervated. In the gastric and duodenal submucosa very few and in the mucosa no vagal fibers and terminals were found. With both normal epifluorescence and laser scanning confocal microscopy, highly varicose or beaded terminal structures of various size and geometry could be identified. The Dil injections, which impregnated the dmnX as well as the adjacent nts, resulted in retrograde and anterograde labeling of all the previously reported forebrain connections with the dorsal vagal complex. We conclude that the myenteric plexus is the primary target of vagal innervation throughout the gastrointestinal tract, and that its innervation is more complete than previously assumed. In contrast, vagal afferent (and efferent) innervation of mucosa and submucosa seems conspicuously sparse or absent. Furthermore, the use of more focal injections of Dil offers the prospect to simultaneously identify specific subsets of vagal preganglionics and their central nervous inputs.

Association of interferon gamma, tumor necrosis factor alpha and interleukin 6 serum levels with systemic lupus erythematosus activity.

We investigated serum level of interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) using an enzyme-linked immunosorbent assay (ELISA) in 59 patients with systemic lupus erythematosus (SLE) and 16 healthy controls. We examined a possible association between serum levels of these cytokines and SLE activity, as well as correlation between IFN-gamma concentration and the level of TNF-alpha and IL-6 and also IL-6 and TNF-alpha. TNF-alpha and IL-6 were detectable in all 59 patients and normal individuals and their level was significantly higher in SLE patients than in the control group (p < 0.001 and p < 0.02, respectively). In contrast IFN-gamma was detectable in 23 (39%) patients and in only 3 (20%) healthy individuals. We found positive correlation between serum concentration of TNF-alpha and IL-6 with SLE activity and no such correlation with IFN-gamma. We also observed positive correlation between serum levels of IFN-gamma and TNF-alpha, IFN-gamma and IL-6 as well as TNF-alpha and IL-6. In conclusion, an increase in the serum levels of TNF-alpha and IL-6 may be useful markers for SLE activity.

Ethanol-induced changes in Purkinje cells of the rat cerebellum. I. The ultrastructural changes following chronic ethanol intoxication (qualitative study).

The ultrastructural changes in the Purkinje cells from rat cerebellum following 3 months' ethanol treatment were investigated. The changes in both smooth (SER) and rough (RER) endoplasmic reticulum, mitochondria, microtubules lipofuscin granules of the Purkinje cells perikarya and of their dendrites were evaluated. The prominent dilatations were found in the hypolemmal cisternae as well as in SER canals. The canals in the lamellar bodies, which are a form of RER, were decreased in number, and sometimes they were disintegrated and dispersed throughout the cytoplasm of both perikarya and dendrites as single distended cisternae. The microtubules within dendrites were often disorderly oriented. The increased amount of lipofuscin granules in the Purkinje cells perikarya were also noticed. Our results suggest that chronic ethanol intoxication lead to disturbances in the synthetic capacity of the Purkinje cells, since the ultrastructure of both SER and RER was greatly changed.

Ethanol-induced changes in Purkinje cells of rat cerebellum. II. The ultrastructural changes after chronic ethanol intoxication. (Morphometric evaluation).

The morphometric approach to evaluation of some organelles of the rat cerebellar Purkinje cells after chronic ethanol intoxication according to the previously elaborated model (Jedrzejewska et al. 1990) was employed. In the experimental rats volumes of both the perikarya and nuclei in the Purkinje cells significantly increased. The quantitative, morphometric changes of both rough and smooth endoplasmic reticulum demonstrated, that in the perikarya and dendrites of the Purkinje cells the volume of rough endoplasmic reticulum decreased and the volume of smooth endoplasmic reticulum increased. The number of lipofuscin granules in the perikarya increased whereas the counts of microtubules per unit area in dendrites decreased. The statistical evaluation of parameters describing mitochondria and Golgi apparatus in ethanol-intoxicated animals did not show significant differences as compared with the control ones.

Intrastriatal grafts of adrenal medulla in hemiparkinsonian rats--ultrastructural study.

The aim of the study was to investigate the ultrastructure of the right striatum after intrastriatal adrenal medulla grafts in Wistar rats with a 6-OHDA unilateral lesion of the compact part of the right substantia nigra (SN). 12 adult rats were investigated. Two rats were intact, 2 received a sham SN-lesion. Ungerstedt's rotational test confirmed a significant lateral SN-lesion in all the animals. Two weeks after the SN lesion small samples of the adrenal medulla of 2-month old Wistar rats were prepared (0.5 mm3) and implanted stereotaxically into the middle-paraventricular region of the right striatum. The animals were perfused with 2.5% glutaraldehyd according to the following patern: 2--after 1 week of survival, 2--after 3 weeks, 2--after 6 weeks, and 2--after 3 months. 10 samples of ca 1 mm3 were taken from 3 regions of the right striatum (1) the region of the graft, (2) the region in the neighbourhood of the graft, (3) tissue at a long distance from the transplant. Macroscopic observation showed granulomatous-like tissue at the place of the implantation of the graft after 1 week of survival. After 3 weeks and later only the evacuated cavity was observed instead of the graft. A routine electron microscopic procedure was used to expose the material in a JEM 100 B electron microscope. The study of the ultrastructure indicated many leucocytes and microglia cells in the region of the graft as well as features of destruction of the adrenal medulla cells in the rats perfused 1 and 3 weeks after transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

[Basilar migraine in children]. / Migrena podstawna u dzieci.

The authors describe 3 children aged 12-15 years with severe basilar artery migraine. The follow-up was 2-3 years. In all cases attacks of throbbing headache occurred which showed varying intensity and lateralization in 2 cases. Only one child had always very strong right-sided headaches. The accompanying symptoms and signs were mostly from the area of vascularization of the basilar artery. In one child attacks of unconsciousness occurred additionally. The authors suggest that the symptoms and signs from brain-stem structures associated with attacks of headache may be due not only to construction of the basilar artery but may be due to a steal effect from certain regions of the brain stem in the phase of vasodilation, although the primary haemodynamic disturbance may not necessarily develop within the basilar artery system.

[Humoral immunological reactivity in subacute sclerosing panencephalitis]. / Odczynnosc immunologiczna humoralna w SSPE (subacute sclerosing panencephalitis).

In a group of 37 children with SSPE serum protein and cerebrospinal fluid electrophoresis was done (in 34 and 25 cases respectively) determining immunoglobulins in the serum and cerebrospinal fluid in all 37 cases. The obtained results demonstrated a lack of correlation between the changes observed in the serum and cerebrospinal fluid. The most frequent change in the serum was a rise in alpha 2 globulin level (85%) and reduced IgA level (58%), while in the cerebrospinal fluid a rise in gamma globulins (92% of cases) and IgG (100%) was observed most frequently. A comparison of these results with past history of measles, with the clinical course of SSPE and with the survival time of the children showed no correlations. Measles antibodies were determined in the serum and cerebrospinal fluid in 37 children, and the determinations, were repeated several times in the serum of all children and in the cerebrospinal fluid of 9 children. Measles antibodies were found in the serum in all children and in the cerebrospinal fluid in 21 children (57%). The highest titres of antibodies above 1:32 in the cerebrospinal fluid were demonstrated in children with measles at the age up to 2 years. The prognosis was worst in children with acute onset of the disease preceded frequently by cranial injury or infection, with a high serum antibody level and absence of antibody in the cerebrospinal fluid.

[Effect of asymmetric respiratory exercise therapy on respiratory system function; evaluation using spirometric examination in children with idiopathic scoliosis]. / Wplyw leczenia metoda asymetrycznych cwiczen oddechowych na czynnosc ukladu oddechowego, oceniana za pomoca badania spirometrycznego u dzieci z idiopatycznym bocznym skrzywieniem kregoslupa.

Current work presents the results of spirometric examinations in 124 children aged 5 to 16 years (mean age 12.1 years) suffering from idiopathic scoliosis. Children were treated according to asymmetric respiratory exercises method applied in period of 24 days. Healthy children living in Upper Silesia industrial region were the control group. Examined scoliotic group was characterized by generally mild lung function impairment, although the values of spirometric indexes tended to deplete with time of duration and severity of the scoliosis. Especially the tendency of the forced expiratory volume in first second (FEV1) decrease was apparent, as well as maximal expiratory flows MEF50 and MEF25, in conjunction with Cobb angle increase. Slight but evident increase of forced vital capacity (FVC) and FEV1 was observed as a result of rehabilitation utilizing asymmetric respiratory exercises method.

Angiotensin converting enzyme inhibition reduces cardiovascular responses to acute stress in myocardially infarcted and chronically stressed rats.

Previous studies showed that chronically stressed and myocardially infarcted rats respond with exaggerated cardiovascular responses to acute stress. The present experiments were designed to elucidate whether this effect can be abolished by treatment with the angiotensin converting enzyme (ACE) inhibitor captopril. Sprague Dawley rats were subjected either to sham surgery (Groups 1 and 2) or to myocardial infarction (Groups 3 and 4). The rats of Groups 2 and 4 were also exposed to mild chronic stressing. Four weeks after the operation, mean arterial blood pressure (MABP) and heart rate (HR) were measured under resting conditions and after application of acute stress. The cardiovascular responses to the acute stress were determined again 24 h after administration of captopril orally. Captopril significantly reduced resting MABP in each group. Before administration of captopril, the maximum increases in MABP evoked by the acute stressor in all (infarcted and sham-operated) chronically stressed rats and also in the infarcted nonchronically stressed rats were significantly greater than in the sham-operated rats not exposed to chronic stressing. These differences were abolished by captopril. The results suggest that ACE may improve tolerance of acute stress in heart failure and during chronic stressing.