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PubMed2003

Effects of sustained post-traumatic shock and initial fluid resuscitation on extravascular lung water content and pulmonary vascular pressures in a porcine model of shock.

BACKGROUND: The temporal evolution of lung injury following post-traumatic shock is poorly understood. In the present study we have tested the hypothesis that manifestations of pulmonary vascular dysfunction may be demonstrable within the first hour after the onset of shock. METHODS: Twenty-nine anaesthetized pigs (mean weight 27.4 kg; (SD) 3.2) were randomly allocated to three groups: control (C, n=9), shock resuscitated with either NaCl 0.9% (S, n=10), or 4% gelatine (G, n=10). Shock was maintained for 1 h followed by fluid resuscitation with either normal saline or 4% gelatine solution. Cardiac output (CO), mean arterial pressure (MAP), mixed venous saturation (Sv(O(2))), blood lactate concentration, mean pulmonary artery pressure (MPAP), MPAP/MAP, pulmonary vascular resistance (PVR), extravascular lung water index (EVLWi), Pa(O(2))/FI(O(2)), venous admixture (Q(.)(S)/Q(.)(T)), and dynamic lung compliance (C(dyn)) were measured at baseline, beginning of shock phase, end of shock phase, and post-resuscitation. RESULTS: At the end of volume resuscitation CO was restored to control values in both shock groups. MAP remained significantly below control values (95% CI: C=70-95, S=28-52, G=45-69 mm Hg) in both shock groups. MPAP/MAP was significantly greater in both shock groups at the end of the shock phase (95% CI; C=0.15-0.24, S=0.28-0.38, G=0.32-0.42) and at the post-resuscitation phase (95% CI: C=0.12-0.30, S=0.43-0.61, G=0.32-0.49) indicating the presence of relative pulmonary hypertension. This was associated with a significant increase in PVR in Group S (F=3.9; P<0.05). There were no significant changes in Pa(O(2))/FI(O(2)), Q(.)(S)/Q(.)(T), EVLWi, or C(dyn). In a small cohort of animals a measurable increase in EVLWi (>30%) and reduction in C(dyn) (>10%) were observed. CONCLUSIONS: Pulmonary vascular injury manifesting as relative pulmonary hypertension and increased PVR may occur within the first hour after the onset of shock. These changes may not be accompanied by overt changes in oxygenation, compliance, or EVLWi. Br J Anaesth 2003; 91: 224-32

Animals↗
PubMed1996

Effect of pre- and post-heat shock temperature on the persistence of thermotolerance and heat shock-induced proteins in Listeria monocytogenes.

The effect of incubation temperature, before and after a heat shock, on thermotolerance of Listeria monocytogenes at 58 degrees C was investigated. Exposing cells grown at 10 degrees C and 30 degrees C to a heat shock resulted in similar rises in thermotolerance while the increase was significantly higher when cells were grown at 4 degrees C prior to the heat shock. Cells held at 4 degrees C and 10 degrees C after heat shock maintained heat shock-induced thermotolerance for longer than cells held at 30 degrees C. The growth temperature prior to inactivation had negligible effect on the persistence of heat shock-induced thermotolerance. Concurrent with measurements of thermotolerance were measurements of the levels of heat shock-induced proteins. Major proteins showing increased synthesis upon the heat shock had approximate molecular weights of 84, 74, 63, 25 and 19 kDa. There was little correlation between the loss of thermotolerance after the heat shock and the levels of these proteins. Thermotolerance of heat shocked and non-heat shocked cells was described by traditional log-linear kinetics and a model describing a sigmoidal death curve (logistic model). Employing log-linear kinetics resulted in a poor fit to a major part of the data whereas a good fit was achieved by the use of a logistic model.

Bacterial Proteins↗
PubMed1999

Proteasome inhibitors lactacystin and MG132 inhibit the dephosphorylation of HSF1 after heat shock and suppress thermal induction of heat shock gene expression.

Recently, we have shown that two proteasome inhibitors, MG132 and lactacystin, induce hyperphosphorylation and trimerization of HSF1, and transactivate heat shock genes at 37 degrees C. Here, we examined the effects of these proteasome inhibitors and, in addition, a phosphatase inhibitor calyculin A (CCA) on the activation of HSF1 upon heat shock and during post-heat-shock recovery, with emphasis on HSF1 hyperphosphorylation and the ability of HSF1 to transactivate heat shock genes. When lactacystin, MG132, or CCA was present after heat shock, HSF1 remained hyperphosphorylated during post-heat-shock recovery at 37 degrees C. Failure of HSF1 to recover to its preheated dephosphorylated state correlated well with the suppression of the heat-induced hsp70 expression. In vitro, HSF1 from heat-shocked cells, when dephosphorylated, showed an increase in HSE-binding affinity. Taken together, these data suggest that phosphorylation of HSF1 plays an important role in the negative regulation of heat-shock response. Specifically, during post-heat-shock recovery phase, prolonged hyperphosphorylation of HSF1 suppresses heat-induced expression of heat shock genes.

Acetylcysteine↗
PubMed1980

Meperidine's effect under shock titration and shock discrimination procedures.

Meperidine's effects were examined under a schedule of shock titration and under a shock intensity discrimination in which squirrel monkeys discriminated between the presence and absence of a low intensity shock. Meperidine did not increase the intensity at which monkeys maintained the shock in the shock titration procedure, nor did meperidine alter the percentage of correct responses under the shock intensity discrimination although meperidine did increase the time to respond in the presence and absence of shock. When meperidine was combined with a dose of SKF-525A, which did not alter responding when given alone, the intensity at which monkeys maintained the shock under the shock titration procedure was increased. Moreover, the percentage of correct responses in the presence of shock under the shock titration procedure was decreased by the combination of meperidine and SKF-525A.

Animals↗
PubMed2006

One-shock versus three-shock defibrillation protocol significantly improves outcome in a porcine model of prolonged ventricular fibrillation cardiac arrest.

BACKGROUND: The success of resuscitation with a 1-shock versus the conventional 3-shock defibrillation protocol was investigated subject to the range of treatment variation imposed by automated external defibrillators (AEDs). METHODS AND RESULTS: Ventricular fibrillation was induced in 44 domestic pigs. After 7 minutes of untreated VF, animals were randomized among 4 groups representing all combinations of the 1- versus 3-shock protocol and 2 different AED regimens (AED1, AED2). Because few AEDs support a 1-shock protocol, manual defibrillators were used to replicate the AED treatment regimen: electrical waveform, dose sequence, and cardiopulmonary resuscitation (CPR) interruption intervals. Initial shock(s) were delivered, followed by 60 seconds of CPR, and the treatment was repeated until resuscitation was successful or for 15 minutes. The 1-shock protocol was associated with improved outcome, reducing CPR interruptions from 45% to 34% of total resuscitation time (P=0.019) and increasing survival from 64% to 100% (P=0.004). Survival was 91% for AED1 versus 36% for AED2 (P=0.024) with a 3-shock protocol but was increased to 100% for both by adoption of a 1-shock protocol. Improvements in postresuscitation left ventricular ejection fraction and stroke volume were observed with AED1 compared with AED2 (difference of means, 15% and 28% of baseline respectively, P<0.001) regardless of defibrillation protocol. CONCLUSIONS: Adoption of a 1-shock versus a 3-shock resuscitation protocol improved survival and minimized outcome differences imposed by variations in AED design and implementation. When a conventional 3-shock defibrillation protocol was used, however, the choice of AED had a significant impact on resuscitation outcome.

Animals↗
PubMed2005

Both heat-shock and cold-shock influence trehalose metabolism in an entomopathogenic nematode.

Heat-shock response is highly conserved in animals and microorganisms, and it results in the synthesis of heat-shock proteins. In yeast, heat-shock response has also been reported to induce trehalose accumulation. We explored the relationship between heat- (35 C) or cold-shock (1 and 10 C) and trehalose metabolism in the entomopathogenic nematode, Heterorhabditis bacteriophora. Because both heat- and cold-shocks may precede desiccation stress in natural soil environments, we hypothesized that nematodes may accumulate a general desiccation protectant, trehalose, under both situations. Indeed, both heat- and cold-shocks influenced trehalose accumulation and activities of enzymes of trehalose metabolism in H. bacteriophora. Trehalose increased by 5- and 6-fold in heat- and cold-shocked infective juveniles, respectively, within 3 hr of exposure, compared with the nematodes maintained at 25 C (culture temperature). The activity of trehalose-6-phosphate synthase (T6PS), an enzyme involved in the synthesis of trehalose, also significantly increased in both heat- and cold-shocked nematodes during the first 3 hr of exposure. Generally, the trehalose levels and activities of T6PS declined to their original levels within 3 hr when nematodes were transferred back to 25 C. In both heat- and cold-shocked nematodes, trehalase activity decreased significantly within the first 3 hr and generally returned to the original levels within 3 hr when these nematodes were transferred back to 25 C. The results demonstrate that the trehalose concentrations in H. bacteriophora are influenced by both heat- and cold-shocks and are regulated by the action of 2 trehalose-metabolizing enzymes, T6PS and trehalase. The accumulated trehalose may enhance survival of nematodes under both cold and warm conditions, but it may also provide simultaneous protection against desiccation that may result from subsequent evaporation or freezing. This is the first report of the relationship between trehalose metabolism and heat-shock for the Nematoda.

Animals↗
PubMed1969

The effects of escape conditioning and shock intensity on responding during inescapable shock.

Eight albino rats, conditioned to press a lever to escape shock, continued to lever press during short inescapable shocks presented subsequently. The rate of this behavior was found to be higher for higher shock intensities regardless of the order in which shock values were presented. Relative to the immediately preceding escape rate, responding during inescapable shock was higher following conditioning at higher fixed-ratio escape requirements. Four subjects not conditioned to escape shock pressed the lever very infrequently during inescapable shock and showed little change with changes in shock intensity. The escape conditioning effects suggest that responding during inescapable shock is superstitious escape behavior. The effects of shock intensity on this behavior appear to be similar to reported effects of shock intensity on escape behavior.

Journal Article↗
PubMed1973

Choice of longer or stronger signalled shock over shorter or weaker unsignalled shock.

Unsignalled, inescapable shocks were presented to four albino rats in one study and to six rats in a second study. By pressing a lever, subjects could change the condition to signalled shock for 3 min after which unsignalled shock was automatically reinstated. All subjects changed frequently to the signalled shock schedule. After a minimum of three 6-hr sessions or after changeover responding stabilized at the previous values, higher values of signalled shock intensity or duration were introduced. In the first study, the duration of signalled shock was increased in increments of 0.5 sec. In the second study, the intensity of signalled shock was increased in increments of either 0.2 or 0.4 mA. Duration subjects chose signalled shock four (2.0 sec) to nine times (4.5 sec) longer than unsignalled shock (0.5 sec). Intensity subjects chose signalled shock two (2.0 mA) to three times (3.0 mA) more intense than unsignalled shock (1.0 mA).

Journal Article↗
PubMed1981

Effects of signaled and unsignaled shock on schedule-controlled lever pressing and schedule-induced licking: Shock intensity and body weight.

Schedule-controlled lever pressing and schedule-induced licking were studied in rats under a multiple fixed-interval fixed-interval schedule of food reinforcement. Following acquisition of stable rates of pressing and licking, a multiple variable-time variable-time schedule of electric-shock delivery was superimposed upon the baseline schedule. In only one component of the multiple schedule, a 5-sec stimulus preceded each shock (signaled shock). In the other component shock was unsignaled. Several shock intensities (Experiment 1) and body weights (Experiment 2) were studied. Lever pressing and licking were affected similarly by experimental manipulations, although with parametric differences. Depending upon shock intensity and body weight, rates of lever pressing and licking were hardly suppressed, suppressed primarily in the unsignaled shock component (differential suppression), or markedly suppressed in both components. Differential suppression during components with signaled and unsignaled shock and conditioned suppression of responding during the preshock stimulus appeared not to be functionally related. Differential suppression depended more on the discriminability of shock-free time, and on shock intensity, body weight, and the type of response than on the "preparatory" behavior preceding shock.

Journal Article↗
PubMed2003

Early revascularization is associated with improved survival in elderly patients with acute myocardial infarction complicated by cardiogenic shock: a report from the SHOCK Trial Registry.

AIMS: The SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK (SHOCK) Trial showed no benefit of early revascularization in patients aged >/=75 years with acute myocardial infarction and cardiogenic shock. We examined the effect of age on treatment and outcomes of patients with cardiogenic shock in the SHOCK Trial Registry. METHODS AND RESULTS: We compared clinical and treatment factors in patients in the SHOCK Trial Registry with shock due to pump failure aged <75 years (n=588) and >/=75 years (n=277), and 30-day mortality of patients treated with early revascularization <18 hours since onset of shock and those undergoing a later or no revascularization procedure. After excluding early deaths covariate-adjusted relative risk and 95% confidence intervals were calculated to compare the revascularization strategies within the two age groups. Older patients more often had prior myocardial infarction, congestive heart failure, renal insufficiency, other comorbidities, and severe coronary anatomy. In-hospital mortality in the early vs. late or no revascularization groups was 45 vs. 61% for patients aged <75 years (p=0.002) and 48 vs. 81% for those aged >/=75 years (p=0.0003). After exclusion of 65 early deaths and covariate adjustment, the relative risk was 0.76 (0.59, 0.99; p=0.045) in patients aged <75 years and 0.46 (0.28, 0.75; p=0.002) in patients aged >/=75 years. CONCLUSIONS: Elderly patients with myocardial infarction complicated by cardiogenic shock are less likely to be treated with invasive therapies than younger patients with shock. Covariate-adjusted modeling reveals that elderly patients selected for early revascularization have a lower mortality rate than those receiving a revascularization procedure later or never.

Aged↗
PubMed2003

Heat shock protein 70-2+1267 AA homozygotes have an increased risk of septic shock in adults with community-acquired pneumonia.

OBJECTIVE: Heat shock protein (HSP)70-2 is an important immunomodulatory protein induced in response to inflammatory stimuli. We assessed whether HSP70-2+1267 genotype influenced the risk of septic shock in a prospective cohort study of community-acquired pneumonia and whether HSP70-2+1267 genotype is a better predictor of septic shock than the genotype at lymphotoxin-alpha +250. DESIGN: Prospective cohort study. SETTING: A large, nonprofit, private hospital system in Memphis, TN. PATIENTS: Adults admitted with community-acquired pneumonia between 1998 and 2001. Septic shock was defined according to consensus criteria (American College of Chest Physicians/Society of Critical Care Medicine, 1992). INTERVENTIONS: Blood sampling. MEASUREMENTS AND MAIN RESULTS: A total of 343 subjects were enrolled; 30 had septic shock. HSP70-2+1267 and lymphotoxin-alpha +250 genotype was determined using polymerase chain reaction and restriction enzyme digestion. HSP70-2+1267 AA genotype was the strongest predictor of septic shock (p =.0005; relative risk, 3.5). Lymphotoxin-alpha +250 AA genotype was also associated with an increased risk of septic shock (p =.002; relative risk, 2.7). Logistic regression analysis found only age (p =.04) and HSP70-2+1267 genotype (p =.006) were predictors of septic shock. The greatest risk of septic shock was associated with carriage of the HSP70-2+1267 A/lymphotoxin-alpha +250 A haplotype (p <.0001). CONCLUSIONS: HSP70-2+1267 genotype is a stronger predictor of septic shock in patients with community-acquired pneumonia than lymphotoxin-alpha +250 genotype.

APACHE↗
PubMed2003

Activation of heat shock genes is not necessary for protection by heat shock transcription factor 1 against cell death due to a single exposure to high temperatures.

Heat shock response, which is characterized by the induction of a set of heat shock proteins, is essential for induced thermotolerance and is regulated by heat shock transcription factors (HSFs). Curiously, HSF1 is essential for heat shock response in mammals, whereas in avian HSF3, an avian-specific factor is required for the burst activation of heat shock genes. Amino acid sequences of chicken HSF1 are highly conserved with human HSF1, but those of HSF3 diverge significantly. Here, we demonstrated that chicken HSF1 lost the ability to activate heat shock genes through the amino-terminal domain containing an alanine-rich sequence and a DNA-binding domain. Surprisingly, chicken and human HSF1 but not HSF3 possess a novel function that protects against a single exposure to mild heat shock, which is not mediated through the activation of heat shock genes. Overexpression of HSF1 mutants that could not bind to DNA did not restore the susceptibility to cell death in HSF1-null cells, suggesting that the new protective role of HSF1 is mediated through regulation of unknown target genes other than heat shock genes. These results uncover a novel role of vertebrate HSF1, which has been masked under the roles of heat shock proteins.

Adenoviridae↗
PubMed1999

Inhibition of heat shock factor activity prevents heat shock potentiation of glucocorticoid receptor-mediated gene expression.

Using mouse L929 cells stably transfected with a glucocorticoid receptor (GR)-responsive murine mammary tumor virus-chloramphenicol acetyltransferase (MMTV-CAT) reporter gene (LMCAT2 cells), we have shown that cellular stress (heat or chemical shock) can cause a dramatic increase in the levels of dexamethasone (Dex)-induced CAT gene expression. We refer to this response as the heat shock potentiation effect, or HSPE. As the cellular heat shock response also involves the activation of heat shock transcription factor (HSF), we have, in the present study, examined the role of HSF in the stress potentiation of GR by use of a flavonoid compound, quercetin, recently shown to selectively inhibit the stress response in a variety of human and murine cell lines. Analysis of the HSPE, as well as heat shock protein synthesis and activation of HSF during time-courses of recovery following heat shock, revealed a similar pattern for each response, with peak activities occurring about 16 h after stress. These data suggest a correlation between the activation of both GR and HSF in stressed cells. In L929 cells stably transfected with a CAT reporter plasmid under the control of the HSF-responsive hsp70 promoter (LHSECAT cells), pretreatment with quercetin was found to cause a dose- and time-dependent inactivation of HSF activity following heat shock, but only when added before the stress event. In LMCAT2 cells, quercetin similarly inhibited both heat and chemical shock potentiation of Dex-induced GR activity. This activity of quercetin was not the result of post-transcriptional or general cytotoxic properties, as quercetin (1) did not significantly affect GR or HSF activities when added after the stress event, (2) did not reduce CAT gene expression as controlled by the constitutive SV40 early promoter, and (3) did not alter normal (non-stress), Dex-induced MMTV-CAT expression. Thus, quercetin appears to be an effective and selective inhibitor of HSF stress-induced activation and its ability to prevent the stress potentiation of GR suggests either a direct or indirect involvement by stress-activated HSF in this process, or the existence of a regulatory step common to both the heat shock and HSPE responses.

Animals↗
PubMed2006

Tetraploid induction by inhibiting mitosis I with heat shock, cold shock, and nocodazole in the hard clam Mercenaria mercenaria (Linnaeus, 1758).

Tetraploid induction by inhibiting mitosis I with heat shock (32, 35, and 38 degrees C), cold shock (1, 4, and 7 degrees C), and nocodazole (0.02 to 1.6 mg/L) was investigated in the hard clam Mercenaria mercenaria. All treatments were applied to fertilized eggs about 5 min before the first cell division at 22 to 23 degrees C, and lasted for 10, 15, and 20 min. Three replicates were produced for each treatment with different parents. The ploidy of resultant larvae and juveniles was determined with flow cytometry. Heat shock of 35 and 38 degrees C was effective in inhibiting mitosis I, producing 54% to 89% tetraploid larvae. Heat shock of 32 degrees C accelerated embryonic development without inhibiting mitosis or producing tetraploids. In all heat-shock groups, the survival to D-stage larvae was lower than in controls, suggesting that heat-shock treatments and tetraploidy were detrimental to larval development. At the juvenile stage, survivors from heat-shock groups contained no tetraploids. Cold shocks suspended the first cell division during the treatment, but produced no tetraploids in the 4 degrees C and 7 degrees C treatment groups. Cold shock of 1 degrees C produced 31% tetraploid larvae in one replicate, with none surviving to juvenile stage. Nocodazole inhibited mitosis I at concentrations of 0.04 mg/L or higher, but did not produce tetraploids. This study indicates that heat shock is most effective in inducing tetraploids through mitosis I inhibition, although none of the induced tetraploids survived to juvenile stage.

Animals↗
PubMed2003

Changes in arterial hydrogen sulfide (H(2)S) content during septic shock and endotoxin shock in rats.

OBJECTIVES: To explore the changes of hydrogen sulfide (H(2)S) in vascular tissues of rats with septic shock and endotoxin shock and its possible pathophysiological implication. METHODS: Rat models of septic shock induced by cecal ligation and puncture and of endotoxic shock induced by injection of endotoxin were used in this study. The authors measured hymodynamic variations, metabolic data, H(2)S and nitric oxide (NO) contents of different arteries in rats with septic shock and endotoxic shock. RESULTS: The results showed that hemodynamic parameters including the heart rate (HR), the mean arterial pressure (BP), and the +dP/dt max decreased markedly, while the left ventricular end-diastolic pressure (LVEDP) increased significantly and the rats developed hypoglycemia and lactic acidosis. Arterial H(2)S contents were significantly increased (P<0.01) in both septic and endotoxic shock (P<0.01). Endogenous H(2)S and NO contents all negatively correlated with BP, cardiac function and the degree of hypoglycemia (P<0.01). CONCLUSIONS: The results of our study demonstrated that endogenous vascular H(2)S increased in rats with septic shock and endotoxic shock. It was suggested that endogenous H(2)S was involved in physiological and pathophysiological process during shock.

Analysis of Variance↗
PubMed1996

Activation of heat-shock transcription factor 1 by hypertonic shock in 3T3 cells.

The exposure of 3T3 cells to a medium made hypertonic by the addition of NaCl induced activation of a heat-shock transcription factor (HSF). This activation, as monitored by gel-mobility-shift assays, occurred within 10 min of hypertonic shock and was dose-dependent in relation to the osmotic strength of the medium up to 0.7 osM. Competition analysis indicated that the effect of hypertonic shock on HSF binding activity was specific. The magnitude of the heat-shock element (HSE)-HSF binding induced by incubating the cells in a 0.7 osM medium was comparable in intensity and time course with that induced by a 44 degrees C heat shock. Following removal of the stressors, the decrease in HSF-HSE binding was more rapid in hypertonicity-shocked than in heat-shocked cells. Treatment of the cells with cycloheximide did not inhibit HSF-HSE binding, indicating that the activation was independent of new protein synthesis. By using a specifically directed polyclonal serum, HSF1 was identified as the transcription factor involved in the hypertonicity-induced activation. HSF was also activated when a membrane-impermeable osmolyte such as sucrose was used to increase the osmolarity of the medium. However, no HSF-HSE binding was observed after addition of glycerol (a freely membrane-permeable osmolyte) in excess. There was a temporal relationship between the hypertonicity-induced volume decrease, the increase in the intracellular K+ concentration and the induction of HSF-HSE binding. In contrast, an increase in the intracellular Na+ concentration was not required to induce HSF-HSE binding. However, unlike the heat-shock response, the activation of HSF by hypertonic shock did not lead to elongation of the RNA transcript of heat-shock protein 70.

3T3 Cells↗
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↗
PubMed1995

Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Results of an International Registry. SHOCK Registry Investigators.

BACKGROUND: Cardiogenic shock remains the leading cause of death of patients hospitalized with acute myocardial infarction (MI). This study was conducted to examine (1) the current spectrum of cardiogenic shock, (2) the proportion of patients who are potential candidates for a trial of early revascularization, and (3) the apparent impact of early revascularization on mortality. METHODS AND RESULTS: Nineteen participating centers in the United States and Belgium prospectively registered all patients diagnosed with cardiogenic shock. Two hundred fifty-one patients were registered. The mean age was 67.5 +/- 11.7 years, and 43% were women. Acute mitral regurgitation or ventricular septal rupture was the cause of shock in 8%. Concurrent conditions contributing to the development of shock were noted in 5%, and 2% had isolated right ventricular shock. Among the remaining 214 patients, nonspecific findings on the ECG associated with "nontransmural" MI were seen in 14%. The median time to shock diagnosis after MI was 8 hours. The overall in-hospital mortality was 66%. Patients clinically selected to undergo cardiac catheterization were significantly younger and had a lower mortality than those not selected (51% versus 85%, P < .0001) even if they were not revascularized (58%). Mortality for patients undergoing percutaneous transluminal coronary angioplasty (PTCA) was 60% (n = 55) and 19% (n = 16) for coronary artery bypass graft surgery (CABG). Sixty percent (n = 150) of registered patients were judged eligible for a trial of early revascularization. Trial-eligible patients were significantly younger (65.4 +/- 11.0 versus 70.6 +/- 11.9 years, P < .001), had an earlier median time to shock onset after MI (6.5 versus 17.5 hours, P = .003), and had lower mortality (62% versus 73%, P = .077) than ineligible patients. CONCLUSIONS: Patients diagnosed with cardiogenic shock complicating acute MI are a heterogeneous group. Those eligible for a trial of early revascularization tended to have lower mortality. Patients selected to undergo cardiac catheterization had lower mortality whether or not they were revascularized. Emergent PTCA and CABG are promising treatment modalities for cardiogenic shock, but biased case selection for treatment may confound the data. Whether PTCA and CABG reduce mortality and which patient subgroups benefit most remain to be determined in a randomized clinical trial.

Aged↗