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SHORT REPOR T Open Access Japanese experience of hydrogen sulfide: the suicide craze in 2008 Daiichi Morii 1,2* , Yasusuke Miyagatani 1 , Naohisa Nakamae 1 , Masaki Murao 1 , Kiyomi Taniyama 3 Abstract Most of hydrogen sulfide poisoning has been reported as industrial accidents in Japan. However, since January 2008, a burgeoning of suicide attempts using homemade hydrogen sulfide gas has become evident. By April 2008, the fad escalated into a chain reaction nationwide. Mortality of the poisoning was very high. There were 220 cases of attempted gas suicides during the period of March 27 to June 15, killing 208. An introduction of new method of making the gas, transmitted through message boards on the internet, was blamed for this “outbreak”. The new method entailed mixing bath additive and toilet detergent. The National Police Agency instructed internet provi- ders to remove information that could be harmful. Of the victims of the fad in 2008, several cases were serious enough that family members wer e involved and died. Paramedics and caregivers were also injured secondarily by the gas. This fad has rapidly spread by internet communication, and can happen anywhere in the world. Overview Hydrogen sulfide poisoning has been a relatively uncom- mon intoxication, with only a few cases a year being reported in Japan. Most incidents occurred in circum- stances of volcano climbing, pharmaceutical product treatments, and man-hole cleaning[1]. Hence, this poi- soning has been categorized as being associated with industrial accidents. However, since January 2008, ther e has been a burgeoning of suicide attempts using home- made hydrogen sulfi de gas. By April 2008, the fad esca- lated into a chain reaction, and cases of H 2 Spoisoning made headlines almost everyday, nationwide. The Japa- nese Cabinet Office reported 220 cases of attempted gas suicides during the period from March 27 to June 15, killing 208, a very high mortality rate (Figure 1). An introduction of new methods of making the gas, trans- mitted through message boards on the internet, was blamed for this “outbr eak.” The new method entailed mixing bath additive and toilet detergent. The main component of the bath additive is lime sulfur, and toilet detergent acts as an oxidant to produce H 2 Sgas.In Japan, the custom of bathing, especially in hot springs ( onsen ), is quite common. As a result, people want to enjoy it in their own homes by using bath additive. These two materials are thus easily available in Japan, and also obtainable through the internet. Given these circumstances, the NationalPoliceAgencyinstructed internet providers to remove information that could be harmful, and MUTOHAP (the most frequently ‘featured’ brand of bath additives in the method) was forced to suspend its production. A few cases of swallowing MUTOHAP itself had already been reported as a means of suicid e. If the sulfur in MUTOHAP were mixed with gastric acid in the stomach, a H 2 S gas-evolving reaction would occur and cause poisoning. When sulfur is mixed with a potent oxidant such as toilet detergent, an even greater quantity of H 2 S gas evolves than it would with gastric acid. In most of the cases, victims lose conscious- ness with a single intake of breath, and die immediately. This has been referred to as knock down and was intro- duced as a painless way to kill oneself. This new method was first reported in 2007. Because of the burst PHIẾU AN TOÀN HÓA CHẤT Phiếu an toàn hóa chất Tên phân loại, tên sản phẩm: Hydrogen Sulfide Số CAS: 7783-06-4 TRUNG TÂM DỮ LIỆU VÀ HỖ TRỢ ỨNG PHÓ SỰ CỐ HÓA CHẤT Địa : 21 Ngô Số UN: 1053 Quyền - Hoàn Kiếm - Hà Nội, Điện thoại : Số đăng ký EC: 231-977-3 04.39362506, Fax : 04.39387120 Email : Số thị nguy hiểm tổ chức xếp dlhoachat@gmail.com, Cở sở : 655 Phạm loại (nếu có): Văn Đồng - Bắc Từ Liêm - Hà Nội Số đăng ký danh mục Quốc gia khác (nếu có): I NHẬN DẠNG HÓA CHẤT - Tên thường gọi chất: Hydrogen Mã sản phẩm (nếu có) Sulfide - Tên thương mại: - Tên khác (không tên khoa học): - Tên nhà cung cấp nhập khẩu, Địa liên hệ trường hợp khẩn cấp: địa chỉ: - Tên nhà sản xuất địa chỉ: Mục đích sử dụng: - Sản xuất hợp chất thio hữu bao gồm: methanethiol , ethanethiol acid thioglycolic - Sản xuất sunfua kim loại kiềm dùng để khử polyme sinh học tẩy bột giấy theo quy trình Kraft II THÔNG TIN VỀ THÀNH PHẦN CÁC CHẤT Tên thành phần nguy hiểm Số CAS Công thức Hàm lượng hóa học (% theo trọng lượng) Hydrogen Sulfide 7783-06-4 H2S 99% III NHẬN DẠNG ĐẶC TÍNH NGUY HIỂM CỦA HÓA CHẤT Mức xếp loại nguy hiểm (theo số liệu hợp lệ có sẵn quốc gia, tổ chức thử nghiệm Ví dụ: EU, Mỹ, OSHA…) Phân loại theo GHS: - Khí dễ cháy (loại 1) - Khí nén áp suất cao - Độc cấp tính, hô hấp (loại 2) - Độc với môi trường nước, cấp tính (loại 1) Cảnh báo nguy hiểm - Hình đồ cảnh báo: - Từ cảnh báo: Nguy hiểm Khuyến cáo nguy hiểm H225 Dạng lỏng có khả cháy cao H315 Causes skin irritation H319 Gây kích ứng mắt nghiêm trọng H361fd Nghi nghờ độc với sinh sản Nghi ngờ gây tổn thương thai nhi H372 Gây tổn thương quan thể tiếp xúc lặp lại kéo dài H220 Chất khí có khả cháy cao H280 Khí nén áp suất cao; Có thể nổ bị đốt nóng H330 Tử vong hít thở phải H400 Rất độc với sinh vật nước Khuyến cáo cáo phòng ngừa P210 Tránh xa sức nóng / tia lửa / lửa / bề mặt nóng - Không hút thuốc P260 TRành hít thở phải bụi/mù/khói/ sương/khí/hơi P273 Tránh xả thải môi trường P284 Trang bị thiết bị bảo vệ hệ hô hấp P310 Ngay gọi đến trung tâm chống độc bác sĩ P410 + P403 Bảo vệ khỏi ánh nắng mặt trời Bảo quản nơi thông thoáng IV BIỆN PHÁP SƠ CỨU VỀ Y TẾ Trƣờng hợp tai nạn tiếp xúc theo đƣờng mắt (bị văng, dây vào mắt) Rửa toàn mắt với lượng lớn nước 15 phút Tham khảo ý kiến bác sĩ Trƣờng hợp tai nạn tiếp xúc da (bị dây vào da) Rửa xà phòng với lượng lớn nước Tham khảo ý kiến bác sĩ Trƣờng hợp tai nạn tiếp xúc theo đƣờng hô hấp (hít thở phải hóa chất nguy hiểm dạng hơi, khí) Di chuyển nạn nhân đến vùng không khí sạch, cung cấp máy trợ thở nạn nhân bị ngừng thở Tham khảo ý kiến bác sĩ Trƣờng hợp tai nạn theo đƣờng tiêu hóa (ăn, uống nuốt nhầm hóa chất) Nếu nuốt phải: không cho thứ vào miệng người bất tỉnh Súc miệng với nước Tham khảo ý kiến bác sĩ Lƣu ý bác sĩ điều trị (nếu có) V BIỆN PHÁP XỬ LÝ KHI CÓ HỎA HOẠN Xếp loại tính cháy (dễ cháy, dễ cháy dễ cháy, không cháy, khó cháy…) Chất dễ cháy Sản phẩm tạo bị cháy Các Sulphur oxides Các tác nhân gây cháy, nổ (tia lửa, tĩnh điện, nhiệt độ cao, va đập, ma sát …) Các chất dập cháy thích hợp hƣớng dẫn biện pháp chữa cháy, biện pháp kết hợp khác Sử dụng vòi phun nước, bọt chống cồn, hóa chất khô hay carbon dioxide (CO 2) Phƣơng tiện, trang phục bảo hộ cần thiết chữa cháy Mặc quần áo bảo hộ mang thiết bị tự cung cấp khí thở để chữa cháy cần thiết Các lƣu ý đặc biệt cháy, nổ (nếu có) Phun nước để làm mát thùng chứa chưa mở nắp VI BIỆN PHÁP PHÕNG NGỪA, ỨNG PHÓ KHI CÓ SỰ CỐ Khi tràn đổ, dò rỉ mức nhỏ - Tìm cách để ngăn chặn nguồn hóa chất tràn đổ, rò rỉ Làm thông thoáng khu vực xảy cố - Phong tỏa khu vực xảy cố tràn đổ, rò rỉ Cắt cử người trông coi cảnh báo cho người phương tiện biết khu vực - Ngăn cấm nguồn lửa tia lửa xảy cố tràn đổ, rò rỉ - Sử dụng cát, giẻ lau, vật liệu thấm chuyên dụng để để làm khu vực hóa chất rò rỉ nhanh tốt, sau thu gom vào thùng chứa chuyên dụng để tiêu hủy cách - Không cho hóa chất chảy lan vào nguồn nước, hệ thống kênh rạch, sông hồ, cống rãnh Khi tràn đổ, dò rỉ lớn diện rộng - Tìm cách để cắt điện, ngừng hoạt động xuất nhập, bơm chuyển hóa chất - Ngăn cấm nguồn lửa tia lửa xảy cố tràn đổ, rò rỉ - Cô lập khu vực hóa chất tràn đổ, rò rỉ Chuẩn bị phương án phòng cháy chữa cháy - Lên phương án bảo vệ khu vực cố, ngăn ngừa hóa chất loang rộng thực phương án thu hồi hóa chất tràn - Thông báo cho quan chức khu vực xảy cố để tổ chức hỗ trợ ứng cứu - Phải có hệ thống thông gió tốt để khống chế bay phân tán khu vực làm việc Cô lập vùng bị tràn hoá chất nguy hiểm Tránh để sản phẩm vào cống rãnh thải môi trường VII YÊU CẦU VỀ CẤT GIỮ Biện pháp, điều kiện cần áp dụng sử dụng, thao tác với hóa chất nguy hiểm (thông gió, dùng hệ thống kín, sử dụng thiết bị điện phòng nổ, vận chuyển nội bộ…) -Phải dùng quạt thông gió (thiết bị phòng nổ) nơi có nhiệt độ cao môi trường để giữ nồng độ thấp giới hạn cho phép - Mở thùng chứa từ từ để giải phóng áp suất bên thùng chứa đựng - Chỉ xuất nhập, bơm rót hóa chất vào thiết bị chứa đựng hóa chất chuyên dụng Phải sử dụng hệ thống nam châm tĩnh điện, tiếp đất xuất nhập hóa chất vào phương tiện vận ...BioMed Central Page 1 of 10 (page number not for citation purposes) Journal of Inflammation Open Access Research Effects of hydrogen sulfide on inflammation in caerulein-induced acute pancreatitis Jenab N Sidhapuriwala 1 , Siaw Wei Ng 2 and Madhav Bhatia* 1 Address: 1 Cardiovascular Biology Research Group, Department of Pharmacology, Yong Loo Lin School of Medicine, CRC MD11, National University of Singapore 117597, Singapore, Singapore and 2 University of Oxford Department of Physiology, Anatomy and Genetics Sherrington Building, Parks Road, Oxford OX1 3PT, UK Email: Jenab N Sidhapuriwala - jenab_n_sidhapuriwala@nuhs.edu.sg; Siaw Wei Ng - swng101@hotmail.com; Madhav Bhatia* - mbhatia@nus.edu.sg * Corresponding author Abstract Background: Hydrogen sulfide (H 2 S), a gaseous mediator plays an important role in a wide range of physiological and pathological processes. H 2 S has been extensively studied for its various roles in cardiovascular and neurological disorders. However, the role of H 2 S in inflammation is still controversial. The current study was aimed to investigate the therapeutic potential of sodium hydrosulfide (NaHS), an H 2 S donor in in vivo model of acute pancreatitis in mice. Methods: Acute pancreatitis was induced in mice by hourly caerulein injections (50 μg/kg) for 10 hours. Mice were treated with different dosages of NaHS (5 mg/kg, 10 mg/kg or 15 mg/kg) or with vehicle, distilled water (DW). NaHS or DW was administered 1 h before induction of pancreatitis. Mice were sacrificed 1 h after the last caerulein injection. Blood, pancreas and lung tissues were collected and were processed to measure the plasma amylase, myeloperoxidase (MPO) activities in pancreas and lung and chemokines and adhesion molecules in pancreas and lung. Results: It was revealed that significant reduction of inflammation, both in pancreas and lung was associated with NaHS 10 mg/kg. Further the anti-inflammatory effects of NaHS 10 mg/kg were associated with reduction of pancreatic and pulmonary inflammatory chemokines and adhesion molecules. NaHS 5 mg/kg did not cause significant improvement on inflammation in pancreas and associated lung injury and NaHS 15 mg/kg did not further enhance the beneficial effects seen with NaHS 10 mg/kg. Conclusion: In conclusion, these data provide evidence for anti-inflammatory effects of H 2 S based on its dosage used. Background Hydrogen sulphide (H 2 S) a novel gaseous messenger, is synthesized endogenously from L-cysteine by two pyri- doxal-5'-phosphate-dependent enzymes, cystathionine β- synthetase (CBS, EC4.2.1.22) and cystathionine γ-lyase (CSE, EC4.4.1.1). Both CBS and CSE are widely distrib- uted in tissues. However, CBS is the predominant source of H 2 S in the central nervous system whereas CSE is the major H 2 S-producing enzyme in the cardiovascular sys- tem. H 2 S dilates blood vessels and relaxes gastrointestinal smooth muscles by opening muscle K ATP channels and promotes hippocampal long-term potentiation by Published: 30 December 2009 Journal of Inflammation 2009, 6:35 doi:10.1186/1476-9255-6-35 Received: 13 August 2009 Accepted: 30 December 2009 This article is available from: http://www.journal-inflammation.com/content/6/1/35 © 2009 Sidhapuriwala et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Journal of Inflammation 2009, 6:35 http://www.journal-inflammation.com/content/6/1/35 Page 2 of 10 (page number not for citation purposes) enhancing the sensitivity of N-methyl-D-aspartate recep- tors to glutamate [1,2]. Since the discovery of endogenous H 2 S, many studies have been performed to understand the physiologic and pathologic roles of this gas and numerous animal studies have shown its beneficial effects Available online http://ccforum.com/content/13/3/213 Page 1 of 9 (page number not for citation purposes) Abstract Hydrogen sulfide (H 2 S), a gas with the characteristic odor of rotten eggs, is known for its toxicity and as an environmental hazard, inhibition of mitochondrial respiration resulting from blockade of cytochrome c oxidase being the main toxic mechanism. Recently, however, H 2 S has been recognized as a signaling molecule of the cardiovascular, inflammatory and nervous systems, and therefore, alongside nitric oxide and carbon monoxide, is referred to as the third endogenous gaseous transmitter. Inhalation of gaseous H 2 S as well as administration of inhibitors of its endogenous production and compounds that donate H 2 S have been studied in various models of shock. Based on the concept that multiorgan failure secondary to shock, inflammation and sepsis may represent an adaptive hypometabolic reponse to preserve ATP homoeostasis, particular interest has focused on the induction of a hibernation-like suspended animation with H 2 S. It must be underscored that currently only a limited number of data are available from clinically relevant large animal models. Moreover, several crucial issues warrant further investigation before the clinical application of this concept. First, the impact of hypothermia for any H 2 S-related organ protection remains a matter of debate. Second, similar to the friend and foe character of nitric oxide, no definitive conclusions can be made as to whether H 2 S exerts proinflammatory or anti-inflam- matory properties. Finally, in addition to the question of dosing and timing (for example, bolus administration versus continuous intravenous infusion), the preferred route of H 2 S administration remains to be settled – that is, inhaling gaseous H 2 S versus intra- venous administration of injectable H 2 S preparations or H 2 S donors. To date, therefore, while H 2 S-induced suspended anima- tion in humans may still be referred to as science fiction, there is ample promising preclinical data that this approach is a fascinating new therapeutic perspective for the management of shock states that merits further investigation. Introduction Hydrogen sulfide (H 2 S), a colorless, flammable and water- soluble gas with the characteristic odor of rotten eggs, has been known for decades because of its toxicity and as an environmental hazard [1,2]. Inhibition of mitochondrial respiration – more potent than that of cyanide [3] – resulting from blockade of cytochrome c oxidase is the main mecha- nism of H 2 S toxicity [4,5]. During recent years, however, H 2 S has been recognized as an important signaling molecule of the cardiovascular system, the inflammatory system and the nervous system. Alongside nitric oxide (NO) and carbon monoxide, therefore, H 2 S is now known as the third endogenous gaseotransmitter [1,6]. Since H 2 S is a small ubiquitous gaseous diffusible molecule, its putative interest for intensive care research is obvious. Consequently, inhibitors of its endogenous production as well as compounds that donate H 2 S have been studied in various models of shock resulting from hemorrhage [7-9], ischemia/reperfusion [10-18], endotoxemia [19-21], bacterial sepsis [22-25] and nonmicrobial inflammation [26-29] – which, however, yielded rather controversial data with respect to the proinflammatory or anti-inflammatory properties of H 2 S. The present article reviews the current literature on the therapeutic potential of H 2 S, with a special focus on clinically relevant studies in – if available – large animal models. Biological chemistry In mammals, H 2 S is synthesized from the sulfur-containing amino acid L-cysteine by either cystathionine-β-synthase or Review Bench-to-bedside review: Hydrogen sulfide – the third gaseous transmitter: applications for critical care Florian Wagner 1 , Pierre Asfar 2,3 , Enrico Calzia 1 , Peter Radermacher 1 and Csaba Szabó 4,5 1 Sektion Anästhesiologische RESEARC H Open Access Effects of hydrogen sulfide on hemodynamics, inflammatory response and oxidative stress during resuscitated hemorrhagic shock in rats Frédérique Ganster 1,2,6 , Mélanie Burban 1 , Mathilde de la Bourdonnaye 1 , Lionel Fizanne 1 , Olivier Douay 1 , Laurent Loufrani 3 , Alain Mercat 1,2 , Paul Calès 1,2 , Peter Radermacher 4 , Daniel Henrion 3 , Pierre Asfar 1,2* , Ferhat Meziani 2,5,6 Abstract Introduction: Hydrogen sulfide (H 2 S) has been shown to improve survival in rodent models of lethal hemorrhage. Conversely, other authors have reported that inhibition of endogenous H 2 S production improves hemodynamics and reduces organ injury after hemorrhagic shock. Since all of these data originate from unresuscitated models and/or the use of a pre-treatment design, we therefore tested the hypothesis that the H 2 S donor, sodium hydrosulfide (NaHS), may improve hemodynamics in resuscitated hemorrhag ic shock and attenuate oxidative and nitrosative stresses. Methods: Thirty-two rats were mechanically ventilated and instrumented to measure mean arterial pressure (MAP) and carotid blood flow (CBF). Animals were bled during 60 minutes in order to maintain MAP at 40 ± 2 mm Hg. Ten minutes prior to retransfusion of shed blood, rats randomly received either an intravenous bolus of NaHS (0.2 mg/kg) or vehicle (0.9% NaCl). At the end of the experiment (T = 300 minutes), blood, aorta and heart were harvested for Western blot (inductible Nitric Oxyde Synthase (iNOS), Nuclear factor-B (NF-B), phosphorylated Inhibitor B (P-IB), Inter-Cellular Adhesion Molecule (I-CAM), Heme oxygenase 1(HO-1), Heme oxygenase 2(HO-2), as well as nuclear respiratory factor 2 (Nrf2)). Nitric oxide (NO) and superoxide anion (O 2 - ) were also measured by electron paramagnetic resonance. Results: At the end of the experiment, control rats exhibited a decrease in MAP which was attenuated by NaHS (65 ± 32 versus 101 ± 17 mmHg, P < 0.05). CBF was better maintained in NaHS-treated rats (1.9 ± 1.6 versus 4.4 ± 1.9 ml/minute P < 0.05). NaHS significantly limited shock-induced metabolic acidosis. NaHS also prevented iNOS expression and NO production in the heart and aorta while significantly reducing NF-kB, P-IB and I-CAM in the aorta. Compared to the control group, NaHS significantly increased Nrf2, HO-1 and HO-2 and limited O 2 - release in both aorta and heart (P < 0.05). Conclusions: NaHS is protective against the effects of ischemia reperfusion induced by controlled hemorrhage in rats. NaHS also improves hemodynamics in the early resuscitation phase after hemorrhagic shock, most likely as a result of attenuated oxidative stress. The use of NaHS hence appears promising in limiting the consequences of ischemia reperfusion (IR). * Correspondence: PiAsfar@chu-angers.fr 1 Laboratoire HIFIH, UPRES EA 3859, IFR 132, Université d’Angers, Rue Haute de Reculée, Angers, F-49035 France Full list of author information is available at the end of the article Ganster et al. Critical Care 2010, 14:R165 http://ccforum.com/content/14/5/R165 © 2010 Ganster et al.; licensee B ioMed Central Ltd. This is an open access article distr ibuted under the terms of the Creative Common s Attribution License (http://creativecommons.org/licenses/by/2.0), w hich permits unrestricted use, distribu tion, and reproduction in any medium, provided the original work is properly cited. Introduction Hemorrhagic shock (HS) is a life-threatening co mplica- tion in both trauma patients and in the operating room [1,2]. The pathophysiology of HS is complex, especially during t he reperfusion phase [3]. During HS, the state of vasoconstriction turns into vasodilatory shock. According to Landry et al. [4], this phenomeno n is related to tissue hypoxia as well as to a proinflammatory immune response [4]. In addition, dur ing the reperfu- sion phase, cellular injuries induced by ischemia are enhanced, and are associated with excessive production of radical oxygen species (ROS), RESEARCH Open Access Administration of hydrogen sulfide via extracorporeal membrane lung ventilation in sheep with partial cardiopulmonary bypass perfusion: a proof of concept study on metabolic and vasomotor effects Matthias Derwall 1,2*† , Roland CE Francis 1† , Kotaro Kida 1 , Masahiko Bougaki 1 , Ettore Crimi 1 , Christophe Adrie 1 , Warren M Zapol 1 , Fumito Ichinose 1 Abstract Introduction: Although inhalation of 80 parts per million (ppm) of hydrogen sulfide (H 2 S) reduces metabolism in mice, doses higher than 200 ppm of H 2 S were required to depress metabolism in rats. We therefore hypothesized that higher concentrations of H 2 S are required to reduce metabolism in larger mammals and humans. To avoid the potential pulmonary toxicity of H 2 S inhalation at high concentrations, we investigated whether administering H 2 S via ventilation of an extracorporeal membrane lung (ECML) would provide means to manipulate the metabolic rate in sheep. Methods: A partial venoarte rial cardiopulmonary bypass was established in anesthetized, ventilated (fraction of inspired oxygen = 0.5) sheep. The ECML was alternately ventilated with air or air containing 100, 200, or 300 ppm H 2 S for intervals of 1 hour. Metabolic rate was estimated on the basis of total CO 2 production ( VCO 2 ) and O 2 consumption ( VO 2 ). Continuous hemo dynamic monitoring was performed via indwelling femoral and pulmonary artery catheters. Results: VCO 2 , VO 2 , and cardiac output ranged within normal physiological limits when the ECML was ventilated with air and did not change after administration of up to 300 ppm H 2 S. Administration of 100, 200 and 300 ppm H 2 S increased pulmonary vascular resistance by 46, 52 and 141 dyn·s/cm 5 , respectively (all P ≤ 0.05 for air vs. 100, 200 and 300 ppm H 2 S, respectively), and mean pulmonary artery pressure by 4 mmHg ( P ≤ 0.05), 3 mmHg (n.s.) and 11 mmHg (P ≤ 0.05), respectively, without cha nging pulmonary capillary wedge pressure or cardiac output. Exposure to 300 ppm H 2 S decreased systemic vascular resistance from 1,561 ± 553 to 870 ± 138 dyn·s/cm 5 (P ≤ 0.05) and m ean arterial pressure from 121 ± 15 mmHg to 66 ± 11 mmHg (P ≤ 0.05). In addition, exposure to 300 ppm H 2 S impaired arterial oxygenation (P a O 2 114 ± 36 mmHg with air vs. 83 ± 23 mmHg with H 2 S; P ≤ 0.05). Conclusions: Administration of up to 300 ppm H 2 S via ventilation of an extracorporeal membrane lung does not reduce VCO 2 and VO 2 , but causes dose-dependent pulmonary vasoconstrictio n and systemic vasodilation. These results suggest that administration of high concentrations of H 2 S in venoarterial cardiopulmonary bypass circulation does not reduce metabolism in anesthetized sheep but confers systemic and pulmonary vasomotor effects. * Correspondence: mderwall@partners.org † Contributed equally 1 Anesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA Full list of author information is available at the end of the article Derwall et al. Critical Care 2011, 15:R51 http://ccforum.com/content/15/1/R51 © 2011 Derwall et al.; licensee BioMed Central Ltd. This is an open ac cess article distributed under the terms of the Creative Commons Attribution License (http://cre ativecom mons.org/licenses/by/2.0), which permits unrestrict ed use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction Balancing cellular oxygen supply and demand is a key therapeutic approach to protecting organs such as the brain, kidneys and heart from ischemic injury. Permis- sive hypothermia and active cooling have been shown to reduce oxygen demands in patients experiencing stroke, cardiac arrest, cardiac surgery, severe trauma and other instances of ischemia and subsequent reperfusion [1-4]. However, hypothermic reduc tion of aerobic metabolism has been ... ngƣỡng Kết Đƣờng tiếp xúc Sinh vật thử phần 700 mg/cu m/35 LC50 Hô hấp Khỉ Hydrogen 380 mg/cu m/410 LC50 Hô hấp Chuột Sulfide 1500 mg/cu m/18 LC50 Hô hấp Chuột Các ảnh hƣởng mãn tính với ngƣời... sinh sản, biến đổi gen …) Các ảnh hƣởng độc khác XII THÔNG TIN VỀ SINH THÁI Tên thành phần Hydrogen Sulfide Loại sinh vật Độc tính với sinh vật Loại ngƣỡng Kết Ruồi, hô hấp LC50 380 mg/cu m/