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PubMed1997

In vitro effects of diazepam on human ciliary function.

This study demonstrated the in vitro effect of diazepam on human ciliary beat frequency (CBF) from fifteen normal subjects using brush cytology. Tube A contained culture medium, tube B the diluent that diazepam intravenous injectate was carried in and culture medium (controls). Tube C, D and E contained, 0.4 mg/l, 4.0 mg/l and 40.0 mg/l of diazepam in culture medium respectively. The mean effective diazepam concentration in plasma is 0.4 mg/l. CBF was measured photometrically. The most vigorous cilia were measured in 5 areas taking 10 readings on each sample, 30 minutes and 1 hour after mixing. Standard deviation (SD) and confidence limits were calculated along with significance testing (p < 0.05) using the paired t-test and ANOVA. The mean of the CBF of tubes A and B were 13.44 (SD 2.65) and 13.67 (SD 2.48). There was a reduction of the CBF with increasing concentrations of diazepam at 30 minutes, 11.32 (SD 2.14), 10.29 (SD 1.58) and 4.14 (SD 1.57) tubes C. D and E respectively. There was a significant lowering in CBF of 17% (p < 0.01) of diazepam at the mean effective plasma level (tube C) when compared against the controls. CBF decreased over time and at 1 hour was 10.57 (SD, 1.36), 9.02 (SD, 1.39) and 3.58 (SD, 1.31) tubes C, D and E respectively. A proposed mechanism of altered intracellular calcium flux via the action diazepam on GABA receptors is described.

Adult↗
PubMed1986

Effect of benzodiazepine derivatives: I. Augmentation of T cell-dependent antibody response by diazepam in mouse spleen cells.

Oral administration of diazepam at doses of 5-10 mg/kg to restraint-stressed mice resulted in almost complete recovery in the stress-induced suppression of the antibody response to sheep red blood cell (SRBC). Moreover, this compound restored the suppression of antibody response to SRBC in cyclophosphamide-treated mice. Diazepam treatment also enhanced the antibody response against SRBC in normal mice only when the animals were immunized with the reduced amount of antigen. It was demonstrated that antigen specific helper T cell activity was promoted by diazepam administration in mice. Addition of diazepam augmented the in vitro anti-SRBC hemolytic plaque-forming cell (PFC) response in mouse splenocytes without altering kinetics of the response. However, the enhancing effect was observed only when the drug was added to the medium at the culture initiation. On the other hand, antibody response to T cell-independent antigens such as trinitrophenylated (TNP)-Ficoll and TNP-lipopolysaccharide were not enhanced by diazepam. Concanavalin A or LPS-induced 3H-thymidine uptake into splenocytes were not stimulated by diazepam. These results suggest that diazepam promotes the antibody response through stimulating helper T cell functions.

Animals↗
PubMed1999

Honokiol, a putative anxiolytic agent extracted from magnolia bark, has no diazepam-like side-effects in mice.

Use of the elevated plus-maze experiment and activity and traction tests in mice have revealed that seven daily treatments with 0.2 mg kg(-1) and higher doses of honokiol, a neolignane derivative extracted from Magnolia bark, had an anxiolytic effect without change in motor activity or muscle tone. Diazepam, 1 mg kg(-1), had the same anxiolytic potential as 0.2 mg kg(-1) honokiol but induced muscle relaxation. The aim of this study was to determine whether honokiol had diazepam-like side-effects. Mice treated with 1-10 mg kg(-1) diazepam, but not those treated with 0.1-2 mg kg(-1) honokiol, for 12 days showed withdrawal symptoms characterized by hyperactivity and running-fit when they were challenge-administered intraperitoneal flumazenil (10 mg kg(-1)) 24 h after the last treatment with diazepam. Oral diazepam (0.5-2 mg kg(-1), 10 min before) dose-dependently prolonged hexobarbital (100 mg kg(-1), i.p.)-induced sleeping, disrupted learning and memory, and inhibited (+)-bicuculline (40 mg kg(-1), i.p.)-induced death. Honokiol (0.2-20 mg kg(-1), p.o., 3 h before) had no such effects. The prolongation by diazepam (1 mg kg(-1)) of hexobarbital-induced sleeping was not modified by honokiol (0.2-20 mg kg(-1)). These results suggest that honokiol is less likely than diazepam to induce physical dependence, central depression and amnesia at doses eliciting the anxiolytic effect. It is also considered that honokiol might have no therapeutic effect in the treatment of convulsion.

Animals↗
PubMed1997

A controlled evaluation of ibuprofen and diazepam for chronic orofacial muscle pain.

The clinical efficacy, side effect liability, and hormonal effects of two prototypic pharmacologic agents were evaluated for the management of chronic myogenous facial pain in a double-blind, randomized, controlled clinical trial. Thirty-nine subjects (35 women,. 4 men) with daily or near-daily orofacial pain of at least 3 months' duration and tenderness to palpation of masticatory muscles participated. Patients were randomly allocated to one of four treatments: placebo, diazepam, ibuprofen, or the combination of diazepam and ibuprofen. Pain, mood, muscle tenderness, maximal interincisal opening, and plasma levels of beta-endorphin were measured following 2-week baseline and 4-week treatment periods. Pain, as measured by a visual analog scale, was significantly decreased in the diazepam and diazepam plus ibuprofen groups but not for the ibuprofen or placebo groups. Analysis of variance showed a significant drug effect for diazepam but not for ibuprofen, indicating that pain relief was attributable to diazepam. No significant changes were noted in muscle tenderness, interincisal opening, or plasma beta-endorphin level. This study supports the efficacy of diazepam in the short-term management of chronic orofacial muscle pain. The lack of effect following administration of an anti-inflammatory analgesic suggests that inflammation is not the basis for chronic muscle pain in the orofacial region, and that the analgesic effect of such medications is not sufficient for pain relief in this condition.

Adult↗
PubMed1999

Ganglioside content and composition in rat cerebellum after prolonged diazepam treatment.

The main purpose of this study was to determine the content and composition of cerebellar gangliosides after prolonged diazepam treatment and their possible recovery after diazepam withdrawal. Male Wistar rats were administered diazepam in a dose of 10 mg/kg/day in drinking water for 3, 5 or 6 months. A additional group of rats had a one-month recovery period after five months of diazepam treatment. Control animals were age-matched and pair-fed. At the end of the experiment, the animals were sacrificed and the total cerebellar contents of ganglioside-NeuAc as well as its content in particular ganglioside fractions were estimated. After three months of diazepam consumption, no changes of ganglioside-NeuAc in investigated fractions (G(Q1b), G(T1b), G(D1b), G(D1a), G(M1), G(M2), and G(M3)) were observed. Five months of diazepam treatment caused a significant decrease in the total amount of gangliosides, which was evident in most of the investigated fractions, with the exception of the monosialoganglioside G(M2). Six months of treatment induced a generalized decrease in all the investigated ganglioside fractions. The diazepam-induced ganglioside reduction found after five months of treatment was also present after a one-month recovery period. The only fraction, which recovered and reached its control value, was monosialoganglioside G(M3).

Animals↗
PubMed2000

Evaluation of route of input on the hepatic disposition of diazepam.

Diazepam, a drug of high intrinsic clearance, was studied in the in situ rat liver dually perfused with Krebs-bicarbonate buffer containing human serum albumin (HSA; 0-1%) and unlabeled diazepam (1 mg/l) under constant hepatic arterial (3 ml/min) and portal venous (PV; 12 ml/min) flow rates. Events after a unit impulse (using [(14)C]diazepam) and at steady state (using unlabeled diazepam) were evaluated. In the absence of HSA the fractional effluent recovery (F) after hepatic arterial infusion (0.046 +/- 0.013) was about twice that after PV infusion (0.019 +/- 0.006). With HSA present, regardless of input route, F increased as unbound diazepam fraction in perfusate decreased (e.g., for PV, F = 0.58 +/- 0.05 and 0.69 +/- 0.02 for unbound diazepam fraction values of 0.18 +/- 0.01 and 0.037 +/- 0.01 at 0.25% and 1% HSA). The effluent [(14)C]diazepam profile was also dependent upon HSA. On decreasing HSA from 1 to 0.25% the early sharp peak (at 12-20 s) was replaced by a flatter unimodal profile with a later peak (at 60-80 s). Comparison of estimated effective permeability-surface area product to perfusate flow ratios (4.4 for 1% HSA and 21 for 0.25% HSA) indicated a shift from a perfusion rate-limited uptake with 0.25% HSA to one intermediate between permeability and perfusion at 1% HSA. Recognizing that orally absorbed drug enters the liver only via PV and i.v. drug via both vascular routes, this study emphasizes the difference in hepatic extraction of compounds depending on route of input, and the role that alteration in perfusate binding has on hepatic drug disposition.

Animals↗
PubMed2001

[Effect of diazepam on the effectiveness of antidote therapy in eliminating the acute lethal effects of soman in mice].

BACKGROUND: The currently used antidotal treatment of intoxication with nerve agents, consisting of an anticholinergic drug and an acetylcholinesterase reactivator, is often completed with the anticonvulsive drug diazepam to prevent poisoned organisms from centrally mediated seizures and subsequent tonic-clonic convulsions. The aim of this study was to find out whether the complementation of the antidotal treatment with diazepam can influence antidotal treatment-induced elimination of acute lethal effects of the chosen nerve agent--soman. METHODS AND RESULTS: In experiments on mice, the values of medium lethal dose of soman in the case of 24 h surviving of soman-exposed mice, treated with the basic antidotes involving various types of anticholinergic drugs and acetylcholinesterase reactivators, were evaluated and compared to the values of medium lethal dose of soman in mice treated with antidotes completed with diazepam. Our findings confirm that diazepam is able to enhance the efficacy of basic antidotal treatment to eliminate acute lethal effects of soman if atropin is used as anticholinergic drug. On the other hand, no ability of diazepam to enhance soman-induced lethal effects was demonstrated if an anticholinergic drug with central effects such as benactyzine, biperiden or scopolamin was used. The ability of diazepam to influence the efficacy of antidotes to eliminate soman-induced acute lethal effects was only observed in the case of using the oxime HI-6 as acetycholinesterase reactivator. CONCLUSIONS: The most perspective antidotal mixture against soman, consisting of the oxime HI-6 and atropine, should be complemented by diazepam no only because of the prevention of poisoned organisms from centrally mediated seizures and subsequent tonic-clonic convulsions but also because of the increase in the ability of antidotal treatment to eliminate soman-induced acute lethal effects.

Acute Disease↗
PubMed2000

Propofol combined with diazepam synergistically potentiates the GABA-activated chloride current in rat sensory neurons.

OBJECTIVE: To investigate the effect of propofol combined with diazepam on the gamma-aminobutyric acid (GABA)-activated chloride current (IGABA) evoked in rat sensory neurons. METHODS: Whole cell patch clamp recordings were made from cultured rat dorsal root ganglionic neurons. GABA (3 mumol/L) was applied by pressure ejection. The anesthetics were dissolved in the external solution and given by the "Y-tube" method. RESULTS: Co-application of propofol (0.3-3 mumol/L) and diazepam (100 nmol/L) potentiated the IGABA which was significantly larger than the sum of that potentiated by drug alone. Diazepam (100 nmol/L) shifted the concentration-response curve for the IGABA potentiation induced by propofol to the left in a parallel fashion. The EC50 value for propofol was decreased by diazepam from 7.6 +/- 1.8 mumol/L to 3.9 +/- 1.1 mumol/L (n = 9). CONCLUSIONS: Our results suggest that propofol combined with diazepam synergistically potentiates the IGABA. Diazepam-induced increase in the apparent binding affinity of propofol for the GABAA receptors is likely responsible for a clinical synergistic hypnotic action during co-application with propofol and diazepam.

Animals↗
PubMed1976

Lorazepam and diazepam in the treatment of neurotic anxiety: a double-blind trial.

Fifty-eight neurotic patients with intense anxiety were treated with either lorazepam or diazepam in a double blind between-patients trial. Statistical analysis indicated that the two groups were homogeneous before treatment and that the results of treatment were similar for both drugs. According to the global rating of illness week after week, after four weeks of treatment more patients on lorazepam than on diazepam were normal or had mild illness (82.1% vs. 70.8%). In the investigators' judgment, 71.9% of the patients treated with lorazepam had an excellent or good response compared with 56.7+ of those treated with diazepam. The mean reduction in score on the Hamilton Anxiety Scale was 17.7 for lorazepam and 16.5 for diazepam. However, none of the above differences in results were statistically significant. The largest dose of lorazepam required in treatment was 6 mg, compared with 30 mg of diazepam. Two patients treated with lorazepam had side effects, against six with diazepam. Six patients in the diazepam group did not complete the trial, including three who discontinued because of side effects (rash, tremors, agitation); no patients in the lorazepam group dropped out.

Adult↗
PubMed1976

The protein binding of diazepam and N-demethyldiazepam in patients with poor renal function.

The plasma protein binding of diazepam and of its main metabolite, N-demethyldiazepam, was measured in patients with renal disease and in healthy volunteers by ultracentrifugation. The total and non-protein bound concentrations of diazepam and N-demethyldiazepam, and the concentration of unconjugated oxazepam in the plasma were determined by gas chromatography after an oral 10 mg dose of diazepam. In the volunteers 98% of diazepam and N-demethyldiazepam were bound to the plasma proteins. In patients with renal disease the corresponding values were 92% and 95%, respectively. In the patients with renal disease no correlation could be found between the percent protein binding of diazepam or N-demethyldiazepam in the plasma and the serum creatinine concentration. Considerable variations in diazepam concentrations at 1 and 24 hours and in N-demethyldiazepam concentrations at 24 hours were found in the patients with renal disease. In contrast to the volunteers, 5 patients out of 28 with renal disease had measurable amounts of unconjugated oxazepam in the plasma. The deficient ability of the plasma proteins of patients with renal disease to bind diazepam may increase its clinical effect.

Adolescent↗
PubMed2003

[How do diazepam and flumazenil influence respiratory control by the activities of both hypoglossal and phrenic nerves in rabbits?].

BACKGROUND: Upper airway obstruction and inadequate ventilation often arise during sedation and anesthesia by benzodiazepines. To estimate the influence of benzodiazepines on the respiratory control, we studied the effect of diazepam and flumazenil on the neural activity and the respiratory response caused by a brief (60 sec) respiratory arrest (RA) observed in the hypoglossal nerve (HG) and phrenic nerve (PH) in rabbits. METHODS: Experiments were preformed on adult rabbits vagotomized, paralyzed and ventilated artificially with 50% N2O, 50% oxygen and 0.3-0.5% sevoflurane. We evaluated and compared the effects of diazepam and flumazenil on the peak amplitude (AMP-HG&PH) and the root mean square (RMS-HG&PH) of HG and PH, and respiratory cycle (Tc). RESULTS: Diazepam depressed HG activity more than PH activity with no influence on Tc. But it did not cause dose-related depression. Flumazenil 0.2 mg.kg-1 completely reversed the respiratory depressions caused by diazepam with the increased Tc. In addition to augmentation of the hypoglossal activity in inspiration, flumazenil caused a rise in its activity in pan-expiratory period in some cases. Additional administration of diazepam 6 mg.kg-1 following flumazenil depressed PH activity again, but did not affect HG activity any more. There was no significant depression in cardiovascular parameters with tested dosages of diazepam and flumazenil. RA response was characterized by raised AMPs and augmented RMSs (delta AMPs, delta RMSs) with marked prolongation in Tc (delta Tc). Diazepam depressed RA response dose dependently, but flumazenil did not seem to antagonize this depression. CONCLUSIONS: These results suggest that 1) flumazenil is not only a specific antagonist of benzodiazepines but also a potential excitatory agent of hypoglossal nerve activity, and that 2) there is some functional diversity in disposition of benzodiazepine-receptor binding GABAA-receptor responsible for neural respiratory control system.

Action Potentials↗
PubMed2004

Case report: Diazepam in severe tetanus treatment.

The causes of death in tetanus are muscle spasms and spasm of the larynx, which are caused by blocking the release of inhibitory neurotransmitters in the spinal synapses, causing the uncontrolled spread of impulses. Diazepam controls the spasms by blocking the polysynaptic reflexes, working peripherally, without depressing the cortical center and has no cardiovascular or endocrine effects. High dose diazepam had been used and proved to be a good muscle relaxant. Diazepam seems to work better with tetanus than pancuronium bromide, but both drugs need mechanical ventilation. In cases where the dose exceeds 240 mg per day in a child, a ventilator should be on hand, and if the dose required is more than 480 mg per day, other drugs should be considered. In three cases of severe tetanus presented here, the first two were managed by diazepam and pancuronium bromide and the last case by high dose diazepam only. In the first case, the dose of diazepam was up to 480 mg/day. By using high dose diazepam in severe tetanus, management of the clinical manifestations of autonomic nerve involvement and the weaning process become easier. Most complications of severe tetanus became more manageable.

Anticonvulsants↗
PubMed2005

Influence of ethanol on the myorelaxant effect of diazepam in rats.

Interaction of ethanol with benzodiazepines can lead to enhanced therapeutic anxyolytic, sedative and hypnotic effects but can also augment unwanted effects such as drowsiness, confusion, amnesia and impaired coordination. In this study we investigated the interaction between ethanol and diazepam and its influence on muscle strength in rats using the grip-strength meter. Three doses of ethanol (0.4, 0.6 and 0.8 g kg(-1) of body mass) and diazepam (0.75, 1.5 and 7.5 mg kg(-1) b.m.) were used in experiments. Single substances and their combinations were tested. The myorelaxant effect of ethanol, measured as grip force (expressed in grams), was dose-dependent. The lowest dose (0.4 g kg(-1) b.m.) failed to affect muscle strength while the strongest effect was observed with the highest dose of ethanol (0.8 g kg(-1) b.m.) and it lasted for 75 min. Diazepam dose-dependently reduced muscle strength too. However, when ethanol was combined with diazepam (1.5 mg kg(-1) b.m.), more enhanced muscle relaxation occurred than by either drug alone. Namely, two lower doses of ethanol (0.4 and 0.6 g kg(-1) b.m) enhanced the myorelaxant effect of diazepam by additional 26 and 46%, respectively, when measured after 15 min. The most pronounced myorelaxation was recorded when the highest dose of ethanol (0.8 g kg(-1) b.m.) was combined with diazepam: from complete muscle relaxation observed after 15 min, it gradually decreased to 91% at the 45th min and to 24% at the 105th min after the beginning of the treatment. The results of this preclinical investigation showed that ethanol enhanced the muscle relaxant effect of diazepam in rats. This enhancement as well as duration of the effect was dependent on the applied dose of ethanol.

Animals↗
PubMed1991

[Studies of midazolam, diazepam and thiopentone on respiratory and cardiovascular function during induction anesthesia].

In this study, the effects of midazolam (M), diazepam (D) and thiopentone (T) on respiratory and cardiovascular systems were compared. The patients were randomly divided into 6 groups, besides minute ventilatory volume (MV), onset of induction and cardiovascular changes were also observed. Induction was performed by a bolus injection of one of the following: midazolam (0.3 mg/kg), diazepam (0.3 mg/kg) or thiopentone (5 mg/kg). Five minutes later, 5 micrograms/kg fentanyl and 1.5-2.0 mg/kg succinylcholine were administered. The results showed that: (1) Inhibitory effect on MV was not prominent and similar after use of midazolam and diazepam but was remarkable after thiopental; (2) As for the onset, midazolam was faster than diazepam but slower than thiopentone; (3) Hemodynamic changes of midazolam, diazepam and thiopentone were similar, however during intubation, cardiovascular response was the least in midazolam, diazepam the intermediate and thiopentone the most significant. We conclude that midazolam is a water-soluble, safe and effective inductive anesthetic with its short eliminated half-life period, and much lesser venous irritation, and it is certainly superior to both diazepam and thiopentone.

Adult↗
PubMed1990

Animal model of anxiety: effect of chronic diazepam treatment in the genetically hypertensive rats of Koletsky type and in the rats of Wistar strain.

Experiments were performed in the adult normotensive rats of Wistar strain in the genetically hypertensive rats of Koltsky type. Diazepam at the dose of 1 mg/kg was applied for five days. The last two days of diazepam treatment the behavior of the animals was traced in holeboard and in the elevated plus-maze. In the control animals the genetically hypertensive rats of both sexes show elevated locomotor-exploratory activity in holeboard in both sessions, genetically hypertensive females show highest degree of directed exploration in holeboard when compared with the other groups of rats; in the elevated plus-maze the normotensive rats of both sexes show lower aversion towards open space and height in elevated plus-maze relative to genetically hypertensive rats. Diazepam only in the genetically hypertensive females increases in the second session locomotor-exploratory activity and reduced the inter-session habituation of the mentioned activity. Directed exploratory activity in holeboard was by diazepam treatment elevated predominantly in the genetically hypertensive rats. In the genetically hypertensive females diazepam caused inter-session sensitization in directed exploration. Considering the number of entries in centre and in open arms of the elevated plus-maze, diazepam in both strains irrespective of sex and session caused increase. Taking into account time spent in centre and in open arms of the elevated plus-maze, the strain dependent effect of diazepam is apparent, i.e., statistical significance of its "anxiolytic" effect was attained only in the genetically hypertensive rats.

Animals↗
PubMed1979

[Effect of diazepam on the Na, K-ATPase state in a penicillin--induced hyperactivity focus in the cerebral cortex].

Intramuscular injection of diazepam to rats at doses of 0.01 and 2 mg/kg 25-30 min after penicillin application to the rat brain cortex leads to alteration of periodic appearance of epileptic seizures (ES), to changes in the seizure pattern, and to emergence of periodic acceleration of epileptiform discharges (ED). Injection of diazepam at a dose of 2 mg/kg 20 min before penicillin application results in the reduction of ED latency in the epileptogenic focus and in a decrease in their frequency before seizures as compared to the control animals without diazepam injection. ES appear irregularly, their quantity is markedly reduced while duration is increased. Diazepam injection leads to disappearance of the rat moving reaction during ER and ES. In vivo experiments diazepam (2 mg/kg) does not influence brain cortex Na, K-ATPase of crude synaptosomes. However, diazepam leads to an increase in Na, K-ATPase activity both in the primary and dependent secondary epileptogenic foci. It is suggested that the anticonvulsant action of diazepam may be underlain by its activating effect on Na, K-ATPase of neuronal membranes in the epileptogenic focus.

Animals↗
PubMedDate not supplied

Comparison of depressant actions of orphenadrine and diazepam on hypertonic skeletal muscle activity.

The muscle relaxant activities of orphenadrine (Norflex) and diazepam (Valium) were compared in several animal models. In mice, tonic extensor seizures evoked by electroshock or pentylenetetrazol were inhibited by both agents. The protective index (ataxic dose divided by protective dose) was greater than 1 for orphenadrine, whereas for diazepam it was greater than 1 only in the case of the pentylenetetrazol-induced seizures. In strychnine-treated mice, diazepam protected against deaths following tonic extensor seizures, but orphenadrine did not. The protective index for diazepam, however, was less than 1. In cats, orphenadrine and diazepam both were capable of blocking decerebrate ridigity, but not in all animals. The protective index for orphenadrine in animals in which it was active, was greater than 1, while that for diazepam, when it was active, was less than 1. Orphenadrine and diazepam were tested in rabbits in the sciatic nerve-gastrocnemius muscle preparation. Neither drug directly affected nerve muscle stimulation. It would appear that both agents are acting via the central nervous system when they suppress hypertonic skeletal muscle activity, but only orphenadrine exhibits protective indices consistently greater than 1.

Animals↗
PubMed1989

Comparison of the hemodynamic effects of midazolam and diazepam in patients with coronary occlusion.

Midazolam is gradually replacing diazepam in neuroleptanalgesia with fentanyl and sufentanil because of its greater water solubility, greater hypnotic potency, shorter half-life, lack of pharmacologically active metabolites and low incidence of thrombophlebitis. In order to substantiate midazolam as being as safe and effective as diazepam in cardiac patients with severe coronary occlusion, hemodynamic measurements were made before and 10 min after completion of intravenous injection of 0.2 mg/kg i.v. midazolam (n = 45) and 0.4 mg/kg i.v. diazepam (n = 30), the doses which are identical to those used in patients undergoing cardiac catheterization. All 75 patients were spontaneously breathing 40% O2 in air. No positional changes or stimulation of patients were allowed before and during the study. Of hemodynamic variables, systemic systolic blood pressure was significantly reduced by both midazolam and diazepam. Midazolam also caused significant reduction in systemic vascular resistance with reduction in diastolic pressure and left ventricular stroke work index. No changes in heart rate, systolic and diastolic pulmonary artery pressures, cardiac output and index, stroke volume and index, pulmonary vascular resistance, right ventricular stroke work index and rate pressure product were observed following either midazolam or diazepam. No statistically significant differences were observed in any hemodynamic variable between those patients receiving midazolam or diazepam. It is concluded that midazolam is as safe as diazepam in cardiac patients with coronary obstruction.

Aged↗