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Biomedical subjects

Lance B Becker

Publications and source records attributed to Lance B Becker.

32 records · Page 2Linked to original sources
PubMed2004

Induced hypothermia by central venous infusion: saline ice slurry versus chilled saline.

OBJECTIVE: Surface cooling improves outcome in selected comatose survivors of cardiac arrest. Internal cooling with considerable volumes of intravenous cold saline may accelerate hypothermia induction. This study compares core temperatures in swine after central catheter infusions of saline ice slurry (saline with smoothed 100-microm-size ice particles) vs. an equal volume of chilled saline. We hypothesized that slurry would achieve core hypothermia (32-34 degrees C) more consistently and at a faster rate. DESIGN: A total of 11 swine were randomized to receive microparticulate ice slurry, chilled saline infusion, or anesthesia alone in a monitored laboratory setting. INTERVENTIONS: Intravenous bolus (50 mL/kg) of slurry or chilled 1.5% NaCl saline. Slurry was composed of a 1:1 mixture of ice and distilled H2O plus NaCl. MEASUREMENTS: Cerebral cortex, tympanic membrane, inferior vena cava, rectal temperatures, electrocardiogram, arterial blood pressure, and arterial oxygen saturation were recorded for 1 hr after bolus. MAIN RESULTS: Compared with anesthetized controls, core brain temperatures of the saline and slurry groups dropped by 3.4 +/- 0.4 degrees C and 5.3 +/- 0.7 degrees C (p = .009), respectively. With an infusion rate of 120 mL/min, cooling rates for the saline and slurry groups were -11.6 +/- 1.8 degrees C/hr and -18.2 +/- 2.9 degrees C/hr, respectively, during the first 20 mins. Four of four animals in the slurry group vs. zero of four animals in the saline group achieved target cortical temperatures of <34 degrees C. CONCLUSIONS: Cold intravenous fluids rapidly induce hypothermia in swine with intact circulation. A two-phase (liquid plus ice) saline slurry cools more rapidly than an equal volume of cold saline at 0 degrees C. Ice-slurry could be a significant improvement over other cooling methods when rate of cooling and limited infusion volumes are important to the clinician.

Animals↗
PubMed2004

Human factors impact successful lay person automated external defibrillator use during simulated cardiac arrest.

OBJECTIVE: With the dissemination of automated external defibrillators in the community, there is increasing lay person use, along with less formal automated external defibrillator training and retraining. Therefore, the "ease of use" factors related to the human-device interface may be vital for successful use. We sought to determine whether human factor differences would result in differences in parameters of successful or safe use by lay persons in the setting of simulated cardiac arrest. METHODS: We measured parameters of successful and safe use with two automated external defibrillator devices among two groups of volunteers, those trained with a brief video tape and those without any training (completely naive). Both devices (the Philips FR2 or the HS1) are used in public access defibrillator settings. Volunteers entered a mock cardiac arrest scenario after randomization to either the naive (untrained) group or to a video-trained group. RESULTS: Both the FR2 and HS1 were found to be completely safe when used by video-trained and by naive groups of participants, with no adverse events observed (total, n = 256). For both devices, video-trained participants demonstrated high rates of successful defibrillation in the simulated testing (86% for FR2 and 89% for HS1). With the FR2, video-trained participants were significantly more successful compared with naive, untrained participants (86% vs. 48% successful use; p < .001). However, for the HS1, there was no significant difference in success rates for the video-trained vs. naive, untrained groups (89% vs. 87%; p = .79). CONCLUSIONS: Both devices are safe with either video-trained or naive users. The successful use of each device is high when participants view the training videotape designed for the device. An important difference in successful use was observed for naive users where the HS1 showed improved successful use compared with the FR2. Because defibrillation in the community may increasingly be attempted by lay persons whose training is remote or who have not been trained at all, the "naive" scenario may be increasingly relevant to automated external defibrillator use. Collectively, these data support the notion that human factors associated with ease of use may play a critical factor in survival rates achieved by specific devices.

Adult↗
PubMed2004

Synergistic effect of Scutellaria baicalensis and grape seed proanthocyanidins on scavenging reactive oxygen species in vitro.

Scutellaria baicalensis (SbE) is a commonly used Chinese herb medicine and grape seed proanthocyanidins is a popular herbal supplement in the United States. Both herbs have been shown to possess potent antioxidant effects. Using an in vitro model to produce the reactive oxygen species (ROS) generation (H2O2/FeSO4 for hydroxyl radicals, xanthine/xanthine oxidase for suproxide), we observed that Scutellaria baicalensis and grape seed proanthocyanidins acted synergistically to scavenge ROS. Our data suggest that a combination of these two herbs can potentially enhance their antioxidant efficacy, allowing lower dosages of each drug to be used. This has the advantage of avoiding possible side effects that may arise when higher doses of a single herb are used in an attempt to achieve a maximum degree of antioxidant activity.

Drug Synergism↗
PubMed2003

Grape seed proanthocyanidin extract attenuates oxidant injury in cardiomyocytes.

This study sought to test whether grape seed proanthocyanidin extract (GSPE) attenuates exogenous and endogenous oxidant stress induced in chick cardiomyocytes and whether this cytoprotection is mediated by PKC activation, mito K(ATP) channel opening, NO production, oxidant scavenging, or iron chelating effects. Cells were exposed to hydrogen peroxide (H(2)O(2)) (exogenous oxidant stress, 0.5mM) or antimycin A (endogenous oxidant stress, 100 micro M) for 2h following pretreatment with GSPE at various concentrations for 2h. Cells were also pretreated with GSPE or with inhibitors of PKC (chelerytherine), mito K(ATP) channel (5-hydroxydecanoate), nitric oxide synthase (nitro-L-arginine methyl ester) for 2h. Oxidant stress was measured by 2',7'-dichlorofluorescin diacetate and cell viability was assessed using propidium iodide. Free radical scavenging and iron chelating ability was tested in vitro. GSPE dose-dependently attenuated oxidant formation and significantly improved cell survival and contractile function. However, inhibitors of PKC, mito K(ATP) channel or NO synthase failed to abolish the protective action of GSPE during H(2)O(2) or antimycin A exposure. In vitro studies suggested that GSPE scavenges H(2)O(2), hydroxyl radical and superoxide, and may chelate iron. These results indicate that GSPE confers cardioprotection against exogenous H(2)O(2)- or antimycin A-induced oxidant injury. Its effect does not require PKC, mito K(ATP) channel, or NO synthase, presumably because it acts by reactive oxygen species scavenging and iron chelating directly.

Animals↗
PubMed2003

Grape seed proanthocyanidins induce pro-oxidant toxicity in cardiomyocytes.

Grape seed proanthocyanidin extract (GSPE), a polyphenolic compound with antioxidant properties, may protect against cardiac ischemia and reperfusion injury. However, its potential toxicity at higher doses is unknown. The authors tested the effects of GSPE on reactive oxygen species (ROS) generation, cell survival, lactate dehydrogenase (LDH) release, and caspase- 3 activity using chick cardiomyocytes incubated with GSPE at 5, 10, 50, 100, or 500 micrograms/mL in medium for 8 h. Exposure to increasing concentrations of GSPE (100 or 500 micrograms/mL) resulted in an increase in ROS generation and cell death as measured by propidium iodide uptake and LDH release. Caspase-3 activity was significantly increased fourfold in cells exposed to GSPE 500 micrograms/ mL compared to controls; this was abolished by the selective caspase-3 inhibitor Ac-Asp-Gln-Thr-Asp-H (50 microM), which also significantly reduced the cell death resulting from GSPE (500 micrograms/mL). The antioxidant N-acetylcysteine (NAC, 100 microM) reduced cell death induced by GSPE (500 micrograms/mL) but failed to attenuate caspase-3 activation. Collectively, the authors conclude that higher doses of GSPE could cause apoptotic cell injury via effector caspase-3 activation and subsequent induction of ROS generation. Consumers may take higher doses of dietary supplements in the belief that natural herbs have no major side effects. This study demonstrates that dosages of GSPE should be optimized to avoid potential harmful pro-oxidant effects.

Acetylcysteine↗
PubMed2002

Public use of automated external defibrillators.

BACKGROUND: Automated external defibrillators save lives when they are used by designated personnel in certain public settings. We performed a two-year prospective study at three Chicago airports to assess whether random bystanders witnessing out-of-hospital cardiac arrests would retrieve and successfully use automated external defibrillators. METHODS: Defibrillators were installed a brisk 60-to-90-second walk apart throughout passenger terminals at O'Hare, Midway, and Meigs Field airports, which together serve more than 100 million passengers per year. The use of defibrillators was promoted by public-service videos in waiting areas, pamphlets, and reports in the media. We assessed the time from notification of the dispatchers to defibrillation, survival rate at 72 hours and at one year among persons with cardiac arrest, their neurologic status, and the characteristics of rescuers. RESULTS: Over a two-year period, 21 persons had nontraumatic cardiac arrest, 18 of whom had ventricular fibrillation. With two exceptions, defibrillator operators were good Samaritans, acting voluntarily. In the case of four patients with ventricular fibrillation, defibrillators were neither nearby nor used within five minutes, and none of these patients survived. Three others remained in fibrillation and eventually died, despite the rapid use of a defibrillator (within five minutes). Eleven patients with ventricular fibrillation were successfully resuscitated, including eight who regained consciousness before hospital admission. No shock was delivered in four cases of suspected cardiac arrest, and the device correctly indicated that the problem was not due to ventricular fibrillation. The rescuers of 6 of the 11 successfully resuscitated patients had no training or experience in the use of automated defibrillators, although 3 had medical degrees. Ten of the 18 patients with ventricular fibrillation were alive and neurologically intact at one year. CONCLUSIONS: Automated external defibrillators deployed in readily accessible, well-marked public areas in Chicago airports were used effectively to assist patients with cardiac arrest. In the cases of survivors, most of the users had no duty to act and no prior training in the use of these devices.

Aged↗
PubMed2002

Reperfusion, not simulated ischemia, initiates intrinsic apoptosis injury in chick cardiomyocytes.

Although ischemia-reperfusion (I/R) can initiate apoptosis, the timing and contribution of the mitochondrial/cytochrome c apoptosis death pathway to I/R injury is unclear. We studied the timing of cytochrome c release during I/R and whether subsequent caspase activation contributes to reperfusion injury in confluent chick cardiomyocytes. One-hour simulated ischemia followed by 3-h reperfusion resulted in significant cell death, with most cell death evident during the reperfusion phase and demonstrating mitochondrial cytochrome c release within 5 min after reperfusion. By contrast, cells exposed to prolonged ischemia for 4 h had only marginally increased cell death and no detectable cytochrome c release into the cytosol. Caspase activation could not be detected after ischemia only, but it significantly increased after reperfusion. Caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, Ac-Asp-Gln-Thr-Asp-H, or benzyloxycarbonyl-Leu-Glu (Ome)-His-Asp-(Ome)-fluoromethyl ketone given only at reperfusion significantly attenuated cell death and resulted in return of contraction. Antixoxidants decreased cytochrome c release, nuclear condensation, and cell death. These results suggest that reperfusion oxidants initiate cytochrome c release within minutes, and apoptosis within hours, significant enough to increase cell death and contractile dysfunction.

Animals↗
PubMed2002

Baicalein attenuates oxidant stress in cardiomyocytes.

Flavonoids within Scutellaria baicalensis may be potent antioxidants on the basis of our studies of S. baicalensis extract. To further this work, we studied the antioxidative effects of baicalein, a flavonoid component of S. baicalensis, in a chick cardiomyocyte model of reactive oxygen species (ROS) generation during hypoxia, simulated ischemia-reperfusion, or mitochondrial complex III inhibition with antimycin A. Oxidant stress was measured by oxidation of the intracellular probes 2',7'-dichlorofluorescin diacetate and dihydroethidium. Viability was assessed by propidium iodide uptake. Baicalein attenuated oxidant stress during all conditions studied and acted within minutes of treatment. For example, baicalein given only at reperfusion dose dependently attenuated the ROS burst at 5 min after 1 h of simulated ischemia. It also decreased subsequent cell death at 3 h of reperfusion from 52.3 +/- 2.5% in untreated cells to 29.4 +/- 3.0% (with return of contractions; P < 0.001). In vitro studies using electron paramagnetic resonance spectroscopy with the spin trap 5-methoxycarbonyl-5-methyl-1-pyrroline-N-oxide revealed that baicalein scavenges superoxide but does not mimic the effects of superoxide dismutase. We conclude that baicalein can scavenge ROS generation in cardiomyocytes and that it protects against cell death in an ischemia-reperfusion model when given only at reperfusion.

Animals↗
PubMedDate not supplied

Glutamine preserves cardiomyocyte viability and enhances recovery of contractile function after ischemia-reperfusion injury.

BACKGROUND: Glutamine has been shown to protect against cellular injury in in vitro gut epithelial cells and in vivo in the septic rat. Glutamine's effect on the cardiomyocyte has not been explored. We tested the hypothesis that glutamine can enhance heat shock protein 72 (HSP 72) expression, attenuate intracellular oxidant generation, and protect cardiomyocytes against ischemia/reperfusion (I/R) injury. METHODS: Chicken cardiomyocytes were supplemented with glutamine (10 mmol/L) or were controls (0 mmol/L). Cells underwent I/R, and HSP 72 content was evaluated using Western blotting. Reactive oxygen species generation was quantified through 2'-7'-dichlorofluorescin diacetate oxidation. Cell viability was quantified using propidium iodide staining. Return of contractile function was analyzed through phase contrast microscopy. RESULTS: Glutamine significantly increased cardiomyocyte HSP 72 expression and markedly reduced cell death after I/R injury. Glutamine did not significantly decrease intracellular oxidant generation. Contractile function returned in all glutamine-treated cells versus none of the control cells postreperfusion. CONCLUSIONS: Glutamine significantly increases cardiomyocytes survival and recovery of contractile function after I/R injury. This protection is associated with enhanced HSP 72 expression. These observations suggest that glutamine may prove beneficial as a protective therapy in patients at risk for cardiac ischemia and reperfusion injury, such as patients undergoing procedures requiring cardiopulmonary bypass and patients with coronary artery disease.

Animals↗