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Mild hypothermia after near drowning in twin toddlers
Ortrud Hein, Andreas Triltsch, Christoph von Buch, Wolfgang J Kox, Claudia Spies
Critical Care , 2004, DOI: 10.1186/cc2926
Abstract: Two twin toddlers (a boy and girl, aged 2 years and 3 months) suffered hypothermic near drowning with protracted cardiac arrest and aspiration. The girl was treated with mild hypothermia for 72 hours and developed acute respiratory dysfunction syndrome and sepsis. She recovered without neurological deficit. The boy's treatment was conducted under normothermia without further complications. He developed an apallic syndrome.Although the twin toddlers experienced the same near drowning accident together, the outcomes with respect to neurological status and postinjury complications were completely different. One of the factors that possibly influenced the different postinjury course might have been prolonged mild hypothermia.Of drowning and near drowning victims who are younger than 20 years, 63–68% are 0–5 years old [1,2]. Of submersion events in the age group 1–4 years, 56% occurred in artificial pools [3]. Death from drowning is the second leading cause of accidental death in children [4], and one-third of all survivors have neurological damage [4]. Hypothermia frequently accompanies submersion accidents, especially in children with a relatively large ratio of surface area to body mass [3]. Mild hypothermia (32–34°C) reduces oxygen consumption by 7% per 1°C decrease in temperature, and reduces cerebral blood flow and cerebral intracranial pressure [5-7]. Temperature under 28°C leads to cardiocirculatory depression and finally cardiac arrest [3]. Hypoxaemia and capillary leak develop due to apnoea, regardless of whether aspiration occurs [3]. The degree of cerebral protection that can be expected due to hypothermia depends, among other factors, on the amount of time that elapses before induction of mild hypothermia [1,3,6]. Induced mild hypothermia for cerebral protection after near drowning accidents has yielded controversial results in terms of mortality and neurological outcome [1,3,8]. However, induced mild hypothermia after cardiac arrest has led to improved neur
Regional mild hypothermia in the protection of the ischemic brain
Prandini, Mirto Nelso;Lacanna, Santino Nunes;Valente, Paulo Roberto;Stavale, Jo?o Norberto;
Acta Cirurgica Brasileira , 2002, DOI: 10.1590/S0102-86502002000400006
Abstract: objective: to demonstrate that mild hypothermia can be a protective element when an ischemic onset occurs in rabbit brains. methods: a rabbit model of focal ischemia was used to test the protection provided by mild hypothermia regionally produced by means of the placement of ice bag on the scalp of a hemicranium which has had previously its bone removed. twenty new zealand white rabbits were divided into two groups as follows: (a) a control group where an ischemic lesion was produced by coagulation of the middle cerebral artery and (b) a brain protected group where mild hypothermia was provided during 80 to 100 minutes after the same ischemic lesion. the brains slices were stained with 2,3,5-triphenyletrazolium (ttc). the sections were photographed with a digital camera and the infarct volume was measured through a computer program. results: the average of infarct volume was 70.53 mm3 in the control group. in the protected group, the average of infarct volume was 41,30 mm3 only in five animals. five animals of this group did not demonstrate macroscopically and microscopically infarct area. conclusions: we concluded that mild hypothermia regionally produced may protect ischemic brains of rabbits.
Regional mild hypothermia in the protection of the ischemic brain  [cached]
Prandini Mirto Nelso,Lacanna Santino Nunes,Valente Paulo Roberto,Stavale Jo?o Norberto
Acta Cirurgica Brasileira , 2002,
Abstract: Objective: To demonstrate that mild hypothermia can be a protective element when an ischemic onset occurs in rabbit brains. Methods: A rabbit model of focal ischemia was used to test the protection provided by mild hypothermia regionally produced by means of the placement of ice bag on the scalp of a hemicranium which has had previously its bone removed. Twenty New Zealand White rabbits were divided into two groups as follows: (A) a control group where an ischemic lesion was produced by coagulation of the middle cerebral artery and (B) a brain protected group where mild hypothermia was provided during 80 to 100 minutes after the same ischemic lesion. The brains slices were stained with 2,3,5-Triphenyletrazolium (TTC). The sections were photographed with a digital camera and the infarct volume was measured through a computer program. Results: The average of infarct volume was 70.53 mm3 in the control group. In the protected group, the average of infarct volume was 41,30 mm3 only in five animals. Five animals of this group did not demonstrate macroscopically and microscopically infarct area. Conclusions: We concluded that mild hypothermia regionally produced may protect ischemic brains of rabbits.
Study on brain protection of mild hypothermia in cardiopulmonary resuscitation
J BingWen, Zhou Bin
Critical Care , 1997, DOI: 10.1186/cc10
Abstract: (i) The SOD levels in blood and CSF after resuscitation were lower than those before CA (P < 0.01), the LPO and LA levels in blood and CSF were significantly higher than those before CA (P < 0.01). (ii) The SOD level in CSF in mild hypothermia group was higher than that in normothermia group (P < 0.05), the LPO level in CSF was significantly lower than that in normothermia (P < 0.01). But the LA level in CSF and the SOD, LPO and LA levels in blood were not significantly different between these two groups, (iii) The total brain histopathologic damage scores in mild hypothermia group were lower than those in normothermia group (P < 0.01).(i) The OFR and LA have some important effect in postischemic-anoxic encephalopathy. (ii) Mild hypothermia induced immediately with reperfusion after CA may improve cerebral outcome. (iii) The mechanism of this beneficial effect may be to reduce the generation of OFR and to mitigate the lipid peroxidation induced by OFR.
Mild hypothermia reduces cardiac post-ischemic reactive hyperemia
Goran K Olivecrona, Matthias G?tberg, Jan Harnek, Jesper Van der Pals, David Erlinge
BMC Cardiovascular Disorders , 2007, DOI: 10.1186/1471-2261-7-5
Abstract: Sixteen 25–30 kg pigs, in a closed chest model, were anesthetized and temperature was established in all pigs at 37°C using an intravascular cooling catheter. The 16 pigs were then randomized to hypothermia (34°C) or control (37°C). The left main coronary artery was then catheterized with a PCI guiding catheter. A Doppler flow wire was placed in the mid part of the LAD and a PCI balloon was then positioned proximal to the Doppler wire but distal to the first diagonal branch. The LAD was then occluded for ten minutes in all pigs. Coronary blood flow was measured before, during and after ischemia/reperfusion.The peak flow seen during post-ischemic reactive hyperemia (during the first minutes of reperfusion) was significantly reduced by 43 % (p < 0.01) in hypothermic pigs compared to controls.Mild hypothermia significantly reduces post-ischemic hyperemia in a closed chest pig model. The reduction of reactive hyperemia during reperfusion may have an impact on cardiac reperfusion injury.Coronary reperfusion injury is believed to occur during reperfusion of an occluded coronary artery in the setting of myocardial infarction. The existence of this injury is still a matter of debate [1], but also the focus of a great deal of research on how to limit the possible additional cell death thought to occur during reperfusion [2]. The mechanism of this proposed reperfusion injury is unclear but several hypotheses have been proposed: oxygen free radical formation, calcium overload, neutrophil-mediated myocardial and endothelial injury, progressive decline in microvascular flow to the reperfused myocardium, and depletion of high energy phosphate stores [3]. Although a number of pharmacological treatments, aimed at the above mentioned mechanism, have been tried in experimental settings, none have yet yielded positive results in a large randomized trial in man.During a coronary artery occlusion, the area of the heart supplied by the artery is deprived of its blood-supply. Upon reperfu
Effect of Mild Hypothermia on the Coagulation-Fibrinolysis System and Physiological Anticoagulants after Cardiopulmonary Resuscitation in a Porcine Model  [PDF]
Ping Gong, Ming-Yue Zhang, Hong Zhao, Zi-Ren Tang, Rong Hua, Xue Mei, Juan Cui, Chun-Sheng Li
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067476
Abstract: The aim of this study was to evaluate the effect of mild hypothermia on the coagulation-fibrinolysis system and physiological anticoagulants after cardiopulmonary resuscitation (CPR). A total of 20 male Wuzhishan miniature pigs underwent 8 min of untreated ventricular fibrillation and CPR. Of these, 16 were successfully resuscitated and were randomized into the mild hypothermia group (MH, n = 8) or the control normothermia group (CN, n = 8). Mild hypothermia (33°C) was induced intravascularly, and this temperature was maintained for 12 h before pigs were actively rewarmed. The CN group received normothermic post-cardiac arrest (CA) care for 72 h. Four animals were in the sham operation group (SO). Blood samples were taken at baseline, and 0.5, 6, 12, 24, and 72 h after ROSC. Whole-body mild hypothermia impaired blood coagulation during cooling, but attenuated blood coagulation impairment at 72 h after ROSC. Mild hypothermia also increased serum levels of physiological anticoagulants, such as PRO C and AT-III during cooling and after rewarming, decreased EPCR and TFPI levels during cooling but not after rewarming, and inhibited fibrinolysis and platelet activation during cooling and after rewarming. Finally, mild hypothermia did not affect coagulation-fibrinolysis, physiological anticoagulants, or platelet activation during rewarming. Thus, our findings indicate that mild hypothermia exerted an anticoagulant effect during cooling, which may have inhibitory effects on microthrombus formation. Furthermore, mild hypothermia inhibited fibrinolysis and platelet activation during cooling and attenuated blood coagulation impairment after rewarming. Slow rewarming had no obvious adverse effects on blood coagulation.
Inhibition of gastric perception of mild distention by omeprazole in volunteers  [cached]
Akihito Iida,Hiroshi Kaneko,Toshihiro Konagaya,Yasushi Funaki
World Journal of Gastroenterology , 2012, DOI: 10.3748/wjg.v18.i39.5576
Abstract: AIM: To evaluate the effects of omeprazole on gastric mechanosensitivity in humans. METHODS: A double lumen polyvinyl tube with a plastic bag was introduced into the stomach of healthy volunteers under fluorography and connected to a barostat device. Subjects were then positioned so they were sitting comfortably, and the minimal distending pressure (MDP) was determined after a 30-min adaptation period. Isobaric distensions were performed in stepwise increments of 2 mmHg (2 min each) starting from the MDP. Subjects were instructed to score feelings at the end of every step using a graphic rating scale: 0, no perception; 1, weak/vague; 2, weak but significant; 3, moderate/vague; 4, moderate but significant; 5, severe discomfort; and 6, unbearable pain. After this first test, subjects received omeprazole (20 mg, after dinner) once daily for 1 wk. A second test was performed on the last day of treatment. RESULTS: No adverse effects were observed. Mean MDP before and after treatment was 6.3 ± 0.3 mmHg and 6.2 ± 0.5 mmHg, respectively. One subject before and 2 after treatment did not reach a score of 6 at the maximum bag volume of 750 mL. After omeprazole, there was a significant increase in the distension pressure required to reach scores of 1 (P = 0.019) and 2 (P = 0.017) as compared to baseline. There were no changes in pressure required to reach the other scores after treatment. Two subjects before and one after omeprazole rated their abdominal feeling < 1 at MDP, and mean (± SE) abdominal discomfort scores at MDP were 0.13 ± 0.09 and 0.04 ± 0.04, respectively. Mean scores induced by each MDP + 2, 4, 6, 8, 10, 12, 14, 16, 18 and 20 (mmHg) were 1.1 ± 0.3, 2.0 ± 0.4, 2.9 ± 0.5, 3.3 ± 0.4, 4.6 ± 0.3, 5.2 ± 0.3, 5.5 ± 0.2, 5.5 ± 0.3, 5.7 ± 0.3, and 5.4, respectively. After omeprazole, abdominal feeling scores for the same incremental pressures over MDP were 0.3 ± 0.1, 0.8 ± 0.1, 2.0 ± 0.4, 2.8 ± 0.4, 3.8 ± 0.4, 4.6 ± 0.4, 4.9 ± 0.3, 5.4 ± 0.4, 5.2 ± 0.6, and 5.0 ± 1.0, respectively. A significant decrease in feeling score was observed at intrabag pressures of MDP + 2 mmHg (P = 0.028) and + 4 mmHg (P = 0.013), respectively, after omeprazole. No significant score changes were observed at pressures ≥ MDP + 6 mmHg. CONCLUSION: Although the precise mechanisms are undetermined, the present study demonstrated that omeprazole decreases mechanosensitivity to mild gastric distension.
Drug-induced mild therapeutic hypothermia obtained by administration of a transient receptor potential vanilloid type 1 agonist
Keld Fosgerau, Uno J Weber, Jacob W Gotfredsen, Magdalena Jayatissa, Carsten Buus, Niels B Kristensen, Mogens Vestergaard, Peter Teschendorf, Andreas Schneider, Philip Hansen, Jakob Rauns?, Lars K?ber, Christian Torp-Pedersen, Charlotte Videbaek
BMC Cardiovascular Disorders , 2010, DOI: 10.1186/1471-2261-10-51
Abstract: First, we screened a heterogeneous group of TRPV1 agonists and secondly we tested the hypothermic properties of a selected candidate by dose-response studies. Finally we tested the hypothermic properties in a large animal. The screening was in conscious rats, the dose-response experiments in conscious rats and in cynomologus monkeys, and the finally we tested the hypothermic properties in conscious young cattle (calves with a body weight as an adult human). The investigated TRPV1 agonists were administered by continuous intravenous infusion.Screening: Dihydrocapsaicin (DHC), a component of chili pepper, displayed a desirable hypothermic profile with regards to the duration, depth and control in conscious rats. Dose-response experiments: In both rats and cynomologus monkeys DHC caused a dose-dependent and immediate decrease in body temperature. Thus in rats, infusion of DHC at doses of 0.125, 0.25, 0.50, and 0.75 mg/kg/h caused a maximal ΔT (°C) as compared to vehicle control of -0.9, -1.5, -2.0, and -4.2 within approximately 1 hour until the 6 hour infusion was stopped. Finally, in calves the intravenous infusion of DHC was able to maintain mild hypothermia with ΔT > -3°C for more than 12 hours.Our data support the hypothesis that infusion of dihydrocapsaicin is a candidate for testing as a primary or adjunct method of inducing and maintaining therapeutic hypothermia.Mild therapeutic hypothermia (target temperature between 32°C and 34°C) has emerged as an effective treatment to improve neurological outcomes among cardiac arrest survivors. Following publication of two pivotal randomized clinical trials [1-3] mild therapeutic hypothermia for 12 to 24 hours following cardiopulmonary resuscitation (CPR) of out of hospital cardiac arrest patients with shockable electrocardiography rhythms is recommended by the European Resuscitation Counsel (ERC) and the American Heart Association (AHA) for prevention of neurological injury. Also, mild therapeutic hypothermia has been su
The metabolic effect of induced mild hypothermia in critically ill patients
M Bitzani, G Vassiliadou, C Iasonidou, S Tsaggalof, T Kontakiotis, D Riggos
Critical Care , 2003, DOI: 10.1186/cc1899
Abstract: During a 2 year period, 12 consecutive critically ill patients under continuous veno-venous hemofiltration (CVVH), due to acute renal failure, were studied prospectively. All patients were mechanically ventilated, nine of them were sedated but none was paralyzed. Core temperature (T) was continuously monitored through a nasopharyngeal sensor, while resting energy expenditure (REE), VO2 and VCO2 were evaluated by means of indirect calorimetry. Baseline measurements were recorded before the onset of CVVH. Serial measurements were performed each time T was decreased by 1°C. After the interruption of CVVH, measurements were also repeated serially with the increase of core temperature of 1°C.Decrease of temperature from 37°C to 35°C has no statistically significant influence on metabolic demands. During the reduction of temperature from 38°C to 35°C a statistically significant decrease in REE (2593 ± 228 kcal vs 2095 ± 618 kcal, P = 0.041), as well as in VCO2 (P = 0.051) was observed. A difference at the limits of significance was also observed in REE from 38°C to 36°C (2593 ± 228 kcal vs 2292 ± 434 kcal, P = 0.056). Rewarming was followed by a gradual reverse of these effects.Statistics were calculated with SPSS version 10, using nonparametric tests. Correlation between T, REE, VO2 and VCO2 was tested by Pearson's correlation coefficient. Comparison between REE, VO2 and VCO2 at different temperatures was performed using Student's paired t test.Mild hypothermia does not affect the metabolic rate in critically ill patients. Cooling in the febrile critically ill patient is followed by a significant decrease in energy expenditure. This may prove beneficial, minimizing the potential for tissue hypoxia, in situations of limited oxygen delivery.
Mild hypothermia reduces polymorphonuclear leukocytes infiltration in induced brain inflammation
Prandini, Mirto N.;Neves Filho, Antonio;Lapa, Antonio J.;Stavale, Jo?o N.;
Arquivos de Neuro-Psiquiatria , 2005, DOI: 10.1590/S0004-282X2005000500012
Abstract: over the last 50 years deep hypothermia (230 c) has demonstrated to be an excellent neuroprotective agent in cerebral ischemic injury. mild hypothermia (31-330 c) has proven to have the same neuroprotective properties without the detrimental effects of deep hypothermia. mechanisms of injury that are exaggerated by moderate hyperthermia and ameliorated by hypothermia include, reduction of oxygen radical production, with peroxidase damage to lipids, proteins and dna, microglial activation and ischemic depolarization, decrease in cerebral metabolic demand for oxygen and reduction of glycerin and excitatory amino acid (eaa) release. studies have demonstrated that inflammation potentiates cerebral ischemic injury and that hypothermia can reduce neutrophil infiltration in ischemic regions. to further elucidate the mechanisms by which mild hypothermia produces neuroprotection in ischemia by attenuating the inflammatory response, we provoked inflammatory reaction, in brains of rats, dropping a substance that provokes a heavy inflammatory reaction. two groups of ten animals underwent the same surgical procedure: the skull bone was partially removed, the duramater was opened and an inflammatory substance (5% carrageenin) was topically dropped. the scalp was sutured and, for the group that underwent neuroprotection, an ice bag was placed covering the entire skull surface, in order to maintain the brain temperature between 29,5-310 c during 120 minutes. after three days the animals were sacrificed and their brains were examined. the group protected by hypothermia demonstrated a remarkable reduction of polymorphonuclear leukocytes (pmnl) infiltration, indicating that mild hypothermia can have neuroprotective effects by reducing the inflammatory reaction.
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