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G T Shires

Publications and source records attributed to G T Shires.

At least 19 recordsLinked to original sources
PubMed1996

Effects of isotonic saline solution resuscitation on blood coagulation in uncontrolled hemorrhage.

BACKGROUND: It has been suggested that fluid resuscitation before surgical control of hemorrhage may lead to increased bleeding because of the elevated blood pressures and clotting factor dilution. This study was designed to assess the effects of isotonic saline solution resuscitation on blood coagulation during uncontrolled hemorrhage. METHODS: Twenty-four female Sprague-Dawley rats were randomized into four groups with different resuscitation regimens: group A, no resuscitation; group B, 40 ml/kg in 4 minutes; group C, 80 ml/kg in 4 minutes; and group D, 80 ml/kg in 1 minute. Baseline blood samples were collected just before a sharp resection of 75% of the tail to initiate the hemorrhage; 15 minutes later the resuscitation began. Additional blood samples were obtained at 60 minutes after resection. The blood was analyzed for platelets, fibrinogen, prothrombin time, and activated partial thromboplastin time. RESULTS: The largest differences between time 0 and 60 minutes were observed in group D with platelets decreasing 43.36% +/- 7.86%, fibrinogen decreasing 57.10% +/- 16.88%, and prothrombin time increasing from an average 16.5 to 19.2 seconds. These differences was statistiacally significant (p <0.05) with the Student's test. CONCLUSIONS: The results suggested that even though the volume of resuscitation fluid did not appear to affect clotting time when compared with that of nonresuscitated animals, the rate of extremely large volume infusions may play an important role in the cessation of bleeding and consequently in the management of uncontrolled hemorrhagic shock.

Animals↗
PubMed1996

The role of tumor necrosis factor and nitric oxide in the acute cardiovascular response to endotoxin.

OBJECTIVE: This study was designed to examine the differential effects of tumor necrosis factor (TNF) and nitric oxide on the acute cardiovascular changes that occur in response to endotoxemia. SUMMARY BACKGROUND DATA: Recent studies have suggested that some, if not all, of the cardiovascular effects of TNF are mediated through release of nitric oxide. However, the mechanisms through which TNF and nitric oxide induce hypotension and shock in vivo in response to systemic endotoxemia remain poorly characterized, despite current interest in the use of nitric oxide antagonists to ameliorate septic shock. METHODS: A reproducible model of endotoxemia was established in adult Sprague-Dawley rats. The acute cardiovascular changes that occur after bolus infusion of endotoxin was then determined in rats treated with either TNF antibody, N-methyl arginine, or both. RESULTS: Inhibition of either TNF or nitric oxide restores mean arterial blood pressure to normal after endotoxemia (p < 0.05). However, nitric oxide exerts its effects principally on the peripheral vasculature, whereas TNF appears to act on the myocardium. A combination of TNF antiserum pretreatment and N-methyl arginine administration is necessary to return mean arterial blood pressure to normal 60 minutes after endotoxin infusion. CONCLUSION: Tumor necrosis factor and nitric oxide mediate the acute cardiovascular effects of endotoxemia through distinct mechanisms. Nitric oxide is released as a result of both TNF-dependent and TNF-independent mechanisms, whereas the cardiovascular effects of TNF are only partially mediated through nitric oxide.

Animals↗
PubMed1995

Influence of hypercortisolemia on soluble tumor necrosis factor receptor II and interleukin-1 receptor antagonist responses to endotoxin in human beings.

BACKGROUND: We have previously reported that the antecedent administration of glucocorticoids altered both the hormonal and proinflammatory cytokine responses to lipopolysaccharide (LPS) when administered to human volunteers. In that study, subjects with vastly exaggerated levels of tumor necrosis factor (TNF) and interleukin (IL)-6 12 and 144 hours after cortisol infusion exhibited hemodynamic and hormonal responses no different from those of untreated subjects after endotoxin. The current study examined levels of the antiinflammatory cytokines interleukin-1 receptor antagonist (IL-1ra) and soluble receptors to tumor necrosis factor (sTNF-R) in the same setting of the previous report. METHODS: Hydrocortisone succinate was infused into healthy volunteers. LPS was then injected immediately or was delayed by 6, 12, or 144 hours (C, C-6, C-12, and C-144, respectively). Subjects receiving LPS alone served as controls. Plasma was analyzed to determine levels of TNF, sTNF-R and IL-1ra by enzyme-linked immunosorbent assay before administration of LPS and at 30-minute intervals after administration of LPS for 6 hours. RESULTS: Levels of sTNF-R increased after LPS administration in all groups (p < 0.05 versus baseline) with a significantly higher level recorded in the subjects having received hydrocortisone 144 hours before (C-144, p < 0.05 versus all other groups). TNF levels remained undetectable in association with immediate infusion of LPS (C) and the relatively short delay group (C6). This cytokine peaked 90 minutes after LPS in all other groups, with a significantly higher peak in the C-144 subjects when compared with controls. IL-1ra levels rose in all groups but to a lesser extent in the C group (p < 0.05). CONCLUSIONS: These data confirm that glucocorticoids influence the production of both sTNF-R and IL-1ra. The potential for an exaggerated response of sTNF-R exists for an extended period of time after exposure to glucocorticoids.

Adult↗
PubMed1995

Isotonic saline resuscitation in uncontrolled hemorrhage under various anesthetic conditions.

OBJECTIVE: The authors evaluated the effect of early fluid resuscitation with isotonic saline (NaCl, 0.9%) on uncontrolled hemorrhage in rats under different anesthetic conditions. SUMMARY/BACKGROUND DATA: Recently, it has been suggested that administration of fluids to patients during uncontrolled hemorrhage may produce adverse effects, and a postponement of resuscitation until surgical control of bleeding was recommended. Past clinical trials were inconclusive, and the results of recent experimental studies were affected by use of vasoactive anesthetics. METHODS: One hundred thirty-five female Sprague-Dawley rats were randomly divided into three groups: group 1--unanesthetized; group 2--anesthetized with sodium pentobarbital; and group 3--anesthetized with a mixture of droperidol and ketamine. Uncontrolled hemorrhage was initiated with a 75% tail resection, and each group was further subdivided into three subgroups for the following treatment: (A) no resuscitation; (B) 40 mL/kg of isotonic saline; or (C) 80 mL/kg of isotonic saline, administered 15 minutes after the initiation of hemorrhage. Blood loss volume and survival time were recorded, and animals were observed up to 360 minutes. RESULTS: At 6 hours, nonresuscitated animals of all groups exhibited the highest mortality rates (93%, 73%, 100% in groups 1, 2, and 3, respectively). Resuscitation significantly improved the survival; lowest mortality rates were observed after resuscitation with 80 mL/kg in groups 1 and 3 (33%) and 40 mL/kg in group 2 (40%). Fluid infusion increased hemorrhage rates in all anesthetized rats. No such increases in bleeding were observed in group 1. CONCLUSIONS: Resuscitation with isotonic saline improved mortality in uncontrolled hemorrhage, even with concomitant increases in hemorrhage rates, under all three anesthetic conditions tested. Unanesthetized rats bled less than the animals under anesthesia and did not exhibit an increased blood loss in response to fluid infusion.

Anesthesia↗
PubMed1995

Effects of anesthesia on a model of uncontrolled hemorrhage in rats.

OBJECTIVES: Excessive blood loss in a rat model of uncontrolled hemorrhage has been attributed to the vasodilatory effects of a droperidol-ketamine mixture used for anesthesia. The present study compared responses to droperidol-ketamine and pentobarbital with those responses of a control group without anesthesia during uncontrolled hemorrhage. DESIGN: Prospective, randomized, controlled trial. SETTING: University surgical research laboratory. SUBJECTS: Forty-five female Sprague-Dawley rats (210 to 275 g). INTERVENTIONS: Rats were randomly divided into three groups of 15 each according to the type of anesthesia: unanesthetized; pentobarbital; and droperidol-ketamine. A 75% tail resection was used to initiate hemorrhage. Mortality, survival time, and blood loss were monitored, and the differences between all three groups were tested using chi 2 test (mortality) and one-way analysis of variance (ANOVA) (survival and blood loss) for statistical significance. MEASUREMENTS AND RESULTS: Mean blood loss amounts at 15 mins were 8.9, 13.6, and 22.4 mL/kg for the unanesthetized, pentobarbital, and droperidol-ketamine groups, respectively. Mortality rates for the three groups were 0%, 0%, and 53% at 30 mins and 60%, 33%, and 93% at 90 mins, respectively. Mean survival times for these groups were 94, 135, and 39 mins, respectively. CONCLUSIONS: An excessive rate of blood loss due to the use of droperidol-ketamine anesthesia renders this model inappropriate for investigation of uncontrolled hemorrhage. The response of rats under pentobarbital anesthesia more closely approximates that of unanesthetized rats. However, the higher mortality rate despite the lesser hemorrhage observed in the latter group seems to indicate the existence of other factors (in addition to blood loss) that may contribute to the early death of these animals.

Analysis of Variance↗
PubMed1995

Protective effect of selenium on hemoglobin mediated lipid peroxidation in vivo.

The toxicity of hemoglobin (Hb) solutions is related, at least in part, to the generation of oxygen free radicals with consequent induction of lipid peroxidation. The present study was designed to examine whether selenium (Se) may prevent the oxidative damage observed after Hb administration. Three groups of rats were compared; (I) the negative control group receiving autotransfusion; (II) the positive control group with replacement of 40% total blood volume (TBV) with modified bovine Hb solution; and (III) the experimental group which received dietary supplemented selenium (Na2SeO3) in daily doses of 5 micrograms.kg body wt-1 in drinking water, 4 days before and 3 days after administration of Hb solution in the same volume as in group II. Three days after Hb injection, all animals were sacrificed. Oxidative stress was determined by measuring conjugated dienes (CD) and thiobarbituric acid reactants (MDA) in homogenates of the perfused liver, heart, lungs, kidney, brain and plasma. Additionally, the 45k x g supernatants of the organs homogenates and plasma were assayed for the antioxidant enzymes activity: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and the intracellular level of reduced glutathione (GSH). Also, a measurement of nonprotein bound intracellular free iron (Fe) and tissue Se concentrations was performed. Simultaneously, injury dysfunction of vital organs was assessed by the measurement of plasma LDH, SGPT, creatinine, blood PaO2 and by histopathological studies. Results indicate that the exchange transfusion with Hb solution introduced significant increases in CD and MDA formation, particularly in the liver and heart tissues, and in plasma. While the values of the SOD and CAT in the liver and heart tissue were generally altered, the SOD/CAT ratio was also increased. After the Hb injection, activity of GSH-Px remained unchanged and was associated with significant depletion of GSH. The plasma levels of SGPT and LDH were increased, but the creatinine and PaO2 was similar to that of the control and corresponded with histopathological findings. The liver and heart intracellular free Fe was found to be higher than that of control. Treatment with Se was very effective in the prevention of oxidative damage introduced by Hb. Full protection from MDA formation was noted in liver tissue (p < 0.001). Also, plasma levels of MDA, SGPT and LDH were significantly decreased and appeared similar to that of the control group (I). Treatment with Se increased liver (p < 0.05) and plasma (p < 0.1) level of GSH-Px.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Extracorporeal life support for the treatment of adult respiratory distress syndrome after burn injury.

The pediatric population comprises 38% of hospital admissions for burns in the United States. In the age group of 1- to 14-year-olds, a 62% total body surface area burn represents the median lethal dose and carries a lower mortality rate for burn size than in infants or adults. Adult respiratory distress syndrome (ARDS) is a common accompaniment to severe burn injury. Mortality rates of 50% to 80% are expected once ARDS occurs. This is a report of an 11-month-old boy who had fulminant ARDS after a 32% total body surface area second degree burn. After conventional therapy with maximum mechanical ventilatory support failed, salvage therapy with extracorporeal membrane oxygenation (ECMO) was instituted. ECMO was successfully terminated after 28 days. Open lung biopsy specimens obtained before instituting ECMO and on ECMO day 26 exhibited severe but histologically reversible lung disease and improved alveolar aeration as a result of treatment. This is the first reported survival of a pediatric patient with thermal injury and ARDS by using ECMO for the treatment of respiratory failure.

Burns↗
PubMed1994

Alterations of pulmonary gas exchange after superimposed carbon monoxide poisoning in acute lung injury.

BACKGROUND: Smoke inhalation injury produces substantial morbidity and mortality caused both by immediate catastrophic pulmonary failure and by the subsequent development of pneumonia. Although carbon monoxide (CO) poisoning is present to a degree in nearly all instances of smoke inhalation, the importance of CO in the pathogenesis of smoke inhalation injury remains controversial because smoke contains numerous other potential pulmonary toxins such as aldehydes, chlorine gas, and hydrochloric acid. This study was performed to determine whether CO poisoning acts as a cofactor in the evolution of inhalation injury. METHODS: Four groups of anesthetized dogs received ventilation with 1% CO in room air alone, intratracheal instillation of 2.0 ml/kg 0.1 N hydrochloric acid (HCl) alone, or acid either immediately or 30 minutes before CO. Ventilation/perfusion relationships were measured for 4 hours thereafter with the multiple inert gas elimination technique. RESULTS: Acid instillation established 30 minutes before CO poisoning resulted in significantly decreased carboxyhemoglobin concentrations after ventilation with 1% CO in air for 10 minutes. However, CO elimination was markedly delayed in both acid-challenged groups ventilated with CO. Moreover, acid instillation immediately before CO poisoning significantly exacerbated the development of ventilation/perfusion inequality caused by the acid, because the development of shunt was accelerated. CONCLUSIONS: CO poisoning is an important cofactor in the development of inhalation injury by acceleration of the development of ventilation/perfusion inequality after inhalation.

Animals↗
PubMed1993

Thulium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetrakis(methylene phosphonate) as a 23Na shift reagent for the in vivo rat liver.

The use of thulium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetrakis(methylene phosphonate (TmDOTP5-) as an in vivo 23Na NMR shift reagent for rat liver was evaluated by collecting interleaved 23Na and 31P spectra. Infusion of 80 mM TmDOTP5- without added Ca2+ produced baseline-resolved peaks from intra- and extracellular sodium without producing any changes in phosphate metabolite resonances or intracellular pH. Several key physiological parameters measured in parallel groups of animals confirmed that liver physiology is largely unaffected by this shift reagent. A direct comparison of TmDOTP5- versus DyTTHA3- showed that after infusion of 5-8 times more DyTTHA3-, the extracellular sodium peak shifted by the same amount as with TmDOTP5-, but the two 23Na resonances were very broad and not resolved. The baseline-resolved peaks with TmDOTP5- allowed us to measure the in vivo T1 and T2 relaxation characteristics of intra- and extracellular Na+. The measured T1, T2s, and T2f values and the relative contributions from the slow and fast T2 components for intracellular Na+ in liver did not differ significantly from the values reported for perfused frog heart. The T1 and T2 relaxation curves of the extracellular Na+ resonances fit a monoexponential function. Analysis of the relative contribution of the fast- and slow-relaxing T2 components from intracellular Na+ resulted in a calculated visibility factor of 69 +/- 4% and the intracellular Na+ concentration calculated from the NMR peak intensity ratio, the measured visibility factor, and literature values of intra- and extracellular volume was 19 mM. These results indicate that TmDOTP5- promises to be quite useful as an in vivo shift reagent for liver and other organs.

Animals↗
PubMed1993

The effects of isotonic saline volume resuscitation in uncontrolled hemorrhage.

In the present study, the effects of early isotonic fluid resuscitation on uncontrolled hemorrhage in rats under pentobarbital anesthesia were assessed. Forty-five female Sprague-Dawley rats, weighing between 230 and 295 grams, were anesthetized and cannulated. Uncontrolled hemorrhage was initiated by a 75 percent tail resection, and the rats were randomly divided into three groups: group 1, no resuscitation; groups 2 and 3, saline solution administration over a four minute interval (40 and 80 milliliters per kilogram, respectively), 15 minutes after the initial hemorrhage. Changes in blood pressure, blood loss and mortality rates were recorded and the rats were observed for up to 360 minutes. The mortality rates were 73, 40 and 53 percent for groups 1, 2 and 3, respectively. The corresponding average survival times for these groups were 135, 195 and 178 minutes. The difference between groups 1 and 2 were above the 95 percent confidence level using the chi-square test (mortality) and the Student's t test. The average total blood loss in groups 2 and 3 was 31.7 and 41.4 milliliters per kilogram of body weight; when compared with group 1 (24.6 milliliters per kilogram), the difference between the two latter groups (1 and 3) was statistically significant with a p < 0.001. These results suggest that early infusion of isotonic fluid improves survival time and reduces short term mortality in uncontrolled hemorrhage regardless of the associated increases in blood loss.

Animals↗
PubMed1992

Macrophage inflammatory protein 1 modulates macrophage function.

Macrophage inflammatory protein 1 (MIP 1), initially purified from the conditioned medium of endotoxin-stimulated macrophages, is a low m.w. heparin-binding protein doublet comprising two peptides, MIP 1 alpha and MIP 1 beta. Although native doublet MIP 1 has previously been shown to exert pyrogenic, mitogenic, and proinflammatory effects on other cell types, its actions on its cell of origin, the macrophage, have not been well catalogued. Our study reports several aspects of macrophage function that are modulated by MIP 1. MIP 1 was not directly cytotoxic for WEHI tumor cells, but MIP 1-treated macrophage exhibited enhanced antibody-independent macrophage cytotoxicity for tumor targets. MIP 1 treatment stimulated proliferation of mature tissue macrophages, and this effect was enhanced upon costimulations with either CSF-1 or granulocyte-macrophage-CSF. Thioglycollate-elicited peritoneal exudate macrophages incubated with native doublet MIP 1-secreted bioactive TNF and IL-6, as well as immunoreactive IL-1 alpha, and these effects were enhanced significantly when the cells were costimulated with IFN-gamma. Purified preparations of the recombinantly derived MIP 1 alpha peptide alone stimulated the secretion of TNF, IL-1 alpha, and IL-6 by peritoneal macrophages, but MIP 1 beta did not. In fact, as little as eightfold excess MIP 1 beta blocked TNF-induction by MIP 1 alpha to a significant degree. By contrast to these apparent "macrophage activating" properties of MIP 1, the cytokine failed to trigger the macrophage oxidative burst, or to up-regulate the expression of Ia on the macrophage surface. Taken together, these data reveal that MIP 1 peptides act as autocrine modulators of their cells of origin, and raise the possibility that MIP 1 peptides may play a role in modulating macrophage responses to inflammatory stimuli in vivo.

Animals↗
PubMed1992

Effect of cyclosporine on adrenocortical response to injury and infection.

The effects of cyclosporine administration on the adrenocortical response to the severe stress of burn wound sepsis were studied in Wistar rats. Animals were treated with cyclosporine (10 mg/kg/day) or saline by gavage for 10 days, then subjected to 30% scald burns with wound inoculation with Pseudomonas. Animals were sacrificed on Postburn Days (PBDs) 1, 4, and 7 for determination of serum corticosterone and ACTH levels and adrenal weights and histology. Adrenal glands from animals sacrificed on PBD 7 were also analyzed for DNA, RNA, and protein content. Cyclosporine treatment without injury had no significant effect on body weight gain, adrenal mass, or baseline ACTH or corticosterone levels. During sepsis, cyclosporine-treated animals demonstrated a significantly diminished adrenocortical response compared to those given only saline. Serum corticosterone levels in the cyclosporine group were 45, 53, and 62% lower on PBDs 1, 4, and 7, respectively, than in saline-treated controls (P < 0.01 on each day). ACTH levels were 43 and 36% lower in cyclosporine-treated animals on PBDs 4 and 7, respectively, compared to the saline-treated group (P < 0.05 on each day). Adrenal hyperplasia occurred in both groups by PBD 7, but increases in adrenal mass and in histologic changes associated with hyperplasia (lipid depletion, vascular dilation) were less pronounced in cyclosporine-treated animals compared to those receiving saline, while adrenal composition remained similar between the two groups. Thus, cyclosporine administration is associated with an attenuated adrenocortical response to the stress of sepsis due to diminished circulating levels of ACTH.

Adrenal Cortex↗
PubMed1992

Hypothermia relieves oxidative stress in reperfused skeletal muscle following partial ischemia.

The impact of hypothermia on reperfusion-associated oxidative stress in postischemic skeletal muscle was evaluated in a small animal model of high-grade partial ischemia. The infrarenal aorta of heparinized Sprague-Dawley rats was clamped for 90 min, declamped, and then reperfused for 60 min. Previous characterization of this model with 51Cr-tagged microspheres revealed that hindlimb perfusion during aortic clamping continued at 16.6% of baseline values. Resting transmembrane potential difference (Em) and tissue malondialdehyde (MDA), lactate and high-energy phosphate content were determined in hindlimb skeletal muscle at baseline, during ischemia, and upon reperfusion. Four experimental groups (N = 7 in each group) were studied: control animals underwent aortic clamping and declamping; hypothermia animals underwent topical cooling of hindlimbs prior to aortic clamping, with muscle temperatures maintained between 5 and 15 degrees C during ischemia; sham animals underwent midline laparotomy only; and hypothermia-sham animals underwent cooling and midline laparotomy only. During ischemia, resting Em (-mV) was significantly depolarized (P < 0.05 versus baseline) in control (74.9 +/- 0.8 from 91.0 +/- 0.1), hypothermia (64.4 +/- 1.1 from 90.9 +/- 0.3), and hypothermia-sham (67.2 +/- 1.4 from 90.9 +/- 0.4) animals. Upon reperfusion, resting Em remained depolarized in control animals (74.7 +/- 1.6), while repolarization occurred in hypothermia (88.8 +/- 1.1) and hypothermia-sham (90.7 +/- 0.3) animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1992

Differential effects of cyclo-oxygenase and thromboxane synthetase inhibition on ventilation-perfusion relationships in acid aspiration-induced acute lung injury.

Cyclo-oxygenase metabolites are important regulators of pulmonary vascular and airway tone and may act to regulate ventilation-perfusion (VA/Q) relationships. Hypoxemia that follows aspiration of gastric acid is associated with increased venous admixture, and plasma levels of thromboxane (TX) B2 and 6-keto-PGF2 alpha are increased after experimental acid-induced acute lung injury. The present study was designed to determine the effects of cyclo-oxygenase metabolites on VA/Q relationships in canine acid aspiration. Eighteen anesthetized dogs received 0.2 mL/kg 0.1 N HCl intratracheally; six were pretreated with ibuprofen (IBU), a cyclo-oxygenase inhibitor, 12.5 mg/kg IV, and six other dogs received OKY-046 (OKY), a TX synthetase inhibitor, 0.5 mg/kg IV. The remaining six animals (ACID) served as controls. Continuous distributions of ventilation and perfusion were evaluated with the multiple inert gas elimination technique. Within 30 minutes, acid injury resulted in significant (p < 0.05) decreases in PaO2 from baseline values by 44.7 +/- 5.4 and 47.6 +/- 4.8 mm Hg in the ACID and OKY groups, respectively. Although decreased, the change in PaO2 of 21.0 +/- 4.8 mm Hg in IBU animals was significantly (p < 0.05) attenuated in comparison with the other groups. Ibuprofen increased pulmonary vascular resistance, attenuated perfusion to shunt and low VA/Q areas, and reduced ventilation to unperfused areas for the first 2 hours after acid injury (all p < 0.05), whereas OKY exacerbated hypoxemia and VA/Q inequality.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Oxygen free radicals affect cardiac and skeletal cell membrane potential during hemorrhagic shock in rats.

Oxygen free radical (OFR) damage of excitable cell membranes (heart and skeletal muscle) during hemorrhagic shock and after resuscitation was studied in control rats and in rats pretreated with superoxide dismutase (SOD) and catalase (CAT; 6,000 U each) before hemorrhage. Their mean arterial pressure (MAP) was lowered to and maintained at 45 mmHg until 30% of the shed blood was spontaneously reinfused. The remaining blood and twice that volume of lactated Ringer solution were then infused. Cardiac output and organ blood flow were measured by the microsphere technique. The resting membrane potential (Em) and tissue ATP content in the heart and skeletal muscle were determined. There was no significant difference between the control and SOD + CAT groups in shock duration, maximal shed blood, hemodynamics, regional blood flow, or in ATP content in both heart and skeletal muscle, both during shock and after resuscitation. Radical scavenger treatment did not prevent muscle depolarization during shock. After resuscitation, however, significant repolarization in hearts and skeletal muscle of the SOD + CAT group (heart, -70.0 +/- 1.1; muscle, -87.0 +/- 0.6 mV) was noted when compared with the controls (heart, -62.5 +/- 1.2; muscle, -82.7 +/- 1.1 mV; P less than 0.05). This implicates OFRs as mediators of excitable cell membrane injury following resuscitation.

Adaptation, Physiological↗