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PubMed1989

[Atrial natriuretic factor in cardiogenic shock, in hypovolemic shock and in the bradycardia-hypotension syndrome following acute myocardial infarction].

The aim of this paper was to study plasma atrial natriuretic factor, renin activity, aldosterone and antidiuretic hormone in low-output heart failure syndromes such as cardiogenic shock, hypovolemic shock and hypotension with bradycardia syndrome. A total of 30 patients were investigated: 10 with cardiogenic shock due to acute myocardial infarction of the anterior wall (systolic and diastolic blood pressure 56.0 +/- 3.7/40.5 +/- 2.0 mmHg; heart rate 119.7 +/- 1.2 beats/min; central venous pressure 16.2 +/- 0.6 cmH2O) (I group), 10 with hypovolemic shock induced by melena in peptic ulcer (systolic and diastolic blood pressure 74.5 +/- 1.5/57.5 +/- 1.7 mmHg; heart rate 111.0 +/- 1.4; central venous pressure 6.3 +/- 0.5 cmH2O) (II group), 10 with hypotension with bradycardia syndrome which occurred in patients during acute myocardial infarction of the inferior wall (systolic and diastolic blood pressure 71.9 +/- 2.0/58.0 +/- 2.6 mmHg; heart rate 52.0 +/- 2.2 beats/min; central venous pressure 4.6 +/- 0.4 cmH2O) (III group). Plasma atrial natriuretic factor values were measured using radioimmunoassay after chromatographic pre-extraction; plasma renin activity, aldosterone and antidiuretic hormone values were calculated using radioimmunoassay. Circulating atrial natriuretic factor was significantly (p less than 0.01) higher in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) than in healthy volunteers (8.4 +/- 0.3 pg/ml). In the former there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the IInd and IIIrd groups of patients were in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Homoharringtonine induces heat protection and facilitates dissociation of heat shock transcription factor and heat shock element complex.

We investigated the effects of combined treatment with homoharringtonine (HHT) and hyperthermia on cytotoxicity and transcriptional regulation of heat shock genes in human colon carcinoma (HT-29) cells. The drug (100 ng/ml) which inhibited protein synthesis by 93% protected cells from killing at 43 degrees C. For example, treatment with HHT 2 hr before and during heating produced a 9-fold increase in survival from 3.7 x 10(-2) to 3.2 x 10(-1) after 10 hr at 43 degrees C. Little or no protection was observed if the drug was added only during heating. Interestingly, adding the drug (100 ng/ml) 2 hr before and during heat facilitated the dissociation of heat shock transcription factor-heat shock element (HSF-HSE) complex during continuous heating at 43 degrees C. These findings related to the literature suggest that the free pool of HSC70 is increased by inhibiting protein synthesis. An increase in the level of free HSC70 may more effectively protect or repair thermolabile targets and consequently affect regulation of heat shock response.

Antineoplastic Agents, Phytogenic↗
PubMed1995

Expression of heat shock factor and heat shock protein 70 genes during maize pollen development.

We have analysed the expression of heat shock protein 70 (HSP70) and heat shock factor (HSF) gene during maize pollen development, HSFs being the transcriptional activators of hsp genes. In order to eliminate the sporophytic tissues of anthers, we have isolated homogeneous cell populations corresponding to five stages of maize pollen development from microspores to mature pollen. We show that in the absence of heat stress, hsp70 genes are highly expressed late-bicellular pollen as compared to other stages. HSP70 transcripts are significantly accumulated in response to a heat shock at the late microspore stage but to a much lower extent than in vegetative tissues. The latest stages of pollen development, i.e. mid-tricellular and mature pollen, do not exhibit heat-induced accumulation of HSP70 transcripts. Therefore, we analysed the expression of hsf genes throughout pollen development. We demonstrate that at least three hsf genes are expressed in maize and that transcripts corresponding to one hsf gene, whose expression is independent of temperature in somatic as well as in microgametophytic tissues, are present at similar levels throughout pollen development. In addition, we show that the expression of the two other hsf genes is heat-inducible in maize vegetative tissues and is not significantly increased after heat shock at any stage of pollen development. These results indicate that the loss of hsp gene expression at late stages of pollen development is not due to a modification of hsf gene expression at the mRNA level and that hsf gene expression is differentially regulated in vegetative and microgametophytic tissues.

Amino Acid Sequence↗
PubMed1994

Skeletal muscle oedema and muscle fibre necrosis during septic shock. Observations with a porcine septic shock model.

In domestic pigs, intermitted application of Escherichia coli-endotoxin was used to create an animal model for a prolonged hypo- and hyperdynamic septic shock-like state and to investigate mechanisms of multiple organ failure. Here, we describe the changes in skeletal muscle after 18 h (2 animals) and 48 h (6 animals) of septic shock. Two pigs for each observation period that received physiologic saline solutions instead of endotoxin served as controls. The earliest lesions were endothelial cell damage with endomysial oedema and swelling of mitochondria in muscle fibres. With increasing degree of endothelial cell damage, pericytes showed degenerative changes with cytoplasmic fragmentation and karyolysis. After 48 h of shock, endomysial oedema was increased with fibrinogen present. Muscle fibre diameters were increased and swollen mitochondria and segmental necrosis of muscle fibres were frequently observed. However, phagocytic reaction or regenerative changes were not detected. In this respect, skeletal muscle lesions in septic shock differ from ischemic damage, which is characterized by early phagocytosis. Tumour necrosis factor alpha (TNF alpha) was increased greatly and significantly in the serum of the pigs that received endotoxin. The lesions described may be the result of both direct damage to muscle fibres by the endotoxin and/or the increased levels of TNF alpha and indirect damage because of the increased diffusion distance, due to the endomysial oedema. The loss of blood proteins into the endomysium may also play a role in generating hypoproteinemia in patients with septic shock.

Animals↗
PubMed1981

[Pathology and pathophysiology of circulatory shock with respect to shock lung (author's transl)].

The circulatory and acute generalized failure of the circulation, in particular of the lesser peripheral circulation, and may possibly but not necessarily be accompanied by a decrease in blood pressure and damage to the tissue due to a lack of oxygen. The main question concerning the causal pathogenesis of shock is still unsettled, but an interaction between a lack of oxygen as well as of other factors, like endotoxin, complements and vasoactive amines, and the presence of a microthrombosis must be held responsible for the appearance of this condition. In modern intensive medicine the lung must be considered as the preferential area for the manifestation of shock. The clinical picture of shock lung may be described as acute respiratory deficiency accompanied by an impaired diffusion of oxygen, an increase in dead-space ventilation together with an increased shunt volume and intensified respiratory activity. The pathology of shock lung shows two phases and has its onset in exudative alveolitis followed by alveolar fibrosis which can be hardly be controlled by therapy. The early phase of shock lung manifesting itself by exudative alveolitis is decisive with regard to diagnosis and further therapeutic measurements. If the condition can be brought under control at this stage there is a chance that the patient may survive.

Disseminated Intravascular Coagulation↗
PubMed2003

Muscle perfusion and oxygen consumption by near-infrared spectroscopy in septic-shock and non-septic-shock patients.

OBJECTIVE: To measure muscle blood flow (Qtis) and oxygen consumption (VO(2)tis) in septic and non-septic critically ill patients by near-infrared spectroscopy (NIRS). SETTING: Surgical intensive care unit of a university hospital. PATIENTS AND PARTICIPANTS: Four patients with septic shock, eight post-surgical critically ill patients and ten healthy volunteers. MEASUREMENTS AND RESULTS: Oxyhaemoglobin (HbO(2)) and deoxyhaemoglobin (HbH) variations after venous occlusion were measured by NIRS in the brachioradialis muscle. We calculated Qtis by the rate of HbO(2) and HbH increase in the first 30 s of venous occlusion divided by haemoglobin blood concentration. VO(2)tis was calculated by subtraction of the arterial HbH from the initial increase of HbH after venous occlusion extrapolated to 1 min. Tissue oxygenation index [TOI = HbO(2)/(HbO(2)+HbH)] was also measured before venous occlusion. Two measurements in patients with septic shock, and one measurement in non-septic-shock patients and healthy subjects, were obtained. Of the measurements, 35% were repeated because of low-quality NIRS signal. VO(2)tis and Qtis were two times larger ( P<0.05) in patients with septic shock than in patients without and in healthy subjects. The TOI was very similar among the three groups. CONCLUSION: In septic-shock patients the increase in VO(2)tis was associated with an equivalent increase in Qtis. Therefore, tissue O(2) supply does not seem to be a limiting factor for muscle O(2) consumption. NIRS combined with venous occlusion allows a rapid, non-invasive and simultaneous assessment of regional perfusion and oxygen consumption. In case of microcirculatory shunt occurrence, the TOI should be cautiously used to assess tissue oxygenation state.

Aged↗
PubMed1984

Culture shock. Synthesis of heat-shock-like proteins in fresh primary cell cultures.

The isolation of Xenopus liver, lung and testis cells by collagenase digestion of the tissue, followed by Percoll density gradient centrifugation, was characterized by the preferential synthesis of two proteins whose size and charge were similar to 70 and 85 kD heat-shock proteins. The synthesis of these two heat-shock-like proteins, relative to that of total protein, declined gradually in the first 3-4 days after the cells were plated out for primary culture. In fresh primary cultures of liver parenchymal cells albumin mRNA concentration declined rapidly and plateaued at 3-4 days of culture. Freshly isolated male Xenopus hepatocytes were refractory to induction by estrogen of vitellogenin gene transcription but they reacquired hormonal response during the first 3 days of culture. Both of these differentiated phenotypic functions of the Xenopus hepatocytes were quantitatively associated with the decline in synthesis of hsp-like proteins in freshly prepared primary cell cultures. Freshly isolated or heat-shocked hepatocytes exhibited a rounded shape with little intercellular contacts, whereas during the recovery period of 3 days they acquired a flattened shape with a high degree of intercellular and cell-substratum interaction. These results present the first evidence for the preferential synthesis of heat-shock-like proteins by procedures for establishing primary cell cultures. They emphasize the necessity of monitoring normal and heat-shock protein synthesis and cell morphology before using primary cell cultures for studying normal regulatory and developmental processes.

Albumins↗
PubMed1987

Accumulation of heat shock protein 70 RNA and its relationship to protein synthesis after heat shock in mammalian cells.

Heat stress induces a set of heat shock proteins (hsps) in a wide variety of species. In response to either a mild (5 min X 45 degrees C) or severe (30 min X 45 degrees C) heat shock, the timing of expression of the hsps and the recovery of general protein synthesis in rat embryonic fibroblasts was dependent on the duration of the hyperthermic exposure. Synthesis of mRNA coding for an hsp of Mr approximately equal to 70,000 (hsp 70) followed immediately after the mild heat shock but was delayed after the severe heat shock. Appearance of the hsps paralleled the synthesis and decay of RNA and was indicative that new RNA synthesis was required for hsp 70 expression. Inhibition of protein synthesis by cycloheximide after the mild heat shock increased the maximal accumulation of hsp 70 encoding mRNA but did not prevent the subsequent decrease in this mRNA species. These results suggest that mammalian cells control the expression of hsp 70 primarily at the level of transcription, and that the normal pattern of hsp 70 mRNA turnover after an inducing heat stress is not dependent on new protein synthesis.

Animals↗
PubMed2004

Coactivator ASC-2 mediates heat shock factor 1-mediated transactivation dependent on heat shock.

Upon exposure to elevated temperatures, mammalian cells increase the expression of the heat shock proteins (HSP) through activation of the heat shock factor 1 (HSF1). Since most transcription factors require coactivators for efficient transcriptional activity, we tried to identify the coactivator(s) that interacts with and modulates the activities of HSF1. In vitro glutathione S-transferase (GST) pull-down assay revealed that HSF1 strongly interacts with activating signal cointegrator (ASC)-2 and weakly with cyclic adenosine monophosphate responsive element binding protein (CBP). We also show that cotransfection of ASC-2, but not CBP, potentiates HSF1-mediated transactivation based on its cognate element (heat shock element, HSE) linked to luciferase reporter. The molecular interaction of HSF1 and ASC-2 was stimulated by heat shock in cells and the overexpression of HSF1-interacting domain of ASC-2 inhibited the specific induced protein association and HSF1-mediated transactivation. Taking these results together, we suggest that ASC-2 in a novel coactivator for HSF1 and heat shock stress may contribute the strong active transcription complex through sequential recruitment of HSF1 and ASC-2.

Binding Sites↗
PubMed2006

Immediate shock deficit in fear conditioning: effects of shock manipulations.

Pavlovian contextual fear conditioning occurs when an aversive unconditional stimulus (US), such as a footshock, is presented to a rat shortly after it is placed in an experimental context. Contextual fear conditioning does not occur when the shock is presented immediately upon placement of the rat in the novel chamber. In the present study, the authors report that increasing either the number of immediate shock sessions (Experiment 1) or the immediate shock duration (Experiment 2) did not reverse this deficit. However, immediate shock seems to sensitize subsequent context conditioning (Experiment 3). These findings suggest that the associative deficit produced by immediate shock is not related to the rat's ability to process the footshock US.

Animals↗
PubMed1991

Selective activation of human heat shock gene transcription by nitrosourea antitumor drugs mediated by isocyanate-induced damage and activation of heat shock transcription factor.

Treatment of cultured human tumor cells with the chloroethylnitrosourea antitumor drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) selectively induces transcription and protein synthesis of a subset of the human heat shock or stress-induced genes (HSP90 and HSP70) with little effect on other stress genes or on expression of the c-fos, c-myc, or beta-actin genes. The active component of BCNU and related compounds appears to be the isocyanate moiety that causes carbamoylation of proteins and nucleic acids. Transcriptional activation of the human HSP70 gene by BCNU is dependent on the heat shock element and correlates with the level of heat shock transcription factor and its binding to the heat shock element in vivo. Unlike activation by heat or heavy metals, BCNU-mediated activation is strongly dependent upon new protein synthesis. This suggests that BCNU-induced, isocyanate-mediated damage to newly synthesized protein(s) may be responsible for activation of the heat shock transcription factor and increased transcription of the HSP90 and HSP70 genes.

Actins↗
PubMed1993

Dual control of heat shock response: involvement of a constitutive heat shock element-binding factor.

Heat shock factor (HSF) has been implicated as the key regulatory protein in the heat shock response. Our studies on the response of rodent cells to heat shock or sodium arsenite indicate that a high level of HSF-DNA-binding activity, by itself, is not sufficient for the induction of hsp70 mRNA synthesis; furthermore, a high level of HSF binding is also not necessary for this induction. Analysis of the binding of protein factors to the heat shock element (HSE) in extracts of stressed rodent cells indicates that the regulation of heat shock response involves the heat-inducible HSF and a constitutive HSE-binding factor. Our results also suggest that overexpression of human hsp70 may decrease the level of heat-induced HSF-HSE-binding activity in rat cells.

Animals↗
PubMed2006

Induction of the heat shock pathway during hypoxia requires regulation of heat shock factor by hypoxia-inducible factor-1.

Activation of heat shock proteins (Hsps) is critical to adaptation to low oxygen levels (hypoxia) and for enduring the oxidative stress of reoxygenation. Hsps are known to be regulated by heat shock factor (Hsf), but our results demonstrate an unexpected regulatory link between the oxygen-sensing and heat shock pathways. Hsf transcription is up-regulated during hypoxia due to direct binding by hypoxia-inducible factor-1 (HIF-1) to HIF-1 response elements in an Hsf intron. This increase in Hsf transcripts is necessary for full Hsp induction during hypoxia and reoxygenation. The HIF-1-dependent increase in Hsps has a functional impact, as reduced production of Hsps decreases viability of adult flies exposed to hypoxia and reoxygenation. Thus, HIF-1 control of Hsf transcriptional levels is a regulatory mechanism for sensitizing heat shock pathway activity in order to maximize production of protective Hsps. This cross-regulation represents a mechanism by which the low oxygen response pathway has assimilated complex new functions by regulating the key transcriptional activator of the heat shock pathway.

Animals↗
PubMed2006

Development of shock wave assisted therapeutic devices and establishment of shock wave therapy.

In order to exploit systems for shock wave therapy, we are working for the development of clinical devices that are based on the concept of shock waves or related phenomena. The paper describes these new therapeutic devices designed for the minimally invasive approach to vascular thromboloysis, selective dissection of tissues, and drug or DNA delivery. To investigate the response of cells to shock loading, a precise method of shock waves generation in space and time has been developed. This method has been studied for application in cardiovascular therapy, cancer treatment, and cranioplasty in close vicinity of the brain. A laser ablation shock wave assisted particle acceleration device has been developed for delivering drug and DNA into soft targets in the human body. The penetration depth of microparticles observed in the experimental targets is believed to be sufficient for pharmacological treatments. In order to achieve an efficient method for rapid revascularization of cerebral thrombosis, a laser induced liquid jet (LILJ) system has been developed. The LILJ has been successfully applied for selective dissection of soft tissue preserving nerve and blood vessels. The system has been further improved by using piezoelectric actuators to drive the liquid jets, as an alternative to pulse laser.

Animals↗
PubMed1998

Mechanism of gram-positive shock: identification of peptidoglycan and lipoteichoic acid moieties essential in the induction of nitric oxide synthase, shock, and multiple organ failure.

The incidence of septic shock caused by gram-positive bacteria has risen markedly in the last few years. It is largely unclear how gram-positive bacteria (which do not contain endotoxin) cause shock and multiple organ failure. We have discovered recently that two cell wall fragments of the pathogenic gram-positive bacterium Staphylococcus aureus, lipoteichoic acid (LTA) and peptidoglycan (PepG), synergize to cause the induction of nitric oxide (NO) formation, shock, and organ injury in the rat. We report here that a specific fragment of PepG, N-acetylglucosamine-beta-[1--> 4]-N-acetylmuramyl-L-alanine-D-isoglutamine, is the moiety within the PepG polymer responsible for the synergism with LTA (or the cytokine interferon gamma) to induce NO formation in the murine macrophage cell line J774.2. However, this moiety is also present in the PepG of the nonpathogenic bacterium Bacillus subtilis. We have discovered subsequently that S. aureus LTA synergizes with PepG from either bacterium to cause enhanced NO formation, shock, and organ injury in the rat, whereas the LTA from B. subtilis does not synergize with PepG of either bacterium. Thus, we propose that the structure of LTA determines the ability of a particular bacterium to cause shock and multiple organ failure (pathogenicity), while PepG acts to amplify any response induced by LTA.

Animals↗
PubMed1990

The differentially expressed 16-kD heat shock genes of Caenorhabditis elegans exhibit differential changes in chromatin structure during heat shock.

The 16-kD heat shock genes of Caenorhabditis elegans are encoded by four highly similar genes, arranged as divergently transcribed pairs. In spite of the high level of identity that exists between the HSP16 genes, after 2 hr of heat shock the mRNA from one locus accumulates at 7-14 times the level of that from the other locus. To determine if differential HSP16 gene transcriptional activity contributes to these differences, we examined the chromatin structure of the HSP16 genes in nonshocked embryos and in embryos undergoing both the initial phases of heat shock and after 2 hr of heat shock. To carry out these studies, we developed a nuclei isolation procedure that has allowed us to prepare large amounts of nuclei from C. elegans embryos, larvae, and adults that are essentially free of endogenous nuclease and protease activities and appear to be an excellent substrate for investigating chromatin structure in C. elegans. This procedure has enabled us to report the first observations of C. elegans basic chromatin structure, as well as characterize HSP16 chromatin structure in detail. The data suggest that differential HSP16 RNA accumulation following 2 hr of heat shock appears to be correlated with a change in the chromatin structure of one of the HSP16 loci to a preinduction, transcriptionally inactive configuration.

Animals↗
PubMed1995

Binding of heat shock factor to and transcriptional activation of heat shock genes in Drosophila.

Heat shock factor (HSF) binds to heat shock elements (HSEs) and the binding can be highly cooperative. Here we report an analysis of binding of Drosophila HSF to both native and synthetic heat shock regulatory regions. We find that cooperative binding of HSF requires close proximity, rather than helical alignment, of HSEs. Two or more trimeric HSEs organized as contiguous 5 bp units show much higher levels of cooperativity than multiple but separated HSEs. We discuss these in vitro observations in the context of the in vivo status of heat shock genes under mild and full heat shock conditions. Finally, we show that the DNA binding and trimerization domains alone may be sufficient for the full level of binding cooperativity between HSF trimers. This last result suggests that close proximity of HSEs for cooperative binding of HSF is a result of protein-protein interactions near the point of DNA contact.

Animals↗
PubMed2006

Systemic NO production during (septic) shock depends on parenchymal and not on hematopoietic cells: in vivo iNOS expression pattern in (septic) shock.

Septic shock is the leading cause of death in noncoronary intensive care units and the 10th leading cause of death overall. Several lines of evidence support an important role for the vasodilator NO in hypotension, a hallmark of septic shock. However, NO may also positively or negatively regulate inflammation, apoptosis, and oxidative stress. These dual effects of NO may relate to its isoform specific production but also to differences in cellular and/or temporal expression. Via bone marrow transplantations, we examined the contribution of hematopoietic cells to the dramatically elevated NO levels seen in (septic) shock. Surprisingly, hematopoietic cells are not responsible at all for the production of circulating NO after systemic tumor necrosis factor or lipopolysaccharide challenge and contribute only marginally in a bacteremic (Salmonella) model of septic shock. Immunohistochemistry identified the nonhematopoietic sources of NO as hepatocytes, paneth cells, and intestinal and renal epithelial cells. In contrast, during granulomatous Bacillus Calmette-Guérin inflammation, the hematopoietic cell population represents the sole source of systemic NO. These mouse data demonstrate that, in contrast to the general conjecture, the dramatically elevated levels of NO during (septic) shock are not produced by hematopoietic cells such as monocytes/macrophages but rather by parenchymal cells in liver, kidney and gut.

Animals↗