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At least 19 recordsLinked to original sources
PubMed1979

Shock as a signal for shock or no-shock: a feature-negative effect in conditioned suppression.

Rats were trained in conditioned suppression discriminations where shock at the beginning of a trial signaled either shock or no-shock at the end of the trial. In the shock-positive condition, shock at the beginning of a presentation of white noise signaled that noise would end with shock; noise that did not begin with shock did not end with shock. In the shock-negative discrimination, shock at the beginning of noise signaled that noise would not end with shock; presentations of noise that did not begin with shock ended with shock. In shock-random training, shock at the beginning of noise did not reliably signal whether the noise presentation would or would not end with shock. Most subjects in shock-negative training quickly developed a differential pattern of suppression on positive (shock reinforced) trials and no suppression on negative (nonreinforced) trials. The shock-positive discrimination was much more difficult to establish and was not acquired by the majority of the rats. This "feature-negative" effect is a clear exception to the general superiority of feature-positive learning commonly observed in discriminations based on a single distinguishing feature. The results are discussed in terms of Pavlovian stimulus-shock contingencies in the shock-positive and shock-negative paradigms, which appear to favor rapid development of the shock-negative discrimination.

Acoustic Stimulation↗
PubMed1976

Effects of electric-shock delivery on schedule-induced water intake: delay of shock, shock intensity, and body-weight loss.

In each of four experiments, schedule-induced water intake in the rat was studied under fixed-time 40-sec food delivery. Experiments I and II studied the temporal relationship between response-independent electric-shock delivery and licking. Shock was delivered under a variable-time 60-sec schedule. A lick-dependent delay was imposed so that licking and shock delivery were systematically separated in time by a minimum of 1 to 15 sec. Over a wide range of shock intensities the data failed to reveal a consistent delay-of-shock effect. Similar shock intensities led to similar reduction of water intake at each delay of shock interval. Experiments III and IV studied the effects of body-weight loss on water intake during independent shock delivery. In Experiment III, shock was delivered under variable-time 60-sec with a minimum separation between shock and licking of 5 sec. In Experiment IV, shock was delivered under variable-time 180-sec. The minimum separation between shock and licking was 10 sec. In each study, the resistance of water intake to suppression by shock delivery increased as the degree of body-weight loss increased. Schedule-induced water intake was affected more by shock when the animal was maintained at 90% of free-feeding weight than at 70%.

Animals↗
PubMed1991

Attenuation of the heat shock response in HeLa cells is mediated by the release of bound heat shock transcription factor and is modulated by changes in growth and in heat shock temperatures.

When HeLa S3 cells are subjected to a continuous 42 degrees C heat shock, activation of heat shock transcription factor (HSF) and transcriptional activation of the heat shock genes hsp70, hsp89 alpha, and hsp60 is transient, peaking at 40-60 min of heat shock, and then attenuating. We have used in vivo genomic footprinting to demonstrate that attenuation of hsp70 transcription is mediated by release of bound HSF from the heat shock element (HSE) of the hsp70 gene promoter. Release of bound HSF in vivo occurs at a higher rate than would be predicted from in vitro measurements of dissociation. Attenuation of HSF activation and heat shock gene transcription occurs only when mild heat shock temperatures are employed (42 degrees C); increasing the heat shock temperature by 1 degree C elicits a much higher level of activation, which does not attenuate during a 4-hr heat shock. Surprisingly, altering the temperature at which cells are grown prior to heat shock modulates the magnitude and temporal pattern of the response to a given heat shock temperature. This finding suggests that HSF does not sense temperature directly but, instead, may be responsive to the magnitude of the difference between growth and heat shock temperatures.

Base Sequence↗
PubMed1991

Expression of heat shock protein 70 and heat shock cognate 70 messenger RNAs in rat cortex and cerebellum after heat shock or amphetamine treatment.

The expression of strictly inducible hsp70 mRNAs and constitutively expressed hsc70 mRNAs was compared in cerebellum and cerebral cortex of control rats, heat-shocked rats, and rats made hyperthermic with amphetamine. An hsc70-specific oligonucleotide probe identified a 2.55-kb mRNA in cerebellum and cerebral cortex of all rats. An hsp70-specific oligonucleotide probe identified a 3.05-kb mRNA and a 3.53-kb mRNA in cerebellum and cerebral cortex of heat-shocked and amphetamine-treated rats, but not in control rats. Quantitation demonstrated that both hsp70 and hsc70 mRNA levels, relative to 18S rRNA levels, were increased following each treatment. The relative levels of both mRNAs were higher in cerebellum than in cerebral cortex. In amphetamine-treated rats, hsc70 mRNA relative levels increased at body temperatures greater than 39 degrees C, whereas hsp70 mRNA synthesis was induced at temperatures greater than 40 degrees C. Total thermal response values and relative levels of both mRNAs were compared. The results suggested that both the transcription and turnover of hsp70 mRNAs differed between cerebellum and cerebral cortex. At equivalent total thermal response values, amphetamine-treated rats had higher relative levels of hsp70 mRNAs than heat-shocked rats, suggesting that amphetamine enhanced the induction of hsp70 mRNAs.

Amphetamine↗
PubMedDate not supplied

Hemorrhagic shock with fixed hypotension and with spontaneous recovery of blood pressure. A comparison of two shock models.

In 26 dogs anesthetized with a barbiturate peripheral blood flow, O2 consumption and acid-base balance have been studied in two kinds of hemorrhagic shock: 1. Hemorrhagic shock with fixed hypotension (hypotensive shock, n = 12) 2. Hemorrhagic shock with spontaneously recovering arterial blood pressure (normotensive shock, n = 14). In both groups the same amount of blood is withdrawn and stored in a reservoir (31-32 ml/kg) to reduce arterial pressure to 40 mm Hg. In hypotensive shock there is a continuous outflow of blood into the reservoir in order to maintain an arterial pressure of 40 mm Hg. After 1 1/2 hours this shift of blood reverses itself spontaneously. In normotensive shock the arterial pressure is allowed to increase after the initial withdrawal of blood. 1 1/2 hours later it reaches a peak of 93 mm Hg after which it starts declining again. The duration of oligemia which the animals control themselves is nearly identical in both groups (4 hours). Both kinds of hemorrhagic shock have a mortality rate of 80%. The survival time is shorter (p less than 0.01) in hypotensive (3 hours) than in normotensive shock (7 1/2 hours). In both kinds of shock heart rate increases to more than 200 beats/min. However, in hypotensive shock it decreases in the late stage of hypovolemia, whereas the increase is continuous in normotensive shock. Cardiac output is significantly higher in the normotensive animals nearly throughout the entire hypovolemic phase although the initial decrease is the same in both groups (71%). Also a greater increase in total peripheral resistance occurs in these animals. The increased cardiac output and total peripheral resistance. A "centralization" of the circulation is also observed in this kind of shock as is made evident by the changes in the relationship between cardiac output and carotid blood flow. Hyperventilation occurs in both kinds of shock. In hypotensive shock respiratory rate decreases at the end of the oligemic phase possibly due to a smaller cerebral blood flow.

Acidosis↗
PubMed1976

[Clinical study on the shock organs in relation to the duration of shock (author's transl)].

To elucidate the mechanism of development of renal, pulmonary and liver insufficiency after serious shock, retrospective analysis was performed in 85 patients with traumatic shock. Among them, 14 patients died of renal, pulmonary or liver insufficiency after the resuscitation of shock, where kidney and lung were damaged concomitantly in most patients. There was a close correlation between the death related to both insufficiency and the duration of the shockp when the shock was treated completely within 10 hours, there was almost no death related to shock organ, but when the shock persisted more than 10 hours, the death rate was increased as the shock persisted longer. On the contrary, no relation was revealed between death caused by liver insufficiency and the duration of the shock. Renal and pulmonary functions were also correlated with the duration of the shock. It was revealed that the lower PaO2/PAO2 ratio was, the higher urea-N was in these patients, when shock persisted more than 10 hours. On the other hand, no relation was found between the change in liver function and the duration of shock. It can be concluded that the kidney and lung have the same nature as a shock organ. In general both functions were impaired concomitantly, where 10 hours of persistence could be regarded as the critical border to develop the shock organ. The liver seemed to be independent of the others as the shock organ, so that it should be discussed separately.

Acute Kidney Injury↗
PubMed1992

Oxygen radicals in experimental shock: effects of spin-trapping nitrones in ameliorating shock pathophysiology.

BACKGROUND: Circulatory shock is accepted as a consequence of an acute oxygen radical overgeneration. Spin-trapping nitrones inactivate free radicals by forming relatively stable adducts. OBJECTIVE: Three spin-trapping nitrones (N-tert-phenyl-butyl-nitrone; alpha-4-pyridyl-oxide-N-tert-butyl-nitrone; 5-5,dimethyl,1,pyrroline-N-oxide) were tested regarding their role in the pathophysiology and evolution of circulatory shock in rats. DESIGN: Prospective, randomized, controlled trial of spin-trapping nitrones in rats experiencing three different models of circulatory shock. EXPERIMENTS AND RESULTS: In the first group, endotoxic, traumatic, and mesenteric artery occlusion shock (all 100% lethal in control experiments) was prevented by the ip administration of N-tert-phenyl-butyl-nitrone (150 mg/kg); alpha-4-pyridyl-oxide-N-tert-butyl-nitrone (100 mg/kg); or 5-5,dimethyl,1,pyrroline-N-oxide (100 mg/kg). However, the evolution of shock was unaffected by the same compounds when all three nitrones had been previously inactivated by exposure to light and air. In the second group, microcirculatory derangements that were provoked by endotoxin and were observed in the mesocecum of rats were completely prevented by pretreatment with either peritoneal administration of each of the three nitrones or by their topical application to the microscopic field. While the rats survived after systemic treatment, those rats receiving topical nitrones died from endotoxic shock. In the third group, cell-membrane stiffness (a sign of peroxidative damage) was measured by spin-probes and electron-spin resonance in mitochondrial and microsomal membranes. Cell membranes obtained from shocked rats were more rigid than those membranes of controls. However, the membranes obtained from rats that were submitted to trauma or endotoxin after pretreatment with N-tert-phenyl-butyl-nitrone had normal stiffness. The fourth group of experiments was carried out to quantify ethane (one of the final products of lipid peroxidation) in the exhaled air of shocked rats. Ethane concentrations increased in direct proportion to the worsening of the condition. Pretreatment of the rats with N-tert-phenyl-butyl-nitrone prevented such an increase. CONCLUSIONS: Since nitrones are effective inactivators of oxygen-radicals, or of their secondary radicals, these data confirm the relationship between oxygen-radicals and experimental shock. The therapeutic use of spin-trapping nitrones should possibly be considered for future use in shock.

Animals↗
PubMed1990

DnaK, DnaJ, and GrpE heat shock proteins negatively regulate heat shock gene expression by controlling the synthesis and stability of sigma 32.

The Escherichia coli DnaK heat shock protein has been identified previously as a negative regulator of E. coli heat shock gene expression. We report that two other heat shock proteins, DnaJ and GrpE, are also involved in the negative regulation of heat shock gene expression. Strains carrying defective dnaK, dnaJ, or grpE alleles have enhanced synthesis of heat shock proteins at low temperature and fail to shut off the heat shock response after shift to high temperature. These regulatory defects are due to the loss of normal control over the synthesis and stability of sigma 32, the alternate RNA polymerase sigma-factor required for heat shock gene expression. We conclude that DnaK, DnaJ, and GrpE regulate the concentration of sigma 32. We suggest that the synthesis of heat shock proteins is controlled by a homeostatic mechanism linking the function of heat shock proteins to the concentration of sigma 32.

Alleles↗
PubMed1989

Frontal cortex lesions block the opioid and nonopioid hypoalgesia elicited by brief shocks but not the nonopioid hypoalgesia elicited by long shocks.

Previous research (Grau, 1987a, 1987b) suggests that forebrain systems play an essential role in the hypoalgesia observed after brief shock but not long shock. Additional research has shown that pentobarbital anesthesia and decerebration block the hypoalgesia observed after 3 brief (0.75-s) shocks but not the hypoalgesia observed after 3 long (25-s) shocks. This is a study of whether a specific forebrain lesion, a frontal cortex lesion, would have a similar impact on hypoalgesia induced by brief (0.75 s) and long (25-s) shocks. Frontal cortex lesions, like decerebration and pentobarbital anesthesia, eliminated the hypoalgesia observed after brief but not long shocks. Because other research suggests that the stress of surgery may influence whether the hypoalgesia elicited by shock is opioid or nonopioid, the 2nd experiment was to examine whether the sham operation per se alters the form of the hypoalgesia observed after brief shock. It does not; in the sham-treated subjects, brief shock induced the usual transient nonopioid hypoalgesia followed by prolonged opioid hypoalgesia. These data suggest that frontal cortex lesions block nonopioid and opioid hypoalgesia observed after brief shock.

Animals↗
PubMed1992

The plasma membrane of yeast acquires a novel heat-shock protein (hsp30) and displays a decline in proton-pumping ATPase levels in response to both heat shock and the entry to stationary phase.

Recent studies have revealed that the action of the proton-translocating ATPase of the plasma membrane of yeast is an important determinant of several stress tolerances and affects the capacity of cells to synthesise heat shock proteins in response to heat shock [Panaretou, B. & Piper, P. W. (1990) J. Gen. Microbiol. 136, 1763-1770; Coote, P. J., Cole, M. B. & Jones, M. V. (1991) J. Gen. Microbiol. 137, 1701-1708]. This study investigated the changes to the protein composition of the Saccharomyces cerevisiae plasma membrane that result from a heat shock to dividing cultures and the entry to stationary growth caused by carbon source limitation. Plasma membranes were prepared from exponential, heat-shocked and stationary yeast cultures. The proteins of these membrane preparations were then analysed by polyacrylamide gel electrophoresis and immunoblot measurement of ATPase levels. The protein composition of plasma membranes displayed two prominent changes in response to both heat shock and the entry to stationary phase: (a) a reduction in the level of the plasma membrane ATPase; and (b) the acquisition of a previously uncharacterised 30 kDa heat-shock protein (hsp30). The ATPase decline with heat shock probably exerts an important influence over the ability of the cell to maintain ATPase activity, and therefore intracellular pH, during extended periods of stress. Through in vivo pulse-labelling of plasma membrane proteins synthesised before and during heat shock, followed by subcellular fractionation, it was shown that hsp30 is the only protein induced by the yeast heat-shock response that substantially copurifies with plasma membranes. It might therefore exert a stress-protective function specifically at this membrane.

Cell Membrane↗
PubMed1990

Biological effects of shock waves: cavitation by shock waves in piglet liver.

Shock waves are known to generate cavitation in vitro. In vivo, extracorporeal shock waves may cause haemorrhages in tissues. Two types of changes were detected by conventional, real-time B-scan ultrasound when shock waves were administered to 5 piglet livers in vivo: transient changes consisting of bright signals in intrahepatic branches of the portal vein and tributaries of the hepatic vein, presumed to originate from gas bubbles, and stationary changes consisting of brightening of the area along the long axis of the high pressure field, presumed to indicate an increased number of gas-filled bubbles in this area. Transient changes appeared from the start of shock wave administration; bright signals were seen in liver vessels for several hundred microseconds before they were flushed away with the blood flow. Stationary changes appeared later, increased in intensity over several hundred shock waves and persisted for minutes after cessation of shock wave administration. Both types of signals were interpreted as direct evidence that lithotripter shock waves generated cavitation in vivo. Similar signals were received in the partly degassed water of the lithotripter tub. At autopsy of the piglets, focal intralobular haemorrhages and thrombi of portal veins were detected in the shock wave path. The occurrence of cavitation and tissue damage in the same gross area suggests that cavitation might be involved in the generation of tissue damage by shock waves.

Animals↗
PubMed1986

Induction of B2 RNA polymerase III transcription by heat shock: enrichment for heat shock induced sequences in rodent cells by hybridization subtraction.

When hybridization subtraction was used to enrich for sequences induced by heat shock in Chinese hamster cells, B2 sequences were found to be one of the major sequences enriched. With cloned B2 probes, we found that the level of the short, 0.1 to 0.6 kb, polyadenylated RNA polymerase III transcripts of this repetitive genetic element increased approximately 10 to 20 fold after heat shock. Transcription of B2 RNA by RNA polymerase III was rapidly induced after heat shock based on time course studies and nuclear runoff experiments. The induction of B2 RNA was not a nonspecific response to lethality or cellular injury because maximum B2 RNA induction was observed with even nontoxic heating while no induction occurred with other agents such as UV or X-radiation. Since B2 RNA increased after heat shock in several different Chinese hamster and mouse cell lines, induction of B2 RNA by heat shock is probably common in rodent cells. B2 RNA may also be the most abundant transcript induced by heat shock because the level of B2 RNA was substantially higher than several other abundant transcripts induced by heat shock including a rodent HSP70. Our finding of the induction of high levels of RNA polymerase III B2 transcripts in different rodent cells raise the possibility of a role in the heat shock response.

Animals↗
PubMed1991

Heat shock in cultured neurons and astrocytes: correlation of ultrastructure and heat shock protein synthesis.

Cultured cerebral cortical neurons and astrocytes were compared after a brief shock. Morphological findings were correlated with the synthesis of the 68 kD heat shock protein (HSP68). Heat shocked neurons demonstrated many severe morphological changes after exposure to temperatures of 43 degrees C for 15 min and 45 degrees C for 10 min. Nuclear membrane 'blebbing' with lysis of the membrane, chromatin clumping, and disappearance of the nucleolus were prominent after both conditions. Lysis of the cell membrane was noted in severely injured neurons; this was more prominent at the higher temperature. In addition, alterations to polyribosomes, Golgi apparatus, rough endoplasmic reticulum and mitochondria were noted in the cytoplasm of neurons after heat shock. In contrast, no significant changes were noted in either the nucleus or cytoplasm of heat shocked astrocytes. The severity of morphological changes in neurons directly correlated with the low level of induction of HSP68 in neurons. Neurons synthesized much less 68 kD heat shock protein than similarly heat shocked astrocytes. We conclude that cultured cerebral cortical neurons are more susceptible to injury after heat shock than heat resistant astrocytes and that one possible mechanism of injury is failure to synthesize adequate amounts of HSP68 after injury.

Animals↗
PubMed1990

DNA binding of heat shock factor to the heat shock element is insufficient for transcriptional activation in murine erythroleukemia cells.

The heat shock response is among the most highly conserved examples of regulated gene expression, being present in all cellular organisms. Transcriptional activation of heat shock genes by increased temperature or other cellular stresses is mediated by the binding of a heat shock factor (HSF) to a conserved nucleotide sequence (the heat shock element) present in the promoter of heat-inducible genes. Despite the high degree of conservation of this response, embryonic stages of development are characterized by the absence of a heat shock response. Murine erythroleukemia (MEL) cells also lack this response, and we report here a detailed characterization of this defect for one of the most highly conserved of these genes, hsp70. Surprisingly, heat-induced transcriptional activation of this gene does not occur, despite the induction of a protein with the binding specificity of murine HSF. However, the MEL HSF differs slightly in apparent size from the HSF in 3T3 cells, which exhibit a normal heat shock response. These data suggest that activation of mammalian HSF by heat requires at least two separate steps: an alteration of binding activity followed by further modification that activates transcription. MEL cells do not respond to heat shock because they lack the ability to perform this secondary modification. These cells provide a useful system for characterizing heat shock activation in mammals.

Animals↗
PubMed1990

Use of polymerase chain reaction to detect the expression of the Mr 70,000 heat shock genes in control or heat shock leukemic cells as correlated to their heat response.

The expression of the Mr 70,000 heat shock protein (HSP-70) in heat-resistant variants or heat-shocked cells has been correlated with development of thermal resistance. In these studies polymerase chain reaction (PCR) was used to detect low levels of HSP-70 mRNA present in control, unheated cells to investigate the possibility of predicting the intrinsic heat response in various leukemic cells. The expression of two human heat shock genes in control or heat-shocked cells was investigated. Synthetic primers and probes from the untranslated region of the two HSP-70 genes sequenced by Hunt and Morimoto (HSP-70A)(C. Hunt and R. I. Morimoto, Proc. Natl. Acad. Sci. USA, 82: 6455-6459, 1985) and Voellmy et al. (HSP-70B)(R. Voellmy et al., Proc. Natl. Acad. Sci. USA, 82: 4949-4953, 1985) were used in PCR reactions to follow expression in control or heat-shocked leukemic K562, KG-1, and HL-60 cells. The PCR results were correlated with heat response and patterns of protein synthesis in these cells. Results indicate that, among leukemic cells, K562 was much more resistant to killing by heat shock than either KG-1 or HL-60 cells. All control cells, however, expressed the HSP-70B gene. Of the three leukemic cells tested, K562 was the most heat resistant and constitutively expressed the HSP-70A mRNA and the heat-inducible HSP-70 protein. KG-1 and HL-60 cells did not express this gene in unheated cells. All heat-shocked cells expressed the HSP-70A mRNA and the heat-inducible HSP-70 protein. However, there was no significant increase in the mRNA level of the HSP-70B in heat-shocked leukemic cells as measured by PCR or the S1-nuclease protection assay. Other cells including normal human bone marrow and normal and tumorous tissues of the colon and breast all expressed both genes in control cells. Normal breast tissue expressed less mRNA for HSP-70B gene than the tumor tissue obtained from the same patient. In all studies the amplified beta-actin mRNA expression was used as an internal standard. These studies indicate that HSP-70B gene is expressed in all control leukemic cells. The expression of this gene did not seem to correlate with intrinsic heat resistance. The HSP-70A expression correlated with intrinsic and transient heat resistance. These studies also indicate that both HSP-70 genes in humans may be expressed in a variety of unheated normal and tumorous tissues more so than previously reported.

Base Sequence↗
PubMed1987

Detection of mRNAs coding for translationally regulated heat-shock proteins in non-heat-shocked thymic lymphocytes.

Heat shock induces 31 proteins in thymic lymphocytes in 1 h, 11 of which are not blocked by cordycepin, suggesting that their induction may be regulated at the level of translation (Maytin, E.V., Colbert, R.A., and Young, D.A. (1985) J. Biol. Chem. 260, 2384-2392). The possibility that mRNAs coding for these 11 cordycepin-insensitive heat-shock proteins would be found in non-heat-shocked thymus cells was investigated. Analysis of 1500 in vitro translation products separated by giant two-dimensional gel electrophoresis revealed that poly(A)+ RNA isolated from non-heat-shocked thymus cells coded for proteins corresponding to 10 of the 11 non-cordycepin-inhibitable heat-shock proteins. Comparison of the relative rates of synthesis of these 10 proteins in whole cells incubated at 37 and 42 degrees C, with their synthesis in vitro directed by poly(A)+ RNA isolated from cells incubated at 37 degrees C, suggests that mRNAs for 7 of them are present in sufficient amounts in non-heat-shocked cells to account for their increased synthesis during heat shock. These results indicate that part of the response of thymic lymphocytes to heat shock involves a rapid increase in the translation of a group of pre-existing mRNAs that are normally translated at very low rates or not at all.

Animals↗
PubMed1990

Biological effects of shock waves: effect of shock waves on the liver and gallbladder wall of dogs--administration rate dependence.

The effect of extracoporeal shock waves on the liver and the gallbladder wall was compared in two groups of dogs exposed to 1500 shock waves generated in an electrohydraulic lithotripter with 15 kV and 80 nF. The waves were focused on the gallbladder wall. In the experimental group, a shock wave burst of 10 consecutive waves with an interval of 10 ms between the waves was administered each second; in the control group, single shocks were released each second. The day following shock wave exposure, the dogs were anaesthetized, killed and then dissected. In the liver, subcapsular and intraparenchymal focal haemorrhages occurred in the high pressure field and venous thrombi in portal veins. There was a nonsignificant trend towards an increased number of venous thrombi after burst application. The gallbladder wall was haemorrhagic and oedematous, the mucosa was ulcerated in the focal area; blood clots were found in nearly all gallbladders. No differences were detected between the groups. The free plasma haemoglobin was only increased after fast shock wave administration. Increased haemolysis and the trend towards an increased number of thrombi favour cavitation as a mechanism of shock wave damage. The similar extent of tissue damage suggests that shock wave bursts can be applied for gallstone destruction in humans if the major liver vessels are kept out of the high pressure field.

Animals↗