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Acetone cyanohydrin (ACH), an organic cyanide, is mainly used in the production of methyl methacrylate (MMA), and it also exists in cassava roots, the main calorie source in some tropical countries. ACH can decompose spontaneously or enzymatically into acetone and highly toxic hydrogen cyanide (HCN) and be potentially toxic to its contacts. Given that limited forensic studies and case reports on fatal ACH poisoning are available, herein, we present a report of two fatal cases of ACH poisoning in which the two victims, with postmortem cyanide blood concentrations of 4.22 μg/ml and 4.07 μg/ml, suffered from acute poisoning of ACH due to a traffic accident. Furthermore, a literature review of cyanide poisoning case reports from 2000 to 2020 was carried out, and 28 subjects with cyanide poisoning were presented, including the age, sex, cause of poisoning, autopsy findings and the cyanide concentration in the blood. ACH poisoning lacks specific and reliable autopsy findings for diagnosis, and relevant toxicological studies are necessary. Due to the chemical properties of ACH that allow it to easily decompose, the toxicological analysis of acetone and cyanide in biological samples is essential for the diagnosis of ACH poisoning.

The high toxicity and availability in industrial production have made cyanide a concern for clinical testing and forensic toxicological analysis. An efficient and accurate method for detecting cyanide in urine sample has been established. The process was carried out by a two-step derivatization reaction. The cyanide reacted with benzaldehyde to form a stable intermediate which reacted with heptafluorobutyryl chloride in the second step. The quantitative MS/MS transition of the cyanide derivative was m/z 330.2→m/z 303.4, and the qualitative MS/MS transition was m/z 330.2→m/z 185.2. The method had good linearity (r2 = 0.999 4) and covered the cyanide poisoning detection window (0.01–10 µg mL− 1), and the limit of detection was 3 ng mL− 1. At the same time, the method demonstrated good accuracy (recoveries = 92.7.0–102.0%) and precision (intra-day precision = 3.3–5.1%, inter-day precision = 4.4–5.3%). The complete derivatization reaction and detection time were controlled within 20 min and successfully applied in a lethal case of ingestion of potassium cyanide.

Cyanide toxicity is common after significant smoke inhalation. Two cases are presented that provide framework for the discussion of epidemiology, pathogenesis, presenting signs and symptoms, and treatment options of inhalational cyanide poisoning. An evidence-based algorithm is proposed that utilizes point-of-care testing to help physicians identify patients who benefit most from antidotal therapy.

The use of complementary and alternative medicine (CAM) is widespread in children with cancer and is poorly regulated. Case report. We describe a case of severe cyanide poisoning arising from CAM use. A severely agitated, encephalopathic, unresponsive 4-year-old boy (initial Glasgow Coma Scale of 3) with a history of metastatic ependymoma was brought to our emergency department by ambulance services. Initial blood gas analysis demonstrated severe metabolic/lactic acidosis. On detailed questioning of the parents, the use of CAM including intravenous and oral “vitamin B 17” (amygdalin) and oral apricot kernel was reported. After administering sodium thiosulfate, rapid improvement in his medical condition with complete recovery without need for further intensive care treatment was seen. Serum cyanide level was markedly elevated. Cyanide poisoning can be the cause of severe encephalopathy in children receiving CAM treatment with substances containing cyanogenic glycosides.

Food (cassava) linamarin is metabolized into neurotoxicants cyanide and cyanate, metabolites of which we sought to elucidate the differential toxicity effects on memory. Young 6–8 weeks old male rats were treated intraperitoneally with either 2.5 mg/kg body weight (bw) cyanide (NaCN), or 50 mg/kg bw cyanate (NaOCN), or 1 μl/g bw saline, daily for 6 weeks. Short-term and long-term memories were assessed using a radial arm maze (RAM) testing paradigm. Toxic exposures had an influence on short-term working memory with fewer correct arm entries (F 2, 19 = 4.57 p

This is a report on an international non-interventional study of patients exposed to fires with smoke development in closed rooms. The objective of the study was to document clinical symptoms, relevant laboratory values and blood cyanide concentrations from fire victims in order to confirm or rule out presumptive correlations between the individual parameters. The study was conducted in five European countries with patients being included if they presented with the characteristic clinical signs, such as soot deposits and altered neurological status. Venous blood samples were taken from victims prior to administration of an antidote in all cases and determination of cyanide concentration was performed in a central laboratory using high performance liquid chromatography. Data from 102 patients (62 % male, average age 49 years) were included in the evaluation with no blood samples being available for analysis from 2 patients. In 25 patients the blood cyanide concentration was below the limit of detection of 1.2 μmol/l. Cyanide levels between 1.2 and 10 μmol/l were measured in 54 patients, 7 patients had values between 10 and 20 μmol/l, 4 patients between 20 and 40 μmol/l while levels above 40 μmol/l were determined in 10 patients. The results of the study could not demonstrate that the cyanide level was influenced either by the interval between smoke exposure and blood sampling or the duration presence at the fire scene. The following clinical signs or laboratory values were recorded as relevant for increased and possibly toxic cyanide levels: respiratory arrest, dyspnea, resuscitation requirement, tracheal intubation, respiratory support measures, low Glasgow coma scale (GCS) score and respiratory frequency. A correlation between cyanide concentration and the total amount of soot deposits on the face and neck, in the oral cavity and in expectoration was confirmed. A correlation between cyanide and carboxyhemoglobin (COHb) levels in the blood of fire victims was also confirmed. As long as it is not possible to immediately determine the blood cyanide concentration in patients exposed to fire with smoke development, a decreased GCS score, soot deposits particularly in expectoration, dyspnea and convulsions are to be regarded as risk markers for intoxication. In their presence immediate administration of hydroxocobalamin as an antidote is recommended.

Recent studies revealed that alpha-ketoglutarate (A-KG) alone or with sodium thiosulfate (STS) provide significant protection against acute and sub-acute cyanide poisoning in rodents. This study addresses the protective effect of A-KG and/or STS in sub-chronic (90 days) cyanide poisoning. Wistar rats were divided into seven groups (n = 10): Control animals, potassium cyanide (KCN) A-KG, STS, KCN + A-KG, KCN + STS and KCN + A-KG + STS. Spontaneous motor activity and motor coordination were recorded every 15th day. Lipid peroxidation (LPO), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) in blood, brain, liver and kidney, and glutamate, aspartate and dopamine in discrete regions of brain were measured following 90 days exposure. Cyanide significantly decreased motor coordination, accompanied by increase in LPO (blood, brain and liver) and dopamine (corpus striatum and cerebral cortex) levels, and depletion in GSH (blood, brain and liver), GPx (brain and liver), SOD (brain and liver), and CAT (blood and brain) levels. Although treatment of A-KG and STS alone significantly blunted the toxicity of KCN, concomitant use of both afforded the maximum protection. This study shows a promising role of A-KG and STS as treatment regime for long term cyanide exposure.

Increased demand for and dependence on toasted cassava granules (gari), and the widespread mechanization of its production has led to shortened periods of fermentation of the cassava mash during processing. The clinicopathologic implications of consumption of gari produced from cassava mash fermented for varied periods was studied. Exclusive diets of gari produced from cassava mash fermented for 0 hr, 24 hrs, 48 hrs, and 72 hrs were fed to different groups of growing male albino rats for a ten week period during which they were observed for clinical abnormalities. The rats were euthanized thereafter, and gross and histopathologic changes in major body organs noted. All the rat groups fed gari manifested varying degrees of clinical signs and histopathologic changes usually associated with chronic cyanide poisoning (CCP) and protein deficiency but the signs and lesions of CCP were most severe in rats fed gari produced from the 24 hour-fermented cassava mash. The findings suggested that shortening the fermentation period of cassava mash to about 24 hours constitutes a health hazard to consumers of gari.

Hydroxocobalamin is a new antidote approved by the FDA for the treatment of cyanide poisoning. Our report describes a patient with cyanide poisoning who survived after treatment with hydroxocobalamin and complications we encountered with hemodialysis. A 34-year-old female presented to the emergency department after a syncopal event and seizures. Her systolic blood pressure was 75 mmHg, her QRS complex progressively widened, and pulses were lost. She was intubated and resuscitated with fluids, sodium bicarbonate for her QRS widening and vasopressors. Venous blood gas demonstrated a pH of 6.36 with an O2 saturation of 99%. Due to the acidemia with a normal pulse oximetry, simultaneous venous and arterial blood gases were obtained. Venous gas demonstrated a pH of 6.80 with a PO2 of 222 mmHg, an O2 saturation of 99%. The arterial blood gas showed a pH of 6.82, a PO2 518 mmHg, an O2 saturation of 100%. Cyanide was suspected and hydroxocobalamin and sodium thiosulfate were given. Within 40 min of hydroxocobalamin administration, vasopressors were discontinued. Initially, nephrology attempted dialysis for metabolic acidosis; however, the dialysis machine repeatedly shut down due to a “blood leak”. This was an unforeseen effect attributed to hydroxocobalamin. Cyanide level, drawn 20 min after the antidote was completed, was elevated at 22 mcg/dL. Her urinary thiocyanate level could not be analyzed due to an “interfering substance”. Hydroxocobalamin is an effective antidote. However, clinicians must be aware of its effects on hemodialysis machines which could delay the initiation of this important treatment modality in the severely acidemic patient.

The high acute toxicity of acrylonitrile may be a result of its intrinsic biological reactivity or of its metabolite cyanide. Intravenous N-acetylcysteine has been recommended for treatment of accidental intoxications in acrylonitrile workers, but such recommendations vary internationally. Acrylonitrile is metabolized in humans and experimental animals via two competing pathways; the glutathione-dependent pathway is considered to represent an avenue of detoxication whilst the oxidative pathway leads to a genotoxic epoxide, cyanoethylene oxide, and to elimination of cyanide. Cases of acute acrylonitrile overexposure or intoxication have occurred within persons having industrial contact with acrylonitrile; the route of exposure was by inhalation and/or by skin contact. The combined observations lead to the conclusion of a much higher impact of the oxidative metabolism of acrylonitrile in humans than in rodents. This is confirmed by differences in the clinical picture of acute life-threatening intoxications in both species, as well as by differential efficacies of antidotes. A combination of N-acetylcysteine with sodium thiosulfate seems an appropriate measure for antidote therapy of acute acrylonitrile intoxications. Clinical observations also highlight the practical importance of human individual susceptibility differences. Furthermore, differential adduct monitoring, assessing protein adducts with different rates of decay, enables the development of more elaborated biological monitoring strategies for the surveillance of workers with potential acrylonitrile contact.

There have been few reported cases of cyanide toxicity following treatment with sodium nitroprusside. We report on the case of a paediatric patient who had received sodium nitroprusside for intractable hypertension in the post-operative period, resulting in cyanide toxicity. Treatment with sodium thiosulphate, sodium nitrate and haemodialysis resulted in the elimination of cyanide from the circulation. The patient made a full recovery with no neurological sequelae.

The physiological role of calcium was demonstrated by Ringer (1883) when he linked the omission of calcium (Ca++) from the bathing medium to the induction of cardiac arrest in the isolated frog heart. This observation established that Ca++ controlled muscle contraction but it was not until the autumn of 1963 that the specific pharmacological significance of this contribution was realised by Fleckenstein (1964), leading to the development of Ca++ antagonism as a concept in drug action (Fleckenstein 1977). Identifying the precise role of Ca++ ions in toxic cell injury and tissue death attributable to drug and chemical intoxication has lagged behind developments in Ca++ physiology and pharmacology and to date, much remains to be learned, although studies aimed at characterising the role of Ca++ in cytotoxic cell injury are receiving intense attention (Bondy Komulainen 1988; Maduh et al. l988a, l99Oa,b; Orrenius et al. 1989; Trump et al. 1989). On the other hand, the importance of cyanide as a poison has been known from antiquity (for references to earlier literature see Baskin Fricke 1992; Solomonson 1981). In experimental cyanide poisoning, recent studies have examined alterations in cell Ca++ and the influence of Ca++ antagonists in the management of this chemical toxicologicalmore » emergency. These efforts have principally focused on the cellular Ca++ homeostasis system, its interrelationship with cellular components, and its susceptibility to cyanide action.« less

Dear Editor, Although cyanide exists in various alimentary sources like manioc, corn, bitter almonds, peach or apricot kernels, food-related cyanide intoxications are rare [1]. A 58-year-old healthy woman was admitted for sudden headaches, dizziness, vomiting, and generalized seizures. Prehospital medical services found her comatose (Glasgow Coma Score: 5) with bradycardia (30/min) and nonmeasurable blood pressure. She was promptly intubated and received fluids. A brain CT scan was normal. On intensive care unit (ICU) admission, her blood pressure was 80/40 mmHg, heart rate 62/min, SpO2 100% (FiO2: 100%), and temperature 37.0 C. Physical examination, electrocardiogram, and echocardiography were unremarkable. Severe lactic acidosis (arterial pH: 6.59, base deficit: 36.0 mmol/l, anion gap: 33.0 mmol/l, and plasma lactate concentration: 26.0 mmol/l) was assessed without ketosis, osmolar gap, liver or renal dysfunction. Fluids (2,000 ml), norepinephrine (0.5 mg/h), insulin, and sodium bicarbonate were infused. Routine toxicological screening was negative. Blood cyanide concentration was 2.77 mg/l (spectrophotometric method; N \0.2 mg/l; limit of detection: 0.06 mg/l) 6 h after coma onset. Hydroxocobalamin (10 g, 140 mg/kg) was immediately infused, resulting in complete recovery: lactate normalization (within 12 h, Table 1), norepinephrine weaning (20 h), acid/base balance correction (36 h), extubation (day 2), and ICU discharge (day 3). Her husband finally remembered that she had ingested a large quantity of bitter almonds (around 50) from the garden, 2 h before symptom onset. Accidental food-related cyanide poisonings are unusual [1]. Signs are delayed after ingestion, in relation to enzymatic processes producing cyanide in the gut from the ingested cyanogenic glucosides. Cyanide poisoning is rapidly fatal if not promptly treated. Clinical features are not specific, misleading the diagnosis. However, when suspicion is based on compatible circumstances, plasma lactate concentrations C8 mmol/l are an excellent predictor of blood cyanide concentrations C1 mg/l [2]. In our case, despite no relevant anamnesis, cyanide poisoning was suspected because of severe lactic acidosis with coma, hypotension, and bradycardia in the absence of sepsis. Reported symptoms of cyanide poisoning following almond/seed ingestion included headaches, dizziness, sweating, pink cyanosis, coma, seizures, hyperthermia, hypotension, polypnea, bradypnea, hypoglycemia, and lactic acidosis [3, 4]. To our knowledge, hyperlactatemia (pH 7.17, lactate: 14.3 mmol/l) was reported in only one case after ingestion of bitter almonds with laetrile tablets (containing amygdaline) given for alternative cancer treatment [3]. The present case is unique for two reasons: the severity of almondinduced lactic acidosis and its dramatic improvement after hydroxocobalamin infusion. Management of cyanide poisoning is based on advanced life support and antidotes. Despite cyanide-induced deficient cell oxygen utilization, increased oxygen delivery (FiO2: 100%) is useful to reactivate mitochondrial enzymes and other oxidative systems. Hydroxocobalamin is an effective and safe antidote binding cyanide on an equimolar ratio to form stable cyanocobalamin, which is excreted in urine [5]. Although we should

Hydroxocobalamin is a rapid and powerful antidote in acute cyanide poisoning. The effects of hydroxocobalamin (0.1, 0.3, and 1 mM) on intrinsic myocardial contractility were studied on isolated rat cardiac papillary muscles (n = 10). Whatever the concentration, hydroxocobalamin did not modify the active isometric force and a slight increase in maximum unloaded shortening velocity was noted at 1 mM. Only 0.3 mM significantly impaired contraction-relaxation coupling under low load, suggesting a slight decrease in sarcoplasmic reticulum function. No changes in contraction-relaxation coupling under heavy load were noted, suggesting the lack of modification of myofilament calcium sensitivity. These results suggest that hydroxocobalamin does not induce noticeable changes in intrinsic myocardial contractility. An indirect mechanism might be involved in the previously reported decrease in cardiac function at supratherapeutic concentrations of hydroxocobalamin.

Single doses of sodium cyanide (60 mumol/kg body weight s.c.) were administered to male Sprague-Dawley rats. The effects of this poison on the content of the trace elements zinc, copper and manganese was investigated in various organs after 30 min, 2 h, 24 h, 48 h and 1 week. The zinc content in the liver was elevated 24 h after this sublethal cyanide dose (by approximately 20%). In contrast, the copper content in the kidneys was lowered (by approximately 15%) at the same time. Almost similar changes were observed in the same organs after daily administration of the poison for 5 days. For comparison, another group of rats was allowed to respire for 30 min the air that contained only 10% oxygen. The above changes in the trace element concentrations were not observed under these conditions. After sublethal cyanide poisoning there seemed be slight but specific alterations in the trace element concentrations in the liver and kidneys of rats. On the other hand, there were no alterations in serum, heart, lung, brain, muscle, bone or testes. Up to now there is no clearcut explanation for the development and the possible biochemical importance of these results.

Six dogs were given sufficient oral 4-dimethylaminophenol (DMAP) to produce a peak methaemoglobin level of 12–15%. Five out of the six dogs then survived an intravenous injection of approximately 2 LD50's of hydrogen cyanide given when the methaemoglobin had reached 8–10%. The sixth dog died after 44 min. When the same dose of hydrogen cyanide was given to dogs, not previously given DMAP, all three died within 11/2 min. It was concluded that prior treatment with oral DMAP provided a large measure of protection against cyanide poisoning. Comparison of cyanide levels in whole blood and plasma in the two groups of dogs lent support to the hypothesis that methaemoglobin complexed with cyanide in the erythrocytes causing the plasma cyanide to remain lower than it did in unprotected animals.

The effects of 4-dimethylaminophenol . HCl (DMAP) and 100% oxygen on cerebral blood flow (CBF) and peripheral circulation, arterial and venous blood gases, and other parameters have been investigated in dogs in the course of slow cyanide infusion. The i.v. infusion of KCN increased the respiratory minute volume, accompanied by a rise in arterial pO2 and pH and a decrease in arterial pCO2 while the venous lactate concentration increased by about 500% and the hemoglobin content and hematocrit by about 30%. Heart rate and carotid artery blood flow decreased. Local CBF in the cingulum as measured with thermocouples rose steadily, and the brain and oesophagus temperature were lowered. The breathing of 100% oxygen raised the local CBF, the temperature, and the arterial pCO2. During the infusion of KCN into the femoral artery of artificially ventilated dogs the femoral venous pO2 increased continuously by some 40 mm Hg, attended with a decrease in pCO2 of 15 mm Hg. The femoral blood flow, however, rose sharply within 3 min. 100% oxygen induced a rise in pCO2 and a diminution of pH in the femoral vein and in the sinus sagittalis, and the femoral flow rose rapidly. After DMAP i.v. the values of most of the parameters returned to normal or finally stabilized below or above the initial level. The rise in the hemoglobin content, hematocrit, and lactate concentration was stopped, but the arterial and venous pH remained or were lowered. DMAP elicited a rapid, strong decrease in the pO2 of the femoral vein and the sinus sagittalis with a concomitant marked increase in pCO2.

The excretion of thiocyanate following the administration of equitoxic doses of cyanide to unprotected mice and to animals pretreated with various cyanide antidotes has been studied. The results demonstrate that cyanide given alone or to animals pretreated with thiosulfate is extensively converted to thiocyanate. Animals pretreated with sodium nitrite or a combination of nitrite and sodium thiosulfate excreted even higher amounts of thiocyanate. This demonstrates that cyanide originally detoxified by combination with methemoglobin is ultimately converted to thiocyanate in the animal body. Pretreatment of animals with cobalt compounds (cobaltous chloride or dicobalt-EDTA) or a combination of cobalt compounds and thiosulfate resulted, on the other hand, in a less efficient conversion of cyanide to thiocyanate. The cyanide detoxified by trapping as highly undissociated cobalt-cyanide complexes is instead excreted in the urine, as demonstrated by detection of high amounts of cobalt ions and strongly complex-bound cyanide in the urine from animals treated with cobalt compounds and cyanide. A method for the determination of cyanide present as cobalt-cyanide complexes is described and its forensic application is proposed.

A 29-year-old chemistry student took 50 ml of a 1% potassium cyanide solution (500 mg) in an attempted suicide. He became comatose, mydriatic, and was admitted to hospital in an apneic state. He woke up after 7 h and developed Parkinsonism in the following weeks. This regressed slowly during the 2 months after the poisoning apart from dysarthria, bradykinesia of the upper limbs, and very brisk monosynaptic reflexes. At 3 weeks after the intoxication, computerized tomography was largely normal, and there was CSF-dense hypodensity in both putamina after 5 months. Sharply delimited signal elevation in T2 corresponding to the two putamina was detected by magnetic resonance imaging 8 weeks and 5 months after ingestion of the poison.

Cyanide in blood, plasma, and urine of dogs after administration of K14CN was determined with the isotope dilution technique. The addition of large amounts of inactive KCN as soon as possible to a sample to be analyzed inhibited the decrease of the original cyanide concentration. After administration of several lethal doses of cyanide into the stomach or by slow intravenous infusion a concentration of about 40 micron cyanide in plasma was found at the moment of respiratory arrest. Since 60% of the cyanide in plasma was bound to proteins the concentration of free cyanide which stopped respiration was about 16 micron. Quick formation of ferrihemoglobin by i.v. injection of 4-dimethylaminophenol after plasma cyanide had risen to or above 40 micron decreased the cyanide concentration in plasma and restored respiration, while cyanide was accumulated in red cells by formation of ferrihemoglobin cyanide. Equilibrium constants calculated for the reaction between ferrihemoglobin and cyanide in vivo indicated that the reaction approached equilibrium in a few minutes. Up to 60% of the radioactive cyanide absorbed was found as non-cyanide radioactivity in the urine.

The effects of the administration of methemoglobin (MetHb) prepared in vitro were evaluated in Sprague–Dawley rats given increasing doses of potassium cyanide (KCN). Median lethal dose (LD50) studies were conducted by giving intraperitoneal injections of KCN (in 0.3- to 0.5-ml volumes), then 2 min later administering intravenous (iv) doses of 1000, 1500, or 2500 mg/kg of MetHb through the tail vein. Control rats received an equivalent volume of saline. The resulting LD50 values for KCN were 7.4 ± 1.1, 11.7 ± 1.1, 13.9 ± 1.0, and 14.2 ± 1.0 mg/kg (mean ± SD) for the control (no MetHb) and 1000-, 1500-, and 2500-mg/kg dose groups, respectively. Additional groups of rats were given 1000, 1500, or 2500 mg/kg MetHb and submitted for necropsy. The gross finding of darkened kidneys was present in both dose groups, but became consistent and more prominent in the 2500-mg/kg dose group. Evidence of pathologic changes was not present in other organs. Single-dose pharmacokinetic studies were conducted using iv doses of 1600 and 2500 mg/kg MetHb. The elimination half-life was similar in both doses (62.6 min), but the volume of distribution (95.3 ± 7.2 and 126.3 ± 5.2 ml/kg, mean ± SE) and clearance (1.1 ± 0.1 and 1.5 ± 0.1 ml/min/kg) were significantly different (P < 0.05) for the 1600-and 2500-mg/kg dose groups, respectively. From these data we conclude that although MetHb is cleared from the vascular system rapidly, it may be an effective and nontoxic antidote for doses of cyanide up to twice that of the control LD50.

Cyanide markedly affected growth and resting metabolic rate while causing degenerative hepatic necrosis in juvenile rainbow trout (Salmo gairdneri, Richardson). This was revealed during two experiments performed in continuously renewed water at 12.5 degree C with fish fed a restricted artificial diet and exposed to assayed cyanide concentrations of 0.00, 0.01, 0.02, or 0.03 mg/L hydrogen cyanide (HCN) for 18 days. At 0.02 and 0.03 mg/L, HCN growth was reduced by 40 to 95% after 18 days. At all concentrations, cyanide caused a severe initial repression of specific growth rate, followed by a highly significant increase which was insufficient to compensate for the original repression. Previous exposure to cyanide promoted a higher resting metabolic rate during the six days following exposure, the effect increasing with cyanide concentration. At all concentrations tested, widespread cyanide-induced degenerative necrosis of hepatocytes was observed; it was more intense at higher cyanide concentrations and well established even at 0.01 mg/L HCN.

Durch geeignete Dosierung einer Cyanid-Dauerinfusion konnte am in situ arbeitenden Herzen des narkotisierten Hundes eine Glykolyse hervorgerufen und uber einen Zeitraum bis zu 58 min beobachtet werden. Die arteriovenose Milchsauredifferenz betragt unter diesen Bedingungen im Mittel+3,13±0,68 mg/100 ml Blut (n=11). Die Coronardurchblutung last sich unter der Cyanidwirkung auf 320 ml/min·100 g Herz schatzen. Daraus errechnet sich eine Milchsaurebildung im Herzen von etwa 10 mg/min · 100 g. Ungefahr die gleiche Menge Glucose wird standig aufgenommen (Arteriovenose Differenz=−3,62±1,1 mg/100 ml Blut, n=11). 12% des Energiebedarfes des Herzens werden unter den genannten Bedingungen anaerob gedeckt. Unter den Ausgangsbedingungen der Versuche (ohne Cyanidintoxikation) entfallen 58% des Sauerstoffverbrauches auf eine Oxydation der Milchsaure und Glucose, der Rest auf unveresterte Fettsauren. Es werden ferner allgemeine Veranderungen von Stoffwechsel, Kreislauf und Atmung bei Cyanidvergiftung diskutiert.

Thirteen of the 15 cases of polioencephalomalacia reported in this article are considered to be idiopathic. These cases are compared with two cases of polioencephalomalacia following from cyanide poisoning and all are discussed in relation to similar entities occurring in dogs and in other species.

In 42 Versuchen an kunstlich beatmeten Katzen in Chloralose-Urethannarkose (50 mg/kg und 250 mg/kg i.v.) wurde gepruft, ob Blutaustauschtransfusionen als therapeutische Masnahme bei der akuten Cyanidvergiftung in Betracht kommen. Dazu wurde eine Aufschwemmung von Rindererythrocyten in Tyrode benutzt, da ausreichende Mengen von gruppengleichem Katzenblut nicht zur Verfugung standen.

A 42-year old patient received a continuous infusion of sodium nitroprusside (SNP) at a dosage rate of 600 microgram/min for approximately four days. On the third day of treatment a dangerous high level of cyanide was measured in the blood. When an additional continuous infusion of sodium thiosulphate at five times the molar concentration of the SNP was given, this cyanide level dropped over a period of 7h to one-seventh of its initial value. The thiosulphate did not reduce the effectiveness of the SNP in lowering the blood pressure.

The respiration rate and intensity of phospholipid metabolism of a rat brain tissue homogenate was studied during incubation at different temperatures (37, 32 and 27°C) in medium with and without cyanide (0.5 and 1 mM). Both these parameters are directly dependent on incubation temperature between 27 and 37°C. The presence of cyanide in the medium inhibits both processes but phospholipid metabolism more so than respiration. The results indicate that phospholipid metabolism during cyanide poisoning is affected both by the toxic action of the cyanide itself directly, and by temperature, the lowering of which potentiates the toxic action.

Potassium cyanide overdosage occurred in a 43-year-old man resulting in convulsions, cardiac arrest, massive lactic acidosis and rhabdomyolysis. Perfect recovery was obtained with only non-specific supportive therapy (100% oxygen ventilation, vascular volume expansion, sodium bicarbonate infusion, anticonvulsivant drugs).

Es wurde der Einflus von Cyanid in verschiedener Dosierung auf den Plasmaspiegel von freiem Cholin der A. femoralis, V. femoralis und V. hepatica des Hundes untersucht. Die Abtrennung des Cholin erfolgte mittels eines Ionenaustauschers, die quantitative Bestimmung durch Fallung als Reineckat und nachfolgende spektrophotometrische Messung.

CYANIDE toxicity is closely associated with respiratory inhibition and, in many forms of life, death is attributed to disruption of oxidative metabolism through inhibition of the enzyme cytochrome oxidase. In insects also, cyanide inhibits the terminal oxidase, and it has been shown that in the insect heart cyanide sensitivity is closely associated with aerobic metabolism1.