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PubMed1998

Heat shock protein 72 restores cyclic AMP accumulation after heat shock in N18TG2 cells.

Although there are several reports on the alteration of intracellular signal transduction during heat shock in somatic cells, the long term effects of heat shock on neuronal cells remain unknown. In this report, we investigated cyclic AMP (cAMP) accumulation and the expression of heat shock proteins following heat shock in mouse neuroblastoma N18TG2 cells. Basal cAMP accumulation, or that stimulated by serotonin (10 microM), cholera toxin (1 microg/ml), and forskolin (1 microM) was suppressed at 0, 3, and 6 h following heat shock (45 degrees C for 30 min). The cAMP levels were restored at 15 and 24 h after heat shock, corresponding with the expression of stress-induced heat shock protein 72 (HSP72). Quercetin, an inhibitor of HSP expression, decreased the expression of HSP72 and inhibited the recovery of cAMP levels 24 h after heat shock. Quercetin also decreased the basal expression of the constitutive heat shock cognate protein 70 (HSC70) and suppressed cAMP accumulation in non-heat shocked cells. These results suggest that stress-induced HSP72 restores cAMP accumulation to control levels following heat shock and that constitutive HSC70 is related to cAMP levels in non-stress conditions.

Animals↗
PubMed2006

Shock-induced changes of Ca(i)2+ and Vm in myocyte cultures and computer model: Dependence on the timing of shock application.

OBJECTIVES: Responses of Ca(i)2+ to electrical shocks are believed to be important in defibrillation but measurements of shock-induced Ca(i)2+ changes during different phases of the action potential (AP) are lacking. The effects of shocks on Ca(i)2+ and Vm were investigated in geometrically defined cell cultures and in a computer model. METHODS: Uniform-field shocks (E = 10.4+/-0.9 V/cm) were applied 15-300 ms after AP upstroke in strands of cultured neonatal rat myocytes. Optical mapping was used to measure shock-induced Ca(i)2+ and Vm changes. A rat ionic model was used to elucidate ionic mechanisms of Ca(i)2+ responses. RESULTS: In experiments and simulations, shocks applied with short delays (15-40 ms) caused a transient decrease of Ca(i)2+ at sites of both DeltaV(+)m and DeltaV(-)m. Simulations indicated that the Ca(i)2+ decrease at DeltaV(+)m sites was caused by reversed outward flow of L-type Ca2+ current (I(CaL)), while the Ca(i)2+ decrease at DeltaV(-)m sites was due to the NaCa exchanger (NCX). At intermediate delays (40-150 ms), shocks caused a Ca(i)2+ decrease at sites of DeltaV(-)m and an increase at sites of DeltaV(+)m. Simulations indicated that the Ca(i)2+ increase at DeltaV(+)m sites was caused by transient reactivation of I(CaL) combined with a reverse-mode operation of NCX. Shocks applied at long delays (150-300 ms) caused a Ca(i)2+ increase at DeltaV(+)m and no change at DeltaV(-)m sites. CONCLUSION: Effects of shocks on Ca(i)2+ depend on the timing of shock application. Shocks applied during the early AP cause a transient Ca(i)2+ decrease, while later in AP shocks induce a Ca(i)2+ increase at sites of DeltaV(+)m. Shock-induced Ca(i)2+ changes in different AP phases are primarily determined by combination of I(CaL) and NCX.

Action Potentials↗
PubMed2006

Does rate matter? The results of a randomized controlled trial of 60 versus 120 shocks per minute for shock wave lithotripsy of renal calculi.

PURPOSE: In this study we prospectively compared 2 rates of shock wave delivery, 60 and 120 shock waves per minute, to determine whether rate affects outcome with the Dornier Lithotripter S, a lithotriptor with an electromagnetic shock wave source, for renal calculi. MATERIALS AND METHODS: A total of 104 patients with uncomplicated single renal calculus were randomized and treated. Following a single treatment patients were reviewed at 3 months to determine outcome. A plain abdominal x-ray was performed and the size of any residual fragments was noted. Four patients were lost to followup, 1 in the 60 shock waves per minute group and 3 in the 120 shock waves per minute group. RESULTS: Of the 100 patients with complete followup 49 were treated at 60 shock waves per minute and 51 at 120 shock waves per minute. There was no statistically significant difference between mean stone area treated (p = 0.32) or additional analgesic use in the form of patient controlled alfentanil (p = 0.82). A successful outcome was defined by fragments smaller than 4 mm or stone-free status. At 60 shock waves per minute 59% of patients had a successful outcome compared with 61% at 120 shock waves per minute (p = 0.87) following a single treatment. Post-treatment complications were similar in both groups at 8% for 120 shock waves per minute and 10% for 60 shock waves per minute (p = 0.68). CONCLUSIONS: There was no significant difference in patient controlled analgesia use, complications or outcome between rates 60 and 120. Contrary to previous studies these results suggest that a slower rate of shock wave delivery during extracorporeal shock wave lithotripsy for renal calculi does not improve treatment efficacy with the Dornier Lithotripter S.

Adolescent↗
PubMed1996

Prospective randomized comparison of anodal monophasic shocks versus biphasic cathodal shocks on defibrillation energy requirements.

Biphasic shocks are believed to be superior to monophasic shocks. Monophasic anodal shocks, as opposed to cathodal shocks, are associated with improved defibrillation energy requirements (DERs). However, it is unclear how the DER of anodal monophasic shocks compare with conventional biphasic shocks. Therefore the purpose of this study was to prospectively compare the DER of an anodal monophasic shock with that of a cathodal biphasic shock. A transvenous defibrillation lead with distal and proximal shocking electrodes was used. The subjects of this study were 20 consecutive patients with a mean age of 64.2 +/- 10.5 years ( +/- SD) and a mean left ventricular ejection fraction of 0.36 +/- 0.18. Six had had cardiac arrest. The DER, defined as the lowest energy that converted ventricular fibrillation to sinus rhythm, was determined twice with a step-down protocol (25 J, 20 J, 15 J, 10 J, 5 J, 3 J, 1 J). If the DER was > or = 25 J, then a subcutaneous patch was deemed necessary for system implantation. In random order the DER was determined with a monophasic anodal shock (distal electrode positive) and then with a cathodal (first phase, distal electrode negative) biphasic shock. The mean DER with anodal monophasic shocks was 15.1 +/- 8.5 J compared with 13.6 +/- 8.1 J with cathodal biphasic shocks (p = 0.4). A DER > or = 25 J was present in three patients with the monophasic waveform and in three patients with the biphasic waveform (p = NS). In conclusion, the DER and frequency of subcutaneous patch use with an anodal monophasic waveform is comparable to that obtained with cathodal biphasic waveform.

Aged↗
PubMed1995

Low voltage shocks have a significantly higher tilt of the internal electric field than do high voltage shocks.

Typically, an implantable cardioverter defibrillator (ICD) uses a cardioversion shock that is a lower voltage pulse of the same morphology and tilt as its defibrillation pulse. We investigated the internal electric field resulting from an ICD low voltage shock to determine whether its field characteristics matched those of the internal electric field of a high voltage shock. We attached epicardial patch electrodes, for shock delivery, to five fresh pig hearts placed in a diluted, heparinized saline bath. We inserted two plunge electrodes into the myocardium to measure an internal voltage proportional to the electric field. Monophasic 20-msec shocks, from a 140-microF capacitor, ranging from 0.1-30 joules, were delivered through the patches. We measured the current, external voltage, and internal voltage every 0.1 msec throughout the duration of a shock. For each shock, we calculated the time point that represented the 65% tilt position as measured across the patch electrodes. At this 65% tilt time position, we measured the pulse widths and calculated the internal tilt from the internal voltage. We found that the initial internal voltage for the 30-joule shock was 173 +/- 40 volts compared to 10 +/- 2 volts for the 0.1-joule shock. Similarly, we found that the final internal voltage for the 30-joule shock was 56 +/- 14 volts compared to 2 +/- 1 volts for the 0.1-joule shock. Thus, the internal tilt for the 30-joule shock was 68 +/- 1% versus 82 +/- 3% for the 0.1-joule shock (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1973

Choice of higher density signalled shock over lower density unsignalled shock.

Unsignalled, inescapable shocks were presented to four albino rats in Experiment 1. By pressing a lever subjects could change the condition to signalled shock for 3-min periods after which unsignalled shock was automatically reinstated. All subjects changed from unsignalled to signalled shock when shock density was the same or when the density of signalled shock was two times greater than unsignalled shock. When the density of signalled shock was four times that of unsignalled shock, three subjects changed to the higher density schedule. One subject changed to a density of signalled shock eight times that of unsignalled shock. The second study showed that the two shock schedules most similar in Experiment 1 were discriminably different because subjects chose lower over higher shock densities when both densities were unsignalled. An analysis stressing safe (signal absent) and unsafe (signal present) periods was discussed.

Journal Article↗
PubMed2000

Implication of a small GTPase Rac1 in the activation of c-Jun N-terminal kinase and heat shock factor in response to heat shock.

Heat shock induces c-Jun N-terminal kinase (JNK) activation as well as heat shock protein (HSP) expression through activation of the heat shock factor (HSF), but its signal pathway is not clearly understood. Since a small GTPase Rac1 has been suggested to participate in the cellular response to stresses, we examined whether Rac1 is involved in the heat shock response. Here we show that moderate heat shock (39-41 degrees C) induces membrane translocation of Rac1 and membrane ruffling in a Rac1-dependent manner. In addition, Rac1N17, a dominant negative mutant of Rac1, significantly inhibited JNK activation by heat shock. Since Rac1V12 was able to activate JNK, it is suggested that heat shock may activate JNK via Rac1. Similar inhibition by Rac1N17 of HSF activation in response to heat shock was observed. However, inhibitory effects of Rac1N17 on heat shock-induced JNK and HSF activation were reduced as the heat shock temperature increased. Rac1N17 also inhibited HSF activation by l-azetidine-2-carboxylic acid, a proline analog, and heavy metals (CdCl)), suggesting that Rac1 may be linked to HSF activation by denaturation of polypeptides in response to various proteotoxic stresses. However, Rac1N17 did not prevent phosphorylation of HSF1 in response to these proteotoxic stresses. Interestingly, a constitutively active mutant Rac1V12 did not activate the HSF. Therefore, Rac1 activation may be necessary, but not sufficient, for heat shock-inducible HSF activation and HSP expression, or otherwise a signal pathway(s) involving Rac1 may be indirectly involved in the HSF activation. In sum, we suggest that Rac1 may play a critical role(s) in several aspects of the heat shock response.

Animals↗
PubMedDate not supplied

The augmentative effect of repeated heat shock preconditioning on the production of heat shock protein 72 and on ischemic tolerance in rat liver tissue.

OBJECTIVE: Heat shock pretreatment induces heat shock protein (HSP)72 strongly in rat livers and provides the tolerance against subsequent ischemia-reperfusion injury. In this study, the effects of repeated heat shock pretreatment on the production of HSP72 in rat livers and on subsequent ischemic tolerance were investigated. METHODS: Rats pretreated with repeated heat shock were compared with those that received a single heat shock pretreatment. The production of HSP72 was analysed using Western-blotting and densitometer. At 48 h after heat shock pretreatment, all rats were subjected to warm liver ischemia for 30 or 45 min and then reperfused. Survival rate of the animals and liver functions during reperfusion were analysed. RESULTS: The production of HSP72 increased in the repeated heat shock group more than in the single heat shock group. Although there were no significant differences in animal survival or in liver functions after a 30-min ischemia between the single heat shock group and the repeated heat shock group, animal survival and liver functions after a 45-min ischemia were significantly better in the repeated heat shock group. CONCLUSION: In rats, repetition of heat shock pretreatment augmented the production of HSP72 in liver tissue and protected the liver from ischemia-reperfusion injury.

Animals↗
PubMed2001

CD14 expression on monocytes and TNF alpha production in patients with septic shock, cardiogenic shock or bacterial pneumonia.

OBJECTIVES: In patients with septic shock, circulating monocytes become refractory to stimulation with microbial products. Whether this hyporesponsive state is induced by infection or is related to shock is unknown. To address this question, we measured TNF alpha production by monocytes or by whole blood obtained from healthy volunteers (controls), from patients with septic shock, from patients with severe infection (bacterial pneumonia) without shock, and from patients with cardiogenic shock without infection. MEASUREMENTS: The numbers of circulating monocytes, of CD14+ monocytes, and the expression of monocyte CD14 and the LPS receptor, were assessed by flow cytometry. Monocytes or whole blood were stimulated with lipopolysaccharide endotoxin (LPS), heat-killed Escherichia coli or Staphylococcus aureus, and TNF alpha production was measured by bioassay. RESULTS: The number of circulating monocytes, of CD14+ monocytes, and the monocyte CD14 expression were significantly lower in patients with septic shock than in controls, in patients with bacterial pneumonia or in those with cardiogenic shock (p < 0.001). Monocytes or whole blood of patients with septic shock exhibited a profound deficiency of TNF alpha production in response to all stimuli (p < 0.05 compared to controls). Whole blood of patients with cardiogenic shock also exhibited this defect (p < 0.05 compared to controls), although to a lesser extent, despite normal monocyte counts and normal CD14 expression. CONCLUSIONS: Unlike patients with bacterial pneumonia, patients with septic or cardiogenic shock display profoundly defective TNF alpha production in response to a broad range of infectious stimuli. Thus, down-regulation of cytokine production appears to occur in patients with systemic, but not localised, albeit severe, infections and also in patients with non-infectious circulatory failure. Whilst depletion of monocytes and reduced monocyte CD14 expression are likely to be critical components of the hyporesponsiveness observed in patients with septic shock, other as yet unidentified factors are at work in this group and in patients with cardiogenic shock.

Antigens, CD↗
PubMed2003

Biphasic shocks compared with monophasic damped sine wave shocks for direct ventricular defibrillation during open heart surgery.

BACKGROUND: Biphasic waveform shocks are more effective than monophasic shocks for transchest ventricular defibrillation, atrial cardioversion, and defibrillation with implantable defibrillators but have not been studied for open chest, intraoperative defibrillation. This prospective, blinded, randomized clinical study compares biphasic and monophasic shock effectiveness and establishes intraoperative energy dose-response curves. METHODS: Patients undergoing cardiothoracic surgery with bypass cardioplegia were randomly assigned to the monophasic or biphasic shock group. Ventricular fibrillation occurring after aortic clamp removal was treated with escalating energies of 2, 5, 7, 10, and 20 J until defibrillation occurred. If ventricular fibrillation persisted, a 20-J crossover shock of the other waveform was used. RESULTS: Cumulative defibrillation success at 5 J, the primary end point of the study, was higher in the biphasic group than in the monophasic group (25 of 50 vs. 9 of 41 defibrillated; P = 0.011). In addition, the biphasic group required lower threshold energy (6.8 vs. 11.0 J; P = 0.003), less cumulative energy (12.6 vs. 23.4 J; P = 0.002), and fewer shocks (2.5 vs. 3.5; P = 0.002). Crossover-shock effectiveness did not differ between groups. Dose-response curves show biphasic shocks to have higher cumulative success rates at all energies tested. CONCLUSIONS: Biphasic shocks are substantially more effective than monophasic shocks for direct defibrillation. The dose-response curve guides selection of first-shock energy for traditional step-up protocols. Starting at 5 J optimizes for lowest threshold and cumulative energy, whereas 10 or 20 J optimizes for more rapid defibrillation and fewer shocks.

Adult↗
PubMed1997

Delivery of noncommitted shocks for nonsustained ventricular arrhythmias by a new implantable cardioverter defibrillator with abortive shock capability.

INTRODUCTION: To describe the delivery of noncommitted implantable cardioverter defibrillator (ICD) shocks despite self-termination of ventricular arrhythmias. Abortive shock capability should eliminate the delivery of shocks for self-terminating ventricular arrhythmias. The delivery of noncommitted shocks despite abortive shock capability is, therefore, unexpected and previously unreported. METHODS AND RESULTS: Among 118 patients who received the Transvene nonthoracotomy lead system and the Jewel ICD (model 7219D), three patients (1.7%) experienced supurious, noncommitted shocks for self-terminating arrhythmias. Only one detection zone (i.e., ventricular fibrillation) had been programmed in the defibrillator in each patient. In all three patients, the ventricular arrhythmias self-terminated during the charging period. One patient received seven shocks during periods of asystole, and the other two patients received one shock each. Two different mechanisms for shock delivery in this setting were identified: one occurring in the absence of electrical activity at the end of the bradycardia escape interval (i.e., associated with bradyarrhythmias), and the other when two sensed electrical events (i.e., escape beats) occurred during the so-called "synchronization" window of the defibrillator. CONCLUSIONS: In rare patients with the Jewel defibrillator, shocks may be delivered for self-terminating arrhythmias despite abortive shock capability. Patients who are dependent upon pacing from their implanted defibrillator are at particular risk for shock in the aftermath of self-terminating ventricular arrhythmias. Defibrillator programming strategies aimed at eliminating or diminishing the incidence of this problem are discussed.

Aged↗
PubMed1980

Maintenance of responding by squirrel monkeys under a concurrent shock-postponement, fixed-interval shock-presentation schedule.

A chain-pulling response was initially developed under a shock-postponement (avoidance) schedule with two squirrel monkeys. Few responses occurred on a lever where responding initially had no scheduled consequence or, subsequently, when a 3-minute fixed-interval shock-presentation schedule was concurrently arranged for lever responses. Appropriate rates and patterns of lever responding developed and were later maintained under the fixed-interval 3-minute shock-presentation schedule alone when the chain and shock-postponement schedule were removed. When both the shock-postponement and shock-presentation schedules were again simultaneously in effect, steady rates of chain pulling were maintained by the shock-postponement schedule and positively accelerated rates and patterns were maintained on the lever by the shock-presentation schedule. Response rates under both schedules were directly related to shock intensity. A history of exposure to a shock-postponement schedule, even though with a topographically different response and manipulandum, was sufficient for the development and eventual maintenance of responding by the presentation of shock. Further, differential performances can be maintained simultaneously by the presentation and postponement of electric shock.

Animals↗
PubMed1994

Deficient induction of human hsp70 heat shock gene transcription in Y79 retinoblastoma cells despite activation of heat shock factor 1.

One of the basic features of the inducible heat shock response is the activation of heat shock factor which results in the rapid transcriptional induction of the heat shock genes. Although it is widely considered that the heat shock response is ubiquitous, several reports have indicated that the transcriptional response can vary in both intensity and kinetics and often in a tissue-specific manner. Of interest have been studies on the expression of heat shock genes in the brain, particularly observations that certain cultured neuronal cells exhibit a diminished heat shock response. We demonstrate that transcription of the gene encoding a 70-kDa heat shock protein (hsp70) is diminished upon heat shock in Y79 human retinoblastoma cells (which are of neuronal origin) despite both the activation of heat shock factor 1 and induced transcription of another heat shock gene, hsp90 alpha. This uncoupling of stress-induced transcription of the hsp70 and hsp90 alpha genes, which are typically coordinately regulated in response to stress, appears to be due to the selective inability of trans-acting factors, including heat shock factor 1, to bind in vivo to the hsp70 promoter as the result of a chromatin-mediated effect.

DNA-Binding Proteins↗
PubMed1994

The yeast and mammalian Ras pathways control transcription of heat shock genes independently of heat shock transcription factor.

Yeast strains in which the Ras-cyclic AMP (cAMP) pathway is constitutively active are sensitive to heat shock, whereas mutants in which the activity of this pathway is low are hyperresistant to heat shock. To determine the molecular basis for these differences, we examined the transcriptional induction of heat shock genes in various yeast strains. Activation of heat shock genes was attenuated in the strains in which the Ras-cAMP pathway is constitutively active. In contrast, in a strain deficient in cAMP production, several heat shock genes were induced by removal of cAMP from the medium. These results indicate that the Ras-cAMP pathway affects the induction of heat shock genes. In all of the mutants, heat shock transcription factor expression and activity were identical to those in wild-type cells. The response to heat shock in Ha-ras-transformed rat fibroblasts was also studied. While no induction of Hsp68 was observed in Ha-ras-transformed cells, proper regulation of heat shock transcription factor was found. Therefore, in mammals, as in Saccharomyces cerevisiae, the Ras pathway controls the transcription of heat shock genes via a mechanism not involving the heat shock transcription factor.

3T3 Cells↗
PubMed1993

Characterization of two maize HSP90 heat shock protein genes: expression during heat shock, embryogenesis, and pollen development.

We have isolated two genes from Zea mays encoding proteins of 82 and 81 kD that are highly homologous to the Drosophila 83-kD heat shock protein gene and have analyzed the structure and pattern of expression of these two genes during heat shock and development. Southern blot analysis and hybrid select translations indicate that the highly homologous hsp82 and hsp81 genes are members of a small multigene family composed of at least two and perhaps three or more gene family members. The deduced amino acid sequence of these proteins based on the nucleotide sequence of the coding regions shows 64-88% amino acid homology to other hsp90 family genes from human, yeast, Drosophila, and Arabidopsis. The promoter regions of both the hsp82 and hsp81 genes contain several heat shock elements (HSEs), which are putative binding sites for heat shock transcription factor (HSF) commonly found in the promoters of other heat shock genes. Gene-specific oligonucleotide probes were synthesized and used to examine the mRNA expression patterns of the hsp81 and hsp82 genes during heat shock, embryogenesis, and pollen development. The hsp81 gene is only mildly heat inducible in leaf tissue, but is strongly expressed in the absence of heat shock during the pre-meiotic and meiotic prophase stages of pollen development and in embryos, as well as in heat-shocked embryos and tassels. The hsp82 gene shows strong heat inducibility at heat-shock temperatures (37-42 degrees C) and in heat shocked embryos and tassels but is only weakly expressed in the absence of heat shock. Promoter-GUS reporter gene fusions made and analyzed by transient expression assays in Black Mexican Sweet (BMS) Maize protoplasts also indicate that the hsp82 and hsp81 are regulated differentially. The hsp82 promoter confers strong heat-inducible expression of the GUS reporter gene in heat-treated cells (60- to 80-fold over control levels), whereas the hsp81 promoter is only weakly heat inducible (5- to 10-fold over control levels).

Amino Acid Sequence↗
PubMed2006

Expression of heat shock protein70 in pig oocytes: heat shock response during oocyte growth.

The heat shock response of growing and fully-grown pig oocytes was analyzed in vitro by determining heat shock protein70 (HSP70) synthesis under both normal conditions (39 degrees C; 0 and 6h) and after heat shock (43 degrees C; 1, 4 and 6h). The expression of HSP70 in oocytes was detected by immunoblotting analysis. Growing oocytes measuring 80-99 microm synthesized a high number of HSP70 without heat shock effect, and these were capable of increasing the synthesis of HSP70 after heat shock to a maximum after 1h. Growing oocytes measuring 100-115 microm also synthesized HSP70 without heat shock and after it, but the HSP70 synthesis was not statistically changed by increasing duration of heat shock. In fully-grown oocytes, great amounts of HSP70 were found without heat shock treatment, and the contents of HSP70 significantly decreased after heat shock. These results indicate that growing oocytes are able to synthesize HSP70 after heat shock. This ability declines at the end of the growth period, and fully-grown oocytes are unable to induce HSP70 synthesis after heat shock. HSP70 is synthesized and stored during oocyte growth. The high HSP70 synthesis in non-heat-treated growing oocytes and a great amount of HSP70 in fully-grown oocytes support the hypothesis that HSP70 is important for oocyte growth and maturation.

Animals↗