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PubMed2001

A time course study of the protective effect of mesenteric lymph duct ligation on hemorrhagic shock-induced pulmonary injury and the toxic effects of lymph from shocked rats on endothelial cell monolayer permeability.

BACKGROUND: We have previously documented that lymphatic duct division protects against shock-induced lung injury when tested 3 hours post-shock and that lymph collected at 3 hours post-shock increases endothelial cell monolayer permeability. However, whether lymph collected at other time points post-shock also increases endothelial cell permeability is not known. We tested the protective effects of lymphatic division on lung permeability at 6, 12, and 24 hours post-shock and the ability of lymph collected before, during, and hourly (up to 6 hours) after shock to increase endothelial cell monolayer permeability. METHODS: At 3, 6, 12, or 24 hours after sham or actual shock (30 mm Hg for 90 min), lung permeability was measured by using Evans blue dye in rats subjected to sham or actual mesenteric duct ligation. In separate experiments, the ability of lymph collected from rats subjected to shock or sham shock to increase human umbilical vein endothelial cell (HUVEC) monolayer permeability to a 40 kd dextran rhodamine permeability probe. Lymph was tested at 10% and 1% concentrations. RESULTS: Hemorrhagic shock induced a 3- to 4-fold increase in lung permeability compared with sham-shock rats when tested at 3, 6, 12, or 24 hours post-shock. Lymphatic division prevented this increase in lung permeability at each of these time points. Sham shock lymph did not increase HUVEC permeability, while lymph from the shocked rats did, whether tested at 1% or 10%. Lymph samples collected during the shock period and hourly for 6 hours post-shock all increased HUVEC permeability; however, the greatest relative increase in HUVEC permeability was observed in the 3- and 6- hour post-shock samples. CONCLUSIONS: Lung injury after hemorrhagic shock appears to be caused by toxic factors carried in the mesenteric lymph, and factors capable of increasing HUVEC permeability initially appear in the lymph during the shock period and increase over time.

Animals↗
PubMed1997

Patterns of cytokine evolution (tumor necrosis factor-alpha and interleukin-6) after septic shock, hemorrhagic shock, and severe trauma.

OBJECTIVE: To compare the patterns of evolution of two proinflammatory cytokines (tumor necrosis factor [TNF]-alpha and interleukin-6 [IL-6]) in two major clinical entities associated with systemic inflammatory response: septic shock and multiple trauma (with and without hemorrhagic shock). DESIGN: Prospective study of two cohorts of patients. SETTING: Critical care unit and Emergency Center of a university hospital. PATIENTS: Twenty-five nontrauma patients with septic shock and 60 multiple trauma patients (of whom eight patients were resuscitated from hemorrhagic shock). INTERVENTIONS: Serial blood samples were collected in each patient for determination of serum cytokine concentrations. Samples were obtained over 7 days in septic shock patients and 11 days in trauma patients. Standard resuscitation techniques were used in each patient. Clinical and laboratory data were prospectively collected. MEASUREMENTS AND MAIN RESULTS: High concentrations of circulating TNF-alpha and IL-6 were found in patients with septic shock. High IL-6 concentrations, but normal TNF-alpha concentrations were detected in trauma patients. At study entry, TNF-alpha concentrations were higher in nonsurvivor septic shock than in nonsurvivor trauma patients (42 +/- 7 vs 13 +/- 2 pg/mL; p < .001). During the whole study period, nonsurvivor septic shock patients maintained higher TNF-alpha concentrations than nonsurvivor trauma patients (p < .001). In survivors in both groups, normal values for TNF-alpha were detected during the whole study period. At study entry, IL-6 concentrations were significantly higher in nonsurvivor septic shock patients than in nonsurvivor trauma patients (15,627 +/- 4336 vs. 317 +/- 124 pg/mL; p < .0001). During the whole study period, much higher concentrations of IL-6 were detected in septic shock patients than in trauma patients (p < .0001). In survivors, at study entry, IL-6 concentrations were much higher in septic shock patients than in trauma patients (3947 +/- 1410 vs. 247 +/- 41 pg/mL; p < .001). Higher IL-6 concentrations were maintained throughout the study period in septic shock patients than in trauma patients (p < .001). In septic shock patients, changes in both TNF-alpha and IL-6 were correlated with outcome, higher values being found in patients likely to die. Neither TNF-alpha nor IL-6 values were of any significant value in predicting outcome of trauma patients. When septic shock patients were compared with traumatized patients resuscitated from hemorrhagic shock, the former had much higher concentrations of both TNF-alpha and IL-6 throughout the study period (p < .01 to p < .00001). Increased IL-6 values were an indicator of the development of a nosocomial infection in trauma patients. In five trauma patients who developed a nosocomial pneumonia during the study period, the IL-6 concentration was 433 +/- 385 pg/mL before the onset of pneumonia, then peaked at 3970 +/- 1478 pg/mL on day 7, and returned to baseline (219 +/- 58 pg/mL) on day 11. CONCLUSIONS: In septic shock patients, high amounts of circulating TNF-alpha and IL-6 are found and then correlate with fatal outcome. In trauma patients (even those patients resuscitated from hemorrhagic shock), much less increased concentrations of IL-6 are detected while normal TNF-alpha circulating concentrations are measured. In these patients, cytokine concentrations do not correlate with outcome. This finding suggests a much higher degree of activation of the immunoinflammatory cascade in septic shock than in multiple trauma patients. Increased IL-6 values are an indicator of the development of a nosocomial infection in trauma patients.

Adult↗
PubMed2005

Shock wave lithotripsy at 60 or 120 shocks per minute: a randomized, double-blind trial.

PURPOSE: The rate of shock wave administration is a factor in the per shock efficiency of shock wave lithotripsy (SWL). Experimental evidence suggests that decreasing shock wave frequency from 120 shocks per minute results in improved stone fragmentation. To our knowledge this study is the first to examine the effect of decreased shock wave frequency in patients with renal stones. MATERIALS AND METHODS: Patients with previously untreated radiopaque stones in the renal collecting system were randomized to SWL at 60 or 120 shocks per minute. They were followed at 2 weeks and 3 months. The primary outcome was the success rate, defined as stone-free status or asymptomatic fragments less than 5 mm 3 months after treatment. RESULTS: A total of 220 patients were randomized, including 111 to 60 shocks per minute and 109 to 120 shocks per minute. The 2 groups were comparable in regard to age, sex, body mass index, stent status and initial stone area. The success rate was higher for 60 shocks per minute (75% vs 61%, p = 0.027). Patients with larger stones (stone area 100 mm or greater) experienced a greater benefit with treatment at 60 shocks per minute. The success rate was 71% for 60 shocks per minute vs 32% (p = 0.002) and the stone-free rate was 60% vs 28% (p = 0.015). Repeat SWL was required in 32% of patients treated with 120 shocks per minute vs 18% (p = 0.018). Fewer shocks were required with 60 shocks per minute (2,423 vs 2,906, p <0.001) but treatment time was longer (40.6 vs 24.2 minutes, p <0.001). There was a trend toward fewer complications with 60 shocks per minute (p = 0.079). CONCLUSIONS: SWL treatment at 60 shocks per minute yields better outcomes than at 120 shocks per minute, particularly for stones 100 mm or greater, without any increase in morbidity and with an acceptable increase in treatment time.

Adult↗
PubMed2006

Changes of Rho kinase activity after hemorrhagic shock and its role in shock-induced biphasic response of vascular reactivity and calcium sensitivity.

The purpose of the present study is to investigate the changes of Rho kinase activity and its role in biphasic response of vascular reactivity and calcium sensitivity after hemorrhagic shock. The vascular reactivity and calcium sensitivity of superior mesenteric artery (SMA) from hemorrhagic shock rats were determined via observing the contraction initiated by norepinephrine (NE) and Ca under depolarizing conditions (120 mmol/L K) with isolated organ perfusion system. At same time, Rho kinase activity in mesenteric artery was measured, and the effects of Rho kinase activity-regulating agents, angiotensin II (Ang-II), insulin, and Y-27632, on vascular reactivity and calcium sensitivity were also observed. The results indicated that the vascular reactivity and calcium sensitivity were increased at early shock (immediate and 30 min after shock) and decreased at late shock (1 and 2 h after shock). The maximal contractions of NE and Ca were significantly increased (P < 0.05 or P < 0.01) at early shock. But they were significantly decreased at late shock (P < 0.05 or P < 0.01). Rho kinase activity was significantly increased at early shock (immediate after shock) (P < 0.05) but significantly decreased at 1 and 2 h after shock (P < 0.05 or P < 0.01). It was positively correlated with the changes of vascular reactivity and calcium sensitivity. Insulin decreased the increased contractile response of SMA to NE and Caat early shock (P < 0.05 or P < 0.01). Angiotensin II increased the decreased contractile response of SMA to NE and Ca at 2-h shock (P < 0.05 or P < 0.01); Y-27632, Rho kinase-specific antagonist, decreased the contractile response of SMA to NE and Ca at 2-h shock, and abolished Ang-II induced the increase of vascular reactivity and calcium sensitivity. The results suggest that Rho kinase may be involved in the biphasic change of vascular reactivity and calcium sensitivity after hemorrhagic shock. Rho kinase may regulate vascular reactivity through the regulation of calcium sensitivity. Rho kinase-regulating agents may have some beneficial effects on shock-induced vascular hyporeactivity.

Amides↗
PubMed1968

Actual versus potential shock in making shock situations function as negative reinforcers.

The relative importance of potential and actual shocks in making shock situations function as negative reinforcers was studied. Shocks were scheduled to occur at the same rate during two stimuli. During one, squirrel monkeys could avoid the shocks; during the other, they were unavoidable. For the two stimuli the potential rate of shocks was the same, but the actual rate was lower during avoidance because of avoidance responding. Fixed-ratio responding was maintained by the change from unavoidable shock to avoidance, indicating that the change was reinforcing when it resulted in a reduction in actual shock rate with no reduction in potential shock rate. Further increases in the rate of potential shock during avoidance had little effect upon the fixed-ratio responding until the rate was increased to the point that the actual shock rate during avoidance was comparable with that during unavoidable shock. At that point, the fixed-ratio response rate decreased nearly to zero. These findings show that actual shocks are more important than potential shocks in determining whether or not a shock situation will function as a negative reinforcer; this explains why the change from unavoidable shock to avoidable shock is reinforcing.

Animals↗
PubMed2001

Cold cardioplegic arrest enhances heat shock protein 70 in the heat-shocked rat heart.

BACKGROUND: Myocardial content of the 70-kd heat shock protein has been found to correlate with improved cardiac recovery after ischemia, but the mechanisms and conditions that regulate its level, particularly under clinical conditions, are unclear. The aim of this study was to assess the effect of hypothermic cardioplegic arrest and reperfusion on the expression of 70-kd heat shock protein in a protocol mimicking conditions of preservation for cardiac transplantation. METHODS: Heat-shocked and control hearts were subjected to 4 hours of cardioplegic arrest and global ischemia at 4 degrees C and then to 20 minutes of reperfusion. Hearts were freeze clamped at different time points-after 15 minutes of Langendorff perfusion, at the end of ischemia, and after 20 minutes of reperfusion, and analyzed for heat shock protein 70 content by Western blotting. Another set of hearts was subjected to 10 minutes of normothermic ischemia and 20 minutes of reperfusion followed by freeze clamping and analysis of heat shock protein 70 content as in cardioplegic arrest protocol. Cardiac function was measured by means of a left ventricular balloon at the end of reperfusion. RESULTS: Preischemic concentration of 70-kd heat shock protein was increased in heat-shocked hearts compared with control hearts. The content of 70-kd heat shock protein in heat-shocked hearts was further increased from 5.0 +/- 2.4 ng/microg at the end of ischemia to 11.0 +/- 4.9 ng/microg (n = 8, mean +/- SD; P <.05) at 20 minutes of reperfusion after cold cardioplegic arrest. No further rise in 70-kd heat shock protein of the heat-shocked hearts was observed after normothermic ischemia. Maximal developed pressure was 120.8 +/- 13.4 mm Hg in control hearts compared with 164.7 +/- 22.5 mm Hg in heat-shocked hearts (n = 5, mean +/- SD; P =.037) after cardioplegic arrest. By contrast, after normothermic ischemia, maximum developed pressure was 111.2 +/- 10.9 mm Hg in control hearts compared with 139.2 +/- 11.0 mm Hg in heat-shocked hearts (n = 4, mean +/- SD; P =.031). CONCLUSION: Hypothermic cardioplegic arrest but not short normothermic ischemia triggered a further increase in the level of 70-kd heat shock protein in heat-shocked rat hearts, which may enhance endogenous cardiac protection.

Analysis of Variance↗
PubMedDate not supplied

Comparison of bacterial translocation during traumatic shock and hemorrhagic shock in rats.

UNLABELLED: Traumatic shock has been classified as a kind of hypovolemic shock similar to hemorrhagic shock. Since bacterial translocation has been observed in shock, this study investigated the difference in bacterial translocation during traumatic shock and hemorrhagic shock, and considered this effect on lung injury during sepsis. METHODS: Forty-eight male or female Sprague-Dawley rats were divided into 2 groups, hemorrhagic shock and traumatic shock. Bacterial translocation, endotoxin, and blood gas were evaluated. Alterations of the lungs morphologically and functionally were observed. RESULTS: Traumatic shock induced more bacterial translocation and endotoxemia from the gut. Blood gas analysis shows a more severe disorder in traumatic shock than in hemorrhagic shock. Pathological morphologic changes of lungs were more severe in traumatic shock than in hemorrhagic shock. CONCLUSIONS: Traumatic shock cause more bacterial translocation and endotoxemia which subsequently caused serial pathological alterations in lung morphologically and functionally than pure hemorrhagic shock does. These results suggest that this trauma activates more severe mechanism to damage lungs.

Animals↗
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↗
PubMed1972

Effects of response-shock interval and shock intensity on free-operant avoidance responding in the pigeon.

Two experiments investigated free-operant avoidance responding with pigeons using a treadle-pressing response. In Experiment I, pigeons were initially trained on a free-operant avoidance schedule with a response-shock interval of 32 sec and a shock-shock interval of 10 sec, and were subsequently exposed to 10 values of the response-shock parameter ranging from 2.5 to 150 sec. The functions relating response rate to response-shock interval were similar to the ones reported by Sidman in his 1953 studies employing rats, and were independent of the order of presentation of the response-shock values. Shock rates decreased as response-shock duration increased. In Experiment II, a free-operant avoidance schedule with a response-shock interval of 20 sec and a shock-shock interval of 5 sec was used, and shock intensities were varied over five values ranging from 2 to 32 mA. Response rates increased markedly as shock intensity increased from 2 to 8 mA, but rates changed little with further increases in shock intensity. Shock rates decreased as intensity increased from 2 to 8 mA, and showed little change as intensity increased from 8 to 32 mA.

Animals↗
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↗
PubMed2002

Stone fragmentation during shock wave lithotripsy is improved by slowing the shock wave rate: studies with a new animal model.

PURPOSE: The current trend toward ungated shock wave lithotripsy means that more patients are being treated with shock waves delivered at a rapid rate (120 shock waves per minute or greater). However, no benefit of an increased shock wave rate has been shown and in vitro studies indicate that slowing the shock wave rate actually improves stone fragmentation. We tested the effect of the shock wave rate on stone comminution in a new animal model. MATERIALS AND METHODS: Gypsum model stones were inserted via upper pole percutaneous access into the lower pole calix of the kidneys of female pigs weighing approximately 100 pounds. Shock wave lithotripsy was performed (400 shock waves uninterrupted at 20 kV. and 30 or 120 shock waves per minute) 2 hours later using an unmodified HM3 lithotriptor (Dornier Medical Systems, Marietta, Georgia). After en bloc excision of the urinary tract stone fragments were collected and sieved through 2 mm. mesh. The particles were weighed and surface area was determined. RESULTS: Stones treated at 30 shock waves per minute broke more completely than stones treated at 120 shock waves per minute. The percent of fragments greater than 2 mm. was significantly higher for stones treated at the fast rate of 120 versus the slow rate of 30 shock waves per minute (mean +/- SEM 81% +/- 14% versus 45% +/- 12%, p <0.005). When stone fragmentation was expressed as the percent increase in fragment surface area, significantly greater fragmentation occurred at the slower than at the more rapid rate (327% +/- 63% versus 135% +/- 136%, p <0.02). CONCLUSIONS: Slowing the rate of shock wave administration during shock wave lithotripsy significantly improves the efficiency of stone fragmentation in vivo.

Animals↗
PubMed1978

Acceleration and suppression of rats' responding to avoid foot shock and tail shock.

Signalled response-independent shocks were superimposed on rats' wheel-turn responding to avoid shock administered to their feet through a grid floor or to their tails through fixed electrodes. In Experiment I, a tone paired with response-independent foot shock increased responding in three of four rats; a tone paired with tail shock increased responding in only one of four rats and suppressed responding in two rats. In Experiment II, a tone presented randomly with respect to response-independent shock had no reliable effect on responding to avoid foot shock or tail shock. In Experiment III, tail shock and foot shock were compared in a within-subject design while the temporal pattern of responding during conditioned stimuli was recorded. Responding during the conditioned stimulus preceding foot shock was characterized by initial suppression of responding at tone onset, followed by increased responding just before response-independent shock. Responding was suppressed throughout the conditioned stimulus preceding tail shock. Foot shock elicited bursts of responding, but tail shock did not.

Journal Article↗
PubMed1996

Astrocyte survival and HSP70 heat shock protein induction following heat shock and acidosis.

Although severe acidosis is an important mediator of brain infarction, recent evidence suggests that mild acidosis may protect ischemic cells. The HSP70 heat shock protein is induced by acidosis in cultured cells and in ischemic brain and protects cells against many types of injury. Therefore, this study determined whether induction of heat shock proteins protects cultured astrocytes against acidosis. Brief exposure of cultured cortical astrocytes to acid (pH 5.2 for 40 min) or heat shock (45 degrees C for 40 min) markedly induced hsp70 mRNA and HSP70 protein. HSP70 protein was detected with the C92 monoclonal antibody (Welch and Suhan: J Cell Biol 103:2035, 1986), which has been shown to recognize the protein product of the full-length rat hsp70 cDNA (Longo et al: J Neurosci Res 36:325, 1993). Heat shock of the cultured cortical astrocytes completely protected the astrocytes from an otherwise lethal heat exposure 24 h later (45 degrees C for 4 h). In contrast, heat pretreatment sensitized the astrocytes to injury from acidosis 24 h later. Acid pretreatment, which markedly induced the HSP70 protein without producing astrocytic cell death, similarly sensitized the cells to injury from acidosis 24 h later (60% survival following pH 5.2 for 3 h versus 90% survival in controls; P < 0.0001). Surprisingly, heat shock pretreatment protected astrocytes against exposure to acid 48 h later (P < 0.05, 1.5-3 h), whereas acid pretreatment had no effect on astrocyte survival 48 h later. Since heat shock did not protect against acidosis at 24 h when HSP70 induction was maximal but did protect at 48 h when HSP70 was markedly diminished, the protective effect of heat shock at 48 h may be related to stress proteins present at 48 h. It is concluded that induction of HSP70 and other heat shock proteins by heat shock protects astrocytes against subsequent lethal heat shock. However, heat shock and acid treatment increase the vulnerability of astrocytes to acidosis 24 h later in spite of the induction of HSP70 heat shock proteins. The finding that heat shock protected astrocytes against acidosis 2 days later may suggest that delayed induction of stress proteins partially protects the astrocytes against damage produced by high concentrations of hydrogen ions.

Acidosis↗
PubMed2003

Cardiogenic shock complicating acute myocardial infarction; prognostic impact of early and late shock development.

AIMS: Cardiogenic shock accounts for the majority of deaths following acute myocardial infarction. The majority of outcome data on this issue are, however, derived from single hospitals, referral centers or selected patients in randomized studies. The purpose of this study was to investigate incidence, outcome and prognostic significance of cardiogenic shock in 6676 consecutive patients with acute myocardial infarction. METHODS AND RESULTS: Demographic and clinical data including the presence of cardiogenic shock were prospectively collected in 6676 non-invasively managed patients with myocardial infarction consecutively admitted to 27 different hospitals during a 2-year period. Six-year mortality data were collected in 99.9% of the population. Cardiogenic shock developed in 444 patients (6.7%). In 59% of these patients cardiogenic shock developed within 48 h, 11% developed shock during days 3 and 4 and 30% later than 4 days after the infarction. Thirty-day and 6-year mortality was 62 and 88% among shock patients compared to 9 and 45% in non-shock patients. Patients with early shock development (days 1-2) had a significantly lower 30-day mortality (45%) than those with intermediate or late shock development (>80%) (P<0.05). In 30-day survivors, survival the following years was lower than in patients without cardiogenic shock but with post-infarction heart failure. CONCLUSIONS: In this nationwide prospectively collected registry, non-invasively managed consecutive myocardial infarct patients with cardiogenic shock had an extremely reduced life expectancy. Every attempt to improve treatment, prevention and identification of patients at risk of shock development should be strongly encouraged.

Aged↗
PubMed2003

Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry.

OBJECTIVES: The purpose of this study was to determine the characteristics and outcomes of patients with acute myocardial infarction (MI) complicated by cardiogenic shock due to predominant right ventricular (RV) infarction. BACKGROUND: Although RV infarction has been shown to have favorable long-term outcomes, the influence of RV infarction on mortality in cardiogenic shock is unknown. METHODS: We evaluated 933 patients in cardiogenic shock due to predominant RV (n = 49) or left ventricular (LV) failure (n = 884) in the SHould we emergently revascularize Occluded coronaries for Cardiogenic shocK? (SHOCK) trial registry. RESULTS: Patients with predominant RV shock were younger, with a lower prevalence of previous MI (25.5 vs. 40.1%, p = 0.047), anterior MI, and multivessel disease (34.8 vs. 77.8%, p < 0.001) and a shorter median time between the index MI and the diagnosis of shock (2.9 vs. 6.2 h, p = 0.003) in comparison to patients with LV shock. In-hospital mortality was 53.1% versus 60.8% (p = 0.296) for patients with predominant RV and LV shock, respectively, and the influence of revascularization on mortality was not different between groups. Multivariate analysis revealed that RV shock was not an independent predictor of lower in-hospital mortality (odds ratio 1.07, 95% confidence interval 0.54 to 2.13). CONCLUSIONS: Despite the younger age, lower rate of anterior MI, and higher prevalence of single-vessel coronary disease of RV compared with LV shock patients, and their similar benefit from revascularization, mortality is unexpectedly high in patients with predominant RV shock and similar to patients with LV shock.

Aged↗
PubMed2003

Hemorrhagic shock induces an S 100 B increase associated with shock severity.

S 100 B is a glial marker of cerebral Injury. In a previous clinical study, we found an S 100 B increase within the first 24 h in patients with multiple trauma and hemorrhagic shock but without cerebral trauma. The aim of our current experimental study was to determine whether this posttraumatic S 100 B increase is caused by extracerebral soft tissue injury or by hemorrhagic shock and whether it is associated with the severity of hemorrhagic shock. Hemorrhagic shock was achieved by bleeding anesthetized rats to a mean arterial pressure (MAP) of 30-35 mmHg through a femoral catheter and maintaining this MAP until incipient decompensation. At incipient decompensation, MAP was either increased immediately to 40-45 mmHg (moderate shock) or was maintained until 40% of shed blood had been returned (severe shock), and then increased to 40-45 mmHg. Resuscitation was provided after 40-45 mmHg MAP had been maintained for 40 min. Soft tissue injury was achieved by midline laparotomy performed at the onset of hemorrhagic shock or without shock and was maintained for 30 min. Hemorrhagic shock caused an early S 100 B increase at the onset of decompensation. S 100 B remained increased for 24 h and was significantly higher after severe than after moderate shock. In contrast, soft tissue injury without hemorrhagic shock caused no S 100 B increase. The data presented demonstrate for the first time that the S 100 B increase is induced by hemorrhagic shock and is associated with the severity of shock.

Acidosis↗
PubMed1998

Cytoprotection and regulation of heat shock proteins induced by heat shock in human breast cancer T47-D cells: role of [Ca2+]i and protein kinases.

Overexpression of heat shock protein 70 kDa alters the susceptibility of tumor cells to chemotherapeutic agents. We conducted experiments to study the regulation of expression of heat shock proteins (HSPs) in heat shock-treated T47-D cells, a human breast cancer cell line that expresses estrogen receptors. Cells exposed to heat shock at 44 degreesC displayed increased expression of heat shock protein 72 kDa (HSP-72), glucose-regulated protein 78 kDa (GRP-78), and GRP-94 in a time-dependent manner, as shown by [35S]methionine incorporation and Western blotting experiments. The maximal rate of synthesis occurred between 2 and 4 h after heat shock. Removal of external Ca2+ inhibited the synthesis of the heat shock-induced GRP-78 but not of HSP-72 and GRP-94, whereas treatment of cells with BAPTA (a Ca2+ chelator) inhibited HSP-72 and GRP-78. Treatment with H89 (a protein kinase A inhibitor) blocked the heat shock-induced GRP-78 synthesis, whereas GF-109203X (a protein kinase C inhibitor) attenuated the heat shock-induced HSP-72 synthesis and completely blocked synthesis of GRP-78 but not of GRP-94. These results indicate that protein kinase C is involved in regulation of the heat shock-induced synthesis of HSP-72, whereas PKA and PKC are involved in the regulation of GRP-78 synthesis. Cells overexpressing HSP-72 and GRPs after heat shock displayed resistance against lethal temperature (47 degreesC for 50 min) -induced death, which was diminished after removal of external Ca2+ and treatment with GF-109203X. Heat shock increased intracellular free Ca2+ concentration ([Ca2+]i) in a temperature- and heating duration-dependent fashion, and the increase was inhibited in the absence of external [Ca2+]i and significantly reduced by pretreatment with H89 and GF-109203X. The results suggest that different pathways are involved in the induction of synthesis of HSP-72, GRP-78, and GRP-94 by heat shock. It is highly likely that only HSP-72 and GRP-78 are involved in the process of cytoprotection from the thermal injury.

Calcium↗