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Comparison of the Antiischaemic and Antianginal Effects of Nicorandil and Amlodipine in Patients with Symptomatic Stable Angina Pectoris: the SWAN Study
Journal of Clinical and Basic Cardiology An Independent International Scientific Journal Journal of Clinical and Basic Cardiology 1999; 2 (2), 213-217 Comparison of the antiischaemic and antianginal effects of nicorandil and amlodipine in patients with symptomatic stable angina pectoris: the SWAN study The SWAN Study Group Homepage: www.kup.at/jcbc Online Data Base Search for Authors and Keywords Indexed in Chemical Abstracts EMBASE/Excerpta Medica Krause & Pachernegg GmbH · VERLAG für MEDIZIN und WIRTSCHAFT · A-3003 Gablitz/Austria ORIGINAL PAPERS, CLINICAL The SWAN study J Clin Basic Cardiol 1999; 2: 213 Comparison of the antiischaemic and antianginal effects of nicorandil and amlodipine in patients with symptomatic stable angina pectoris: the SWAN study The SWAN Study Group1 This multicentre, double-blind, randomised study compared the antiischaemic and antianginal effects of nicorandil and amlodipine in patients with symptomatic stable angina pectoris. Nicorandil is a new coronary and balanced peripheral vasodilating agent that operates through two mechanisms of action: activation of ATP-dependent K-channels and stimulation of guanylate cyclase. A total of 121 patients with symptomatic stable angina pectoris were randomised to receive nicorandil 10 mg twice daily (bd) or amlodipine 5 mg once daily (od) for 8 weeks (optional dosage increase after 2-4 weeks to 20 mg bd and 10 mg od, respec- tively). Symptom-limited exercise tolerance tests were performed at baseline, and after 2 and 8 weeks treatment, respectively. In addition, the number of anginal attacks, nitroglycerin (NTG) usage, blood pressure (BP), heart rate (HR) and adverse events were recorded, and a subjective assessment of quality of life performed. -
NINDS Custom Collection II
ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC -
NON-HAZARDOUS CHEMICALS May Be Disposed of Via Sanitary Sewer Or Solid Waste
NON-HAZARDOUS CHEMICALS May Be Disposed Of Via Sanitary Sewer or Solid Waste (+)-A-TOCOPHEROL ACID SUCCINATE (+,-)-VERAPAMIL, HYDROCHLORIDE 1-AMINOANTHRAQUINONE 1-AMINO-1-CYCLOHEXANECARBOXYLIC ACID 1-BROMOOCTADECANE 1-CARBOXYNAPHTHALENE 1-DECENE 1-HYDROXYANTHRAQUINONE 1-METHYL-4-PHENYL-1,2,5,6-TETRAHYDROPYRIDINE HYDROCHLORIDE 1-NONENE 1-TETRADECENE 1-THIO-B-D-GLUCOSE 1-TRIDECENE 1-UNDECENE 2-ACETAMIDO-1-AZIDO-1,2-DIDEOXY-B-D-GLYCOPYRANOSE 2-ACETAMIDOACRYLIC ACID 2-AMINO-4-CHLOROBENZOTHIAZOLE 2-AMINO-2-(HYDROXY METHYL)-1,3-PROPONEDIOL 2-AMINOBENZOTHIAZOLE 2-AMINOIMIDAZOLE 2-AMINO-5-METHYLBENZENESULFONIC ACID 2-AMINOPURINE 2-ANILINOETHANOL 2-BUTENE-1,4-DIOL 2-CHLOROBENZYLALCOHOL 2-DEOXYCYTIDINE 5-MONOPHOSPHATE 2-DEOXY-D-GLUCOSE 2-DEOXY-D-RIBOSE 2'-DEOXYURIDINE 2'-DEOXYURIDINE 5'-MONOPHOSPHATE 2-HYDROETHYL ACETATE 2-HYDROXY-4-(METHYLTHIO)BUTYRIC ACID 2-METHYLFLUORENE 2-METHYL-2-THIOPSEUDOUREA SULFATE 2-MORPHOLINOETHANESULFONIC ACID 2-NAPHTHOIC ACID 2-OXYGLUTARIC ACID 2-PHENYLPROPIONIC ACID 2-PYRIDINEALDOXIME METHIODIDE 2-STEP CHEMISTRY STEP 1 PART D 2-STEP CHEMISTRY STEP 2 PART A 2-THIOLHISTIDINE 2-THIOPHENECARBOXYLIC ACID 2-THIOPHENECARBOXYLIC HYDRAZIDE 3-ACETYLINDOLE 3-AMINO-1,2,4-TRIAZINE 3-AMINO-L-TYROSINE DIHYDROCHLORIDE MONOHYDRATE 3-CARBETHOXY-2-PIPERIDONE 3-CHLOROCYCLOBUTANONE SOLUTION 3-CHLORO-2-NITROBENZOIC ACID 3-(DIETHYLAMINO)-7-[[P-(DIMETHYLAMINO)PHENYL]AZO]-5-PHENAZINIUM CHLORIDE 3-HYDROXYTROSINE 1 9/26/2005 NON-HAZARDOUS CHEMICALS May Be Disposed Of Via Sanitary Sewer or Solid Waste 3-HYDROXYTYRAMINE HYDROCHLORIDE 3-METHYL-1-PHENYL-2-PYRAZOLIN-5-ONE -
Nitroglycerin Sublingual Tablets, USP)
NDA 021134/S-004 Page 4 Nitrostat® (Nitroglycerin Sublingual Tablets, USP) DESCRIPTION Nitrostat is a stabilized sublingual compressed nitroglycerin tablet that contains 0.3 mg , 0.4 mg , or 0.6 mg nitroglycerin; as well as lactose monohydrate, NF; glyceryl monostearate, NF; pregelatinized starch, NF; calcium stearate, NF powder; and silicon dioxide, colloidal, NF. Nitroglycerin, an organic nitrate, is a vasodilating agent. The chemical name for nitroglycerin is 1, 2, 3 propanetriol trinitrate and the chemical structure is: NO2 O O N O CH2CHCH2 O NO 2 2 C3H5N309 Molecular weight: 227.09 CLINICAL PHARMACOLOGY The principal pharmacological action of nitroglycerin is relaxation of vascular smooth muscle. Although venous effects predominate, nitroglycerin produces, in a dose-related manner, dilation of both arterial and venous beds. Dilation of postcapillary vessels, including large veins, promotes peripheral pooling of blood, decreases venous return to the heart, and reduces left ventricular end-diastolic pressure (preload). Nitroglycerin also produces arteriolar relaxation, thereby reducing peripheral vascular resistance and arterial pressure (afterload), and dilates large epicardial coronary arteries; however, the extent to which this latter effect contributes to the relief of exertional angina is unclear. Therapeutic doses of nitroglycerin may reduce systolic, diastolic, and mean arterial blood pressure. Effective coronary perfusion pressure is usually maintained, but can be compromised if blood pressure falls excessively, or increased heart rate decreases diastolic filling time. Elevated central venous and pulmonary capillary wedge pressures, and pulmonary and systemic vascular resistance are also reduced by nitroglycerin therapy. Heart rate is usually slightly increased, presumably due to a compensatory response to the fall in blood pressure. -
Effect of L-Canavanine, an Inhibitor of Inducible Nitric Oxide Synthase, on Myocardial Dysfunction During Septic Shock
J Nippon Med Sch 2002; 69(1) 13 ―Original― Effect of L-canavanine, an Inhibitor of Inducible Nitric Oxide Synthase, on Myocardial Dysfunction During Septic Shock Norihito Suzuki, Atsuhiro Sakamoto and Ryo Ogawa Department of Anesthesiology, Nippon Medical School Abstract Overproduction of nitric oxide(NO)by inducible NO synthase(iNOS)plays aroleinthe pathophysiology of septic shock. The depression of cardiac contractilityinsuchsituationsis mediated by proinflammatory cytokines, including interleukin-1β(IL-1β), and tumor necrosis factor-α(TNF-α). The effects of two NOS inhibitors with different isoform selectivity were compared in isolated working rat hearts. The depression of contractility by IL-1β and TNF-α was prevented by administration of a nonselective nitric oxide synthase inhibitor, NG-nitro-L- arginine methyl ester(L-NAME)or an inhibitor of inducible nitric oxide synthase, L-canavanine. In contrast, when L-NAME was administered in the absence of IL-1β and TNF-α, it depressed contractility over the 2h perfusion period by significantly reducing coronary flow. These results support current thinking that the depression of myocardial functionbyIL-1β and TNF-α is mediated, at least in part, by an intracardiac increase in inducible nitric oxide synthase, and that in contrast to L-NAME, the decline in coronary conductance seen in cytokine-treated is not prevented by L-canavanine hearts. L-canavanine shows selective inhibition of inducible nitric oxide synthase unlike the vasopressor action of L-NAME in cytokine-treated hearts. (J Nippon Med Sch 2002; 69: 13―18) Key words: nitric oxide(NO), nitric oxide(NO)synthase, working heart, L-canavanine, NG-nitro-L-arginine methyl ester(L-NAME) We have previously demonstrated that admini- Introduction stration of L-canavanine or L-NAME attenuated the endotoxin-induced hypotension and vascular hypore- Nitric oxide(NO)may be produced within the activity to adrenaline, and the beneficial hemody- heart by either constitutive or inducible NO1,2. -
1 SAFETY DATA SHEET Product Name: Nitroglycerin in 5% Dextrose
SAFETY DATA SHEET Product Name: Nitroglycerin in 5% Dextrose Injection 1. CHEMICAL PRODUCT AND COMPANY IDENTIFICATION Manufacturer Name And Hospira, Inc. Address 275 North Field Drive Lake Forest, Illinois 60045 USA Emergency Telephone CHEMTREC: North America: 800-424-9300; International 1-703-527-3887; Australia - 61-290372994; UK - 44-870-8200418 Hospira, Inc., Non-Emergency 224 212-2000 Product Name Nitroglycerin in Dextrose Injection Synonyms 1,2,3-propanetriol trinitrate 2. HAZARD(S) IDENTIFICATION Emergency Overview Nitroglycerin in Dextrose Injection is a solution containing nitroglycerin, an organic nitrate vasodilator. Clinically, this material is indicated for treatment of peri-operative hypertension; for control of congestive heart failure in the setting of acute myocardial infarction; for treatment of angina pectoris. In the workplace, this material should be considered potentially irritating to the eyes and respiratory tract and a potent drug. Based on clinical use, possible target organs include the cardiovascular system and blood. U.S. OSHA GHS Classification Physical Hazards Hazard Class Hazard Category Not Classified Not Classified Health Hazards Hazard Class Hazard Category Not Classified Not Classified Label Element(s) Pictogram NA Signal Word NA Hazard Statement(s) NA Precautionary Statement(s) Prevention Do not breathe vapor or spray. Wash hands thoroughly after handling. Response Get medical attention if you feel unwell. IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing. If eye irritation persists, get medical attention. 1 Product Name: Nitroglycerin in 5% Dextrose Injection 3. COMPOSITION/INFORMATION ON INGREDIENTS Active Ingredient Name Nitroglycerin Chemical Formula C3H5N3O9 Component Approximate Percent by Weight CAS Number RTECS Number Nitroglycerin ≤ 0.04 55-63-0 QX2100000 Non-hazardous ingredients include Water for Injection and dextrose. -
NITROGYLCERIN and ETHYLENE GLYCOL DINITRATE Criteria for a Recommended Standard OCCUPATIONAL EXPOSURE to NITROGLYCERIN and ETHYLENE GLYCOL DINITRATE
CRITERIA FOR A RECOMMENDED STANDARD OCCUPATIONAL EXPOSURE TO NITROGYLCERIN and ETHYLENE GLYCOL DINITRATE criteria for a recommended standard OCCUPATIONAL EXPOSURE TO NITROGLYCERIN and ETHYLENE GLYCOL DINITRATE U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE Public Health Service Center for Disease Control National Institute for Occupational Safety and Health June 1978 For »ale by the Superintendent of Documents, U.S. Government Printing Office, Washington, D.C. 20402 DISCLAIMER Mention of company name or products does not constitute endorsement by the National Institute for Occupational Safety and Health. DHEW (NIOSH) Publication No. 78-167 PREFACE The Occupational Safety and Health Act of 1970 emphasizes the need for standards to protect the health and provide for the safety of workers occupationally exposed to an ever-increasing number of potential hazards. The National Institute for Occupational Safety and Health (NIOSH) evaluates all available research data and criteria and recommends standards for occupational exposure. The Secretary of Labor will weigh these recommendations along with other considerations, such as feasibility and means of implementation, in promulgating regulatory standards. NIOSH will periodically review the recommended standards to ensure continuing protection of workers and will make successive reports as new research and epidemiologic studies are completed and as sampling and analytical methods are developed. The contributions to this document on nitroglycerin (NG) and ethylene glycol dinitrate (EGDN) by NIOSH staff, other Federal agencies or departments, the review consultants, the reviewers selected by the American Industrial Hygiene Association, and by Robert B. O ’Connor, M.D., NIOSH consultant in occupational medicine, are gratefully acknowledged. The views and conclusions expressed in this document, together with the recommendations for a standard, are those of NIOSH. -
Sustained Formation of Nitroglycerin-Derived Nitric Oxide
Supplemental material to this article can be found at: http://molpharm.aspetjournals.org/content/suppl/2018/01/22/mol.117.110783.DC1 1521-0111/93/4/335–343$35.00 https://doi.org/10.1124/mol.117.110783 MOLECULAR PHARMACOLOGY Mol Pharmacol 93:335–343, April 2018 Copyright ª 2018 The Author(s). This is an open access article distributed under the CC BY Attribution 4.0 International license. Sustained Formation of Nitroglycerin-Derived Nitric Oxide by Aldehyde Dehydrogenase-2 in Vascular Smooth Muscle without Added Reductants: Implications for the Development of Nitrate Tolerance s Marissa Opelt, Gerald Wölkart, Emrah Eroglu, Markus Waldeck-Weiermair, Roland Malli, Wolfgang F. Graier, Alexander Kollau, John T. Fassett, Astrid Schrammel, Bernd Mayer, and Antonius C. F. Gorren Downloaded from Institute of Pharmaceutical Sciences, Department of Pharmacology and Toxicology, Karl-Franzens University (M.O., G.W., A.K., J.T.F., A.S., B.M., A.C.F.G.), and Institute of Molecular Biology and Biochemistry, Center of Molecular Medicine, Medical University Graz (E.E., M.W.-W., R.M., W.F.G.), Graz, Austria Received October 4, 2017; accepted January 18, 2018 molpharm.aspetjournals.org ABSTRACT According to current views, oxidation of aldehyde dehydrogenase-2 ALDH2, thiol-refractive inactivation was observed, particularly under (ALDH2) during glyceryltrinitrate (GTN) biotransformation is essen- high-turnover conditions. Organ bath experiments with rat aortas tially involved in vascular nitrate tolerance and explains the de- showed that relaxation by GTN lasted longer than that caused by the pendence of this reaction on added thiols. Using a novel fluorescent NO donor diethylamine/NONOate, in line with the long-lasting intracellular nitric oxide (NO) probe expressed in vascular smooth nanomolar NO generation from GTN observed in VSMCs. -
Nitric Oxide Synthase Inhibitors As Antidepressants
Pharmaceuticals 2010, 3, 273-299; doi:10.3390/ph3010273 OPEN ACCESS pharmaceuticals ISSN 1424-8247 www.mdpi.com/journal/pharmaceuticals Review Nitric Oxide Synthase Inhibitors as Antidepressants Gregers Wegener 1,* and Vallo Volke 2 1 Centre for Psychiatric Research, University of Aarhus, Skovagervej 2, DK-8240 Risskov, Denmark 2 Department of Physiology, University of Tartu, Ravila 19, EE-70111 Tartu, Estonia; E-Mail: [email protected] (V.V.) * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +4577893524; Fax: +4577893549. Received: 10 November 2009; in revised form: 7 January 2010 / Accepted: 19 January 2010 / Published: 20 January 2010 Abstract: Affective and anxiety disorders are widely distributed disorders with severe social and economic effects. Evidence is emphatic that effective treatment helps to restore function and quality of life. Due to the action of most modern antidepressant drugs, serotonergic mechanisms have traditionally been suggested to play major roles in the pathophysiology of mood and stress-related disorders. However, a few clinical and several pre-clinical studies, strongly suggest involvement of the nitric oxide (NO) signaling pathway in these disorders. Moreover, several of the conventional neurotransmitters, including serotonin, glutamate and GABA, are intimately regulated by NO, and distinct classes of antidepressants have been found to modulate the hippocampal NO level in vivo. The NO system is therefore a potential target for antidepressant and anxiolytic drug action in acute therapy as well as in prophylaxis. This paper reviews the effect of drugs modulating NO synthesis in anxiety and depression. Keywords: nitric oxide; antidepressants; psychiatry; depression; anxiety 1. Introduction Recent data from Denmark and Europe [1,2], indicate that brain disorders account for 12% of all direct costs in the Danish health system and 9% of the total drug consumption was used for treatment of brain diseases. -
Metabolomics-Driven Elucidation of Cellular Nitrate Tolerance Reveals Ascorbic Acid Prevents Nitroglycerin-Induced Inactivation of Xanthine Oxidase
fphar-09-01085 September 21, 2018 Time: 16:31 # 1 ORIGINAL RESEARCH published: 25 September 2018 doi: 10.3389/fphar.2018.01085 Metabolomics-Driven Elucidation of Cellular Nitrate Tolerance Reveals Ascorbic Acid Prevents Nitroglycerin-Induced Inactivation of Xanthine Oxidase Elizabeth Rose Axton1,2,3, Eleonso Cristobal1,2, Jaewoo Choi1, Cristobal L. Miranda1,2 and Jan Frederik Stevens1,2* 1 The Linus Pauling Institute, Oregon State University, Corvallis, OR, United States, 2 Department of Pharmaceutical Sciences, Oregon State University, Corvallis, OR, United States, 3 Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR, United States Glyceryl trinitrate (GTN) has found widespread use for the treatment of angina pectoris, a pathological condition manifested by chest pain resulting from insufficient blood supply Edited by: to the heart. Metabolic conversion of GTN, a nitric oxide (NO) pro-drug, into NO induces Pedro D’Orléans-Juste, vasodilation and improves blood flow. Patients develop tolerance to GTN after several Université de Sherbrooke, Canada weeks of continuous use, limiting the potential for long-term therapy. The mechanistic Reviewed by: Carlos F. Sánchez-Ferrer, cause of nitrate tolerance is relatively unknown. We developed a cell culture model 15 Universidad Autonoma de Madrid, of nitrate tolerance that utilizes stable isotopes to measure metabolism of N3-GTN Spain into 15N-nitrite. We performed global metabolomics to identify the mechanism of GTN- InKyeom Kim, Kyungpook National University, induced nitrate tolerance and to elucidate the protective role of vitamin C (ascorbic acid). South Korea Metabolomics analyses revealed that GTN impaired purine metabolism and depleted *Correspondence: intracellular ATP and GTP. GTN inactivated xanthine oxidase (XO), an enzyme that Jan Frederik Stevens [email protected] is critical for the metabolic bioactivation of GTN into NO. -
Original Article Acute Effects of Intracoronary Nicorandil and Nitroglycerin in Patients with Coronary Slow Flow
Int J Clin Exp Med 2016;9(6):11852-11858 www.ijcem.com /ISSN:1940-5901/IJCEM0022210 Original Article Acute effects of intracoronary nicorandil and nitroglycerin in patients with coronary slow flow Quanfang Zhang1, Zebo Xiu2, Wei Wang3, Zuoyuan Chen1, Zehua Dong4, Rongsun Zhang5 Departments of 1Cardiology, 3Pharmacy, 4ICU, 5Traditional Chinese Medicine, The Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong, China; 2Department of Cardiology, Liaocheng People’s Hospital and Lia- ocheng Clinical School of Taishan Medical College, Liaocheng 252000, Shangdong Province, China Received December 18, 2015; Accepted March 5, 2016; Epub June 15, 2016; Published June 30, 2016 Abstract: Objective: This study aimed to assess the acute effects of intracoronary nicorandil and nitroglycerin in pa- tients with coronary slow flow (CSF). Methods: Totally, 60 patients with CSF were enrolled in this retrospective study and divided into nicorandil group (n = 30) and nitroglycerin group (n = 30). Coronary angiography was administered to intracoronary nitroglycerin or nicorandil 30 seconds later. The coronary blood flow of patients was evaluated by thrombolysis in myocardial infarction (TIMI) frame count (TFC) method. Heart rate, systolic and diastolic blood pressures, and TFCs in left anterior descending artery (LAD), left circumflex artery (LCX), and right coronary artery (RCA) were recorded before and after administration with nicorandil or nitroglycerin. Results: After nitroglycerin administration, systolic and diastolic blood pressures decreased, heart rates significantly increased (P < 0.001). However, systolic and diastolic blood pressures, heart rate had no significant changes after the application of in- tracoronary nicorandil. In addition, after administration with nicorandil or nitroglycerin, TFCs in LAD, LCX, and RCA were significantly decreased (P < 0.001) compared with before administration; however, TFCs recovered to the normal level in the nicorandil group but not nitroglycerin group. -
United States Patent Office Patented Sept
3,208,890 United States Patent Office Patented Sept. 28, 1965 2 3,208,890 From the table, it is thus evident that the two propyl GELATNIZED EXPLOSIVE ene glycol dinitrates, and especially the 1,2-compound, Carl Torsten Edlund and Gustav Allan Wetterholm, Gyttorp, Sweden, assignors to Nitroglycerin Aktiebola are decidedly less soluble in water than nitroglycol, where get, a company of Sweden by they are absorbed by the blood to a less degree. No Drawing. Filed Feb. 27, 1963, Ser. No. 261,521 Claims priority, application Sweden, Feb. 28, 1962, THE PRESENT INVENTION 2,232/62 The present invention relates to an explosive having an 5 Claims. (Cl. 149-47) improved physiological acceptance and a low sensitivity to impact, consisting of or containing propylene-glycol di The present invention generally relates to a novel ex 0. nitrate, and one or more inorganic oxygen-delivering plosive of the gelatinized type having improved physio salts. One important characterizing feature of the ex logical acceptance and a low sensitivity to impact. More plosive according to the invention is that the oxygen-de specifically the present invention pertains to an explosive livering inorganic salt or salts are present in a sufficient comprising an oxygen-delivering inorganic salt and an ex amount to substantially oxygen-balance the explosive. plosive oil consisting of propylene-glycol dinitrate or a 15 Because the explosives according to the invention mixture of propylene-glycol dinitrate with no more than possess a combination of high insensitivity to impact with 50 percent of nitroglycerine. an excellent physiological acceptance, they represent a BACKGROUND valuable advance in the field of explosives.