Intravenous Injection Of Adrenaline Research Articles

Is It Safe to Use Vasoconstrictors in Association Treated with Amitriptyline or Can It Potentiate Cardiovascular Effects? In Vivo Animal Study

This study aimed to evaluate changes in blood pressure of rats treated or not with amitriptyline after infiltration in the buccal sulcus and intravenous injection of epinephrine, felypressin and phenylephrine in equivalent doses (ED) to the amounts present in 2, 8 and 32 local anesthetic tubes. 42 male Wistar rats, with 45-day-old, treated for seven days with amitriptyline hydrochloride (0.3 mg/kg). On the eighth day, the animal was submitted to general anesthesia and surgery for direct blood pressure rate. The significance level was 5%. The treatment with amitriptyline caused a significant decrease in blood pressure of the treated group compared to the control group (101.80 ± 2.52 and 110.12 ± 2.91 mmHg, respectively, * p < 0.05), and slightly potentiates the hypertensive response after infiltration of epinephrine (4.11 ± 0.54; 7.15 ± 0.55; 9.03 ± 0.87 mmHg, respectively, 2, 8 and 32 tubes, p > 0.05). Felypressin promotes lower blood pressure changes and phenylephrine proved to be the most potent vasoconstrictor of the three studied, producing important changes in blood pressure and, even though infiltration, in doses greater than 8 tubes (15.43 ± 1.15; 70.62 ± 3.70 mmHg, respectively, 8 and 32 tubes, * p < 0.05). The infiltration of the three vasoconstrictors in doses equal to or less than 8 tubes does not cause significant changes in blood pressure, both in the control and amitriptyline treated groups.

The Temporal Topography of Central Serous Chorioretinopathy in the Chinchilla Rabbits Induced by Intravenous Injection of Adrenaline: An in vivo Study.

PurposeTo explore the temporal topography of the chorioretinopathy in an animal model of central serous chorioretinopathy (CSC) induced by intravenous injection of adrenalin in the Chinchilla rabbits.MethodsTen Chinchilla rabbits received a daily intravenous injection of adrenaline at 0.04 mg/kg for 8 weeks. Fluorescence fundus angiography (FFA) and electroretinogram (ERG) were performed every week afterwards to see whether there was fluorescence leakage in the fundus and to evaluate the retinal function. Indocyanine green angiography (ICGA) and optical coherence tomography (OCT) were also conducted to detect the change of choroidal vessels. Finally, the eyes of the rabbits were enucleated to make the retinal sections for histological examination with hematoxylin–eosin (HE) staining.ResultsWithin 8 weeks of the adrenalin administration, 7 out of the 10 rabbits showed different degrees of fluorescence leakage on FFA. The leakage was more obvious during 2–3 weeks after the adrenalin administration. With the progress of disease, the leakage subsided gradually and a scar-like lesion formed. ICGA revealed the local choroidal ischemia and the dilated choroidal vessels. An obvious detachment of retina and an increased thickness of the choroid were found on OCT, which was most obvious 2 weeks after the adrenalin administration (P<0.01). ERG revealed no obvious decline of the b-wave amplitude before and after the adrenalin administration (P>0.05). A circumscribed retinal detachment, the depigmentation of retinal pigment epithelium and enlarged choroidal vessels were shown by the histological examination.ConclusionThe temporal topography of the chorioretinopathy in the Chinchilla rabbits by intravenous injection of adrenaline somewhat mimicked that of the human CSC, which could enhance its application in the exploration for the pathogenesis and the therapeutic measures for human CSC.

CALCIFICATION OF ARTERIES IN PATIENTS WITH ATHEROSCLEROSIS: CAUSES AND MECHANISMS OF DEVELOPMENT

The paper shows analogies between the mechanisms of calcification of arteries, various tissues and bone mineralization. In calcification the same mechanisms are involved, as at ossification of an organic matrix of a bone, including participation of stem cells. In the arteries and capillaries of various organs found polypotent precursors – mesenchymal stem cells, presumably responsible for the pathological mineralization of the arterial wall. Circulating in the blood and present in the intima of the human atheromatous aorta colony-forming stem cells of the stromal line of differentiation. Adventitia cells or pericytes are considered as a pluripotent mesenchymal reserve for replenishment of some cellular forms of connective tissue. Bone marrow stem cells of the stromal line of differentiation with the presence of pluripotent stromal cells in the blood and granulomas (plaques) and their transformation into bone tissue cells are involved in atherogenesis. Smooth muscle cells (SMCs) and myofibroblasts of the arterial wall adventitia have an osteoblast-like phenotype. Collagen and elastic fibers are involved in the calcification of blood vessels and soft tissues. Calcification of granulomas (plaques) accompanies their inflammatory morphogenesis, accompanied by the development of scar tissue. It often accompanies and completes the inflammation in them. This process is observed with the gradual replacement of the parenchyma of some organs with connective tissue. The mineral phase in bones and soft tissues, represented by calcium (Ca) and phosphate (P), contacts with nucleators - specific areas of collagen fibers. Non-collagen proteins are also involved in arterial calcification. With the progression of atherosclerosis and calcification of granulomas/plaques by cells present in the arterial wall, osteonectin is expressed. Osteopontin content is associated with Ca deposits in them; in particular, it correlates with the Ca level in the coronary arteries. In the processes of ossification and calcification, phosphatases play a certain role. In areas of calcification of granulomas/plaques, osteoprotegerin is found, which inhibits the activity of alkaline phosphatase in the aorta and prevents calcification of the media. Arterial wall calcification and inflammation are inhibited by fetuin-A and matrix γ-carboxyglutaric protein (MGP). The rate of bone formation and tissue calcification depends on the concentration of Ca and P in plasma and extracellular fluid. With their high concentration in the extracellular fluid, the mineral phase appears where it normally does not exist. Lipids are among the initiators of granuloma / plaque calcification in the arteries. The role of inflammation and necrosis in the calcification of the arteries is confirmed by experiments on animals with repeated intravenous injections of adrenaline, which causes focal necrosis of the middle membrane, which then undergoes calcification. In arterial walls, heart muscle, bone and cartilage tissue, osteonectin, osteocalcin, osteopontin, bone sialoprotein are often formed. In general, the mechanisms of arterial and soft tissue calcification are poorly understood. There are no effective remedies for calcification.

Editor Note on Adrenaline: A Few Seconds and Life Saves

Adrenaline is a hormone also called epinephrine, its purpose is to allow the body to overcome the "danger" perceived by the brain (it is the pituitary gland that requires the production of this hormone to the medulla adrenal glands (just above the kidneys)). Adrenaline has a short duration of action (of the order of two minutes) because it is rapidly degraded by two enzymes, catechol-oxymethyltransferase (COMT) and monoamine oxidase (MAO). Intravenous injection of adrenaline is used primarily to treat cardiac arrest, in small doses, used in anaphylactic shock .It intervenes particularly on the heart rate. Mixed with procaine, it was used in dentistry to perform local anesthesia. But at too high a dose, it acts on the heart to the point of causing death.

Melanocyte-Stimulating Hormone Response to Exercise, Twitching, Epinephrine Injection, Substance P Injection, and Prostaglandin-F2α Administration in Mares

Five experiments were performed to test the hypothesis that α-melanocyte–stimulating hormone (MSH) is secreted in response to various stressors in horses similar to prolactin, growth hormone, and adrenocorticotropin (ACTH). There was considerable variation in resting concentrations of MSH and in the degree of stimulation in responders; thus all data sets were tested for heterogeneity of variance and corrected for as needed before analysis. In experiment 1, 12 mares were used in a switchback design to test the effect of a 2-minute exercise bout on MSH secretion. Plasma MSH concentrations were constant when mares were not exercised but increased (P < .05) immediately (2 minutes) after exercise and were still elevated 5 minutes later. In experiment 2, six mares were twitched for 2 minutes and six mares were not twitched. Twitching stimulated (P < .05) both MSH and ACTH relative to controls. Experiments 3, 4, and 5 tested the acute effects of intravenous injection of epinephrine at 5 μg/kg of body weight, intravenous injection of 100 μg substance P, and intramuscular injection of 10 mg prostaglandin-F2α in mares compared to controls (6, 5, and 6 mares per treatment group, respectively). Concentrations of MSH increased (P ≤ .05) after treatment in all three experiments. Plasma concentrations of ACTH also increased (P < .01) after administration of epinephrine and prostaglandin-F2α in experiments 3 and 5; plasma ACTH was not measured in experiment 1 or 4 because we have previously reported that exercise and substance P stimulate plasma ACTH concentrations. As hypothesized, MSH is secreted in response to various stimuli similar to that observed previously for prolactin, growth hormone, and ACTH.

Beta-adrenergic activation induces cardiac collapse by aggravating cardiomyocyte contractile dysfunction in bupivacaine intoxication.

In order to determine the role of the adrenergic system in bupivacaine-induced cardiotoxicity, a series of experiments were performed. In an animal experiment, male Sprague-Dawley (SD) rats under chloral hydrate anesthesia received intravenous bupivacaine, followed by an intravenous injection of adrenalin or isoprenalin, and the electrocardiogram (ECG), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), the maximum rate of rise of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease (-dP/dtmax) were continually monitored. In a cellular experiment, freshly isolated adult SD rat ventricular myocytes were perfused with bupivacaine at different concentrations in the presence or absence of isoprenalin, with or without esmolol. The percentage of the sarcomere shortening (bl% peak h), departure velocity (dep v) of sarcomere shortening and time to 50% of the peak speed of myocyte contraction (Tp50) was assessed by a video-based edge-detection system. In an additional experiment, Swiss mice pretreated with saline, isoprenalin, esmolol or dexmedetomidine received bupivacaine to determine the 50% lethal dose (LD50) of bupivacaine. Electron microscopy of myocardial mitochondria was performed to assess damage of these structures. To test mitochondrial reactive oxygen species (ROS) production, freshly isolated SD rat ventricular myocytes were incubated with bupivacaine in the presence of isoprenalin, with or without esmolol. First, our results showed that bupivacaine significantly reduced the LVSP and +dP/dtmax, as well as enhanced the LVEDP and -dP/dtmax (P < 0.05, vs. control, and vs. baseline). Adrenalin and isoprenalin induced a further reduction of LVSP and +dP/dtmax (P < 0.05, vs. before adrenalin or isoprenalin delivery, and vs. control). Second, bupivacaine induced a dose-dependent cardiomyocyte contractile depression. While 5.9 μmol/L or 8.9 μmol/L of bupivacaine resulted in no change, 30.0 μmol/L of bupivacaine prolonged the Tp50 and reduced the bl% peak h and dep v (P < 0.05, vs. control and vs. baseline). Isoprenalin aggravated the bupivacaine-induced cardiomyocyte contractile depression, significantly prolonging the Tp50 (P < 0.05, vs. bupivacaine alone) and reducing the dep v (P < 0.05, vs. bupivacaine alone). Third, esmolol and dexmedetomidine significantly enhanced, while isoprenalin significantly reduced, the LD50 of bupivacaine in mice. Fourth, bupivacaine led to significant mitochondrial swelling, and the extent of myocardial mitochondrial swelling in isoprenalin-pretreated mice was significantly higher than that compared with mice pretreated with saline, as reflected by the higher mitochondrial damage score (P < 0.01). Meanwhile, esmolol pretreatment significantly reduced the mitochondrial damage score (P < 0.01). Fifth, bupivacaine significantly increased the ROS in freshly isolated cardiomyocytes, and added isoprenalin induced a further enhancement of ROS production (P < 0.05, vs. bupivacaine alone). Added esmolol significantly decreased ROS production (P < 0.05, vs. bupivacaine + isoprenalin). Our results suggest that bupivacaine depressed cardiac automaticity, conductivity and contractility, but the predominant effect was contractile dysfunction which resulted from the disruption of mitochondrial energy metabolism. β-adrenergic activation aggravated the cellular metabolism disorder and therefore contractile dysfunction.

Hemodynamics in experimental acute myocardial ischemia against the background of the use of substance PK-66 in comparison with the cordarone

The aim of the study was to study the effect of PK-66 substances on hemodynamic parameters under experimental acute myocardial ischemia compared with cordarone.Materials and methods. The experiments were carried out on 21 rabbits of the chinchilla breed. Acute myocardial ischemia (AMI) was modeled by intravenous injection of epinephrine at a dose of 0.2 mg / kg and caffeine sodium benzoate at a dose of 25 mg / kg. In the studies carried out, the Cordarone compounds and the PC-66 test sample were used. The maximum pressure in the left ventricle (MPLV), mean arterial pressure (MAP), total peripheral vascular resistance (TPVR), and minute volume (MV) were recorded. The initial values of the parameters studied were recorded immediately after the administration and after 30 minutes. after administration of the test substance, immediately after the introduction of the analyzers, and also after 15 and 30 minutes. after modeling pathology.Results Simulation of AMI in rabbits, accompanied by a decrease in MV, caused by a decrease in contractile activity of the myocardium, also showed a simultaneous decrease MPLV in and a significant increase in TPVR, which is caused by a sudden decrease in MV and a decrease in MAP. The introduction of cordarone reduces the changes observed in the modeling of pathology (6.33–10.36 %). The use of PK-66 neutralizes changes in maximum pressure in the left ventricle observed immediately after modeling AMI, followed by a decrease in this parameter after 15 minutes. and normalization after 30 minutes. The prophylactic administration of the PK-66 test sample did not significantly influence the modeling of AMI. Substance PK-66 and cordarone showed a close unidirectional effect in AMI, reducing the changes in SAT, MPLV, MAP, and TPVR in pathology.Conclusions. Acute ischemia of the myocardium in rabbits is characterized by an increase: total peripheral resistance of blood vessels, a decrease in the minute volume of blood and systolic blood pressure. Prophylactic administration of PK-66 leads to normalization of indicators of general hemodynamics in AMI, not inferior in effectiveness to the drug comparison kordaronu.

Induction of chorioretinopathy by adrenaline injection in different strains of rabbits

Objective To establish a central serous chorioretinopathy(CSC) model on different strains of rabbits by intravenous injection of adrenaline, which may contribute to related researches of CSC. Methods This study was approved by Bioethics Committee of Fourth Military University and complied with Statement for the Use of Animals in Ophthalmic and Visual Research.Fundus fluorescein angiography(FFA) was initially performed on male New Zealand white rabbits (10), Belgium rabbits (5) and Chinchilla rabbits(10) to make sure that the retinas of subjects were normal.For the New Zealand white rabbits, adrenaline was injected via ear vein at a dose of 0.04 mg/kg once per day for the first 8 weeks and followed by a dose of 0.08 mg/kg for the next 4 weeks, while 0.04 mg/kg adrenaline was injected in the same way for 8 weeks in the Belgium rabbits and Chinchilla rabbits.FFA was performed every week after injection of adrenaline to evaluate the fluorescence leakage in ocular fundus.New Zealand white rabbits were sacrificed in 4 (3 rabbits), 8 (3 rabbits) and 12 weeks (4 rabbits) after injection respectively, and Belgium rabbits and Chinchilla rabbits were sacrificed in the 8 weeks after injection.The eyeballs of the rabbits were enucleated to prepare the retinal sections for histopathological examination after hematoxylin-eosin staining.The results of FFA and retinal structure were compared among different strains of rabbits. Results No fluorescence leakage was found by FFA in ocular fundus, and the retinal structure was normal in all the 10 New Zealand white rabbits during the experiment.Fluorescence leakage was found by FFA in 2 Belgium rabbits at 1 week and 2 weeks after injection respectively, and retinal detachment and depigmentation of retinal pigment epithelium (RPE) with an enlarged intercellular space were shown by hematoxylin-eosin staining.For the Chinchilla rabbits, fluorescence leakages were found in 7 rabbits throughout the whole period of adrenaline administration.Circumscribed retinal detachment, depigmentation of RPE with enlarged intercellular space were also found in leakage lesions. Conclusions Repeated intravenous injection of adrenaline can induce CSC-like lesions in colored rabbits but not in albino rabbits. Key words: Adrenaline; Central serous chorioretinopathy; Disease model, animal/drug induction; Fundus fluorescein angiography; New Zealand rabbit; Belgium rabbit; Chinchilla rabbit

Proton Pump Inhibitor-induced Hypersensitivity Reaction: A Case Report

: Introduction: Drug induced allergy or hypersensitivity reaction is of great clinical significance in therapeutics. Various factors may contribute like age, genetic composition, disease of the patients and the types of drugs used. Such reactions increases the patient’s suffering and lowers the therapeutic efficacy of any drug. Therefore, it is essential to collect data and investigate important drug reactions for safe therapy. Presentation of Case: A 27-years old female patient, with a history of drug allergy to ranitidine, experienced severe anaphylactic shock immediately after cesarean delivery. Post-operative medications include Ceftriaxone, Metronidazole, Tramadol, Metoclopramide and Pantoprazole. With intravenous injections of Adrenaline, Hydrocortisone, Dexamethasone, Atropine, Promethazine and intubation, she slowly recovered after three days and was discharged. Conclusion: Past history of the patient suggested a rare case of drug allergy to ranitidine. Therefore, instead of ranitidine, pantoprazole was used for this patient. Clinicians suspected this anaphylactic reaction may be induced by drug. However, the drug responsible for this reaction was not detected clearly but Pantoprazole may be a possibility. Though allergy due to H2 receptor antagonists and proton-pump inhibitors are rare but may cause fatal consequences. Thus proper investigation of this case may help in designing the treatment schedule in an effective way, in future.Key words: Anaphylactic shock, Drug Hypersensitivity, H2 Receptor Antagonist, Pantoprazole, Proton-pump Inhibitors, Ranitidine.

Natural IgM Against Oxidation-Specific Epitopes Inhibit Microvesicle-Driven Coagulation

Increasing evidence demonstrates an important role for immune functions in coagulation and thrombosis, and both microbial and sterile triggers have been implicated in these responses. Oxidation-specific epitopes (OSE) are products of lipid peroxidation that are present on oxidized low-density lipoproteins and dying cells, and represent important sterile triggers of inflammation in cardiovascular diseases. We have previously shown that a large part of naturally occurring IgM antibodies have specificity for OSEs and that 50% of circulating procoagulant microvesicles (MV) carry OSEs, such as malondialdehyde-adducts (MDA), on their surface. Because OSE-specific natural IgM bind MVs and increased levels of circulating MVs have been implicated in an increased thrombotic risk, we studied the capacity of these antibodies in directly modulating the procoagulant potential of MVs in vitro and in vivo. We first showed that increasing concentrations of three different monoclonal IgM antibodies with specificity for MDA (LR04, NA17, E014) significantly delayed MV-induced fibrin formation in plasma, while an MDA-specific IgG antibody or F(ab')2 fragments of LR04 had no effect. Moreover, peak thrombin generation of normal, factor VII- or factor XII- deficient microvesicle poor plasma (MVPP) substituted with tissue factor positive MVs was significantly reduced in the presence of LR04 but not a control IgM antibody, indicating that it exerts its effect on the common pathway of the coagulation cascade. A similar anticoagulatory effect of LR04 was observed in freshly drawn whole blood analyzed by rotational thrombelastometry. Addition of LR04, compared to a control IgM antibody, increased clotting time, clot formation time, and the time to reach maximum clot firmness, and decreased maximum clot firmness. Finally, in a murine pulmonary embolism model, we could show that 30-minute survival of mice that received intravenous injections of epinephrine together with pro-coagulant MVs derived from the pancreatic cancer cell line HPAFII was significantly increased in mice co-injected with LR04 compared to controls. Our study identifies an inhibitory role of MDA-specific IgM antibodies in MV-induced coagulation. These effects are exerted on the common pathway of the coagulation cascade and require the intact structure of IgM antibodies. The findings may offer novel diagnostic and therapeutic approaches in the prevention and treatment of thrombosis. DisclosuresNo relevant conflicts of interest to declare.

Protective effect of naloxone injected into cisterna magna on brain tissues of rats following cardiopulmonary resuscitation

Objective To investigate the effects of naloxone injected into cisterna magna on S100βprotein and neuronspecific enolase(NSE)levels in serum and the histopathology of brain tissue of rats following cardiopulmonary resuscitation(CPR).Methods Thirty adult male SD rats were randomly divided into 3groups:Sham group,Conventional CPR group(intravenous injection of epinephrine,0.2mg/kg)and Naloxone CPR group(cisterna magna injection of naloxone,2mg/kg).Asphyxiation was used to set up rat cardiac arrest model,and corresponding drugs were given when the resuscitation was carried out.The blood samples were taken from orbital venous plexus at 0.5h,3h,6hand 24 hafter restoration of spontaneous circulation(ROSC).Enzyme-linked immunosorbent assay(ELISA)was used to detect serum levels of S100βprotein and NSE.Brain tissue was taken after the last blood sampling and the pathology of brain was observed by hematoxylineosin(H-E)staining.Results Serum S100βprotein levels of the Conventional CPR group and Naloxone CPR group were significantly higher than those of the Sham group at all time points(P0.01);compared with the Conventional CPR group,S100βprotein levels in Naloxone CPR group were significantly decreased at 3h,6h,and 24 hafter ROSC(P0.05 or P0.01).Serum NSE protein level of the Conventional CPR group at all time points and Naloxone CPR group at 6hand 24 hafter ROSC were significantly higher than those of the Sham group(P0.05 or P0.01).Serum NSE protein levels were significantly decreased at 6hand 24 hafter ROSC in Naloxone CPR group compared with the Conventional CPR group(P0.05 or P0.01).Moreover,hippocampus glial cells of Conventional CPR group were scattered and decreased,with condensed eosinophilic cytoplasm,narrowed nuclues,unclear nucleolus,and swollen and deformed capillaries.However,most nerve cells of Naloxone CPR group had rich cytoplasm and the nucleolus was clear;only a few nerve cells and capillaries showed edema-like changes of different degrees.Conclusion Naloxone injected into cisterna magna has a prominent protective effect on the brain of rats following cardiopulmonary resuscitation.

Intraoperative ventricular fibrillation arrest caused by accidental intravenous injection of epinephrine

We describe a 25-year old male who experienced ventricular fibrillation (V-Fib) arrest induced by inadvertent intravenous injection of epinephrine instead of the routine reversal medication. Under general anesthesia with Desflurane inhalation, 1.5% Lidocaine containing 1:100,000 Epinephrine was injected into the nasal mucosa for septoplasty and the procedure went smoothly. Near the end of the surgery, the patient suddenly developed sinus tachycardia followed by V-Fib arrest which responded to a single shock of 300J. Sinus rhythm was restored immediately. The patient developed severe lactic acidosis and a bedside echocardiography showed global hypokinesia and normal right sided pressures. The patient was intubated and admitted to the ICU on mechanical ventilation before being weaned and extubated. Retrospectively while investigating the cause after it was discovered that epinephrine had been given as opposed to the anesthesia reversal medication. This case illustrates an unusual response to epinephrine with cardiac arrest in a healthy young male.

An experimental model of Stanford type B aortic dissection with intravenous epinephrine injection

The aim of this study was to create an experimental model of aortic dissection (AD) with a long-term patent false lumen to develop new treatments for Stanford type B aortic dissection. Sixteen adult beagle dogs (weight 14–18 kg) were used. After exposure and partially clamping, the descending aorta was cut through the adventitia to one-third of the depth of the tunica media. The aortic wall was divided into two layers by raspatory. Then half the circumference of the inner layer was cut transversely. All of the proximal layers and the distal outer layers were anastomosed together. Epinephrine was immediately used to expand the false lumen, and the effect was terminated using nitroglycerin when necessary. All dogs underwent both digital subtraction angiography (DSA) and computed tomography angiography (CTA) immediately after and 1 week and 1 month after surgery. The dogs were followed up at 1 day, 3 months, 1 year, and 2 years. The surgery was successful in 12 dogs. Dissection formation was observed immediately after epinephrine administration and confirmed by DSA and CTA. Our results showed typical characteristics of AD, such as a tear, septum, and true and false lumens. This is an easy and feasible way of developing a Stanford type B AD model by intravenous injection of epinephrine. In this canine model of AD, the false lumen has excellent long-term patency and the dissection plane is histologically similar to that in human AD. This model may contribute to the development of new treatments for Stanford type B AD.

Multiple cross-reactivity to several types of neuromuscular blocking agents in a patient with rocuronium anaphylaxis

Anaphylaxis that occurs during anesthesia is a major cause of morbidity and mortality. Muscle relaxant is the most frequent cause of perioperative anaphylaxis [1]. Although it is believed that there is a risk of anaphylaxis to the drug in some patients, a similar incidence of anaphylaxis has been observed with use of other members of the same drug class. We report on a case of anaphylactic reaction to rocuronium in a male patient confirmed as having multiple cross-reactivity to various neuromuscular blocking agents (NMBAs) on an allergic skin test at three months after discharge. A 31-year-old, 174 cm, 85 kg man with congenital cystic ad enomatoid malformation was scheduled to undergo lobectomy of the right lower lung. He did not have a history of allergy or surgery. Results of routine preoperative tests showed no abnormalities. In the operating room, routine monitoring devices, including a blood pressure (BP) cuff, pulse oximetry, and elec trocardiography (ECG) were placed on the patient. He showed stable vital signs, including oxygen saturation (SpO2) 100%, BP 115/78 mmHg, and heart rate (HR) 90 beats/min. Epidural catheter insertion was performed for control of intraoperative and postoperative pain. Propofol target-controlled infusion was performed for induc tion of general anesthesia. After loss of eyelash reflex, rocuronium 60 mg was administered, and endotracheal intubation was performed after two minutes of facemask ventilation. After endotra cheal intubation, his vital signs showed moderate hypotension; BP 85/40 mmHg, HR 75 beats/min. However, his breath sounds were normal. A 20-gauge arterial cannula was inserted into the left radial artery for continuous monitoring of arterial BP and a central venous catheter was placed in the right subclavian vein. He was treated with intravenous injection of ephedrine 10 mg and rapid infusion of Ringer’s lactate solution. BP did not improve; therefore, we stopped propofol infusion. We injected midazolam 3 mg and rocuronium 20 mg. A few minutes after injection, his vital signs indicated severe hypotension (BP 50/30 mmHg). We observed a skin rash, urticaria, and edema on his face, neck, arms, and legs. On arterial blood gas analysis, the measured values were pH 7.230, PCO2 50.4 mmHg, PO2 124 mmHg and SpO2 98%. The patient was treated with intravenous injection of epinephrine 0.1 mg and continuous infusion of dopamine, dobutamine, and phenylephrine. After a few minutes of infusion, his vital signs became stable; BP 90/45 mmHg, HR 105 beats/min, and SpO2 100%. Hydrocortisone 100 mg and chloropheniramine 4 mg were administered intravenously. Seventy

Epinephrine Induces Rapid Deterioration in Pulmonary Oxygen Exchange in Intact, Anesthetized Rats

Previous studies indicate epinephrine adversely affects arterial oxygenation when administered in a rat model of local anesthetic overdose. The authors tested whether epinephrine alone exerts similar effects in the intact animal. Anesthetized rats received a single intravenous injection of epinephrine (25, 50, or 100 mcg/kg); matched cohorts were pretreated with phentolamine (100 mcg/kg); n = 5 for each of the six treatment groups. Arterial pressure and blood gases were measured at baseline, 1 and 10 min after epinephrine administration. Pulmonary capillary pressures during epinephrine infusion with normal and increased flows were measured in an isolated lung preparation. Epinephrine injection in the intact animal caused hypoxemia, hypercapnia, and acidosis at all doses. Arterial oxygen tension was reduced within 1 min of injection. Hyperlactatemia occurred by 10 min after 50 and 100 mcg/kg. Rate pressure product was decreased by 10 min after 100 mcg/kg epinephrine. Pretreatment with phentolamine attenuated these effects except at 100 mcg/kg epinephrine. In the isolated lung preparation, epinephrine in combination with increased pulmonary flow increased pulmonary capillary pressure and lung water. Bolus injection of epinephrine in the intact, anesthetized rat impairs pulmonary oxygen exchange within 1 min of treatment. Effects were blunted by α-adrenergic receptor blockade. Edema occurred in the isolated lung above a threshold pulmonary capillary pressure when epinephrine treatment was coupled with an increase in pulmonary flow. These results potentially argue against using traditional doses of epinephrine for resuscitation, particularly in the anesthetized patient.

A Case of Successful Recovery from High Dose Intravenous Nicorandil Infusion in Refractory Coronary Vasospasm with Hemodynamic Collapse

A 70-year-old male came to the emergency room of the authors’ hospital because of sudden cardiac arrest due to inferior wall ST elevation myocardial infarction. His coronary angiography revealed multiple severe coronary spasms in his very long left anterior descending artery. After an injection of intracoronary nitroglycerine, his stenosis improved. The cardiac arrest relapsed, however, accompanied by ST elevation of the inferior leads, while the patient was on diltiazem and nitrate medication to prevent coronary spasm. Recovery was not achieved even with cardiac massage, intravenous injection of epinephrine and atropine, and intravenous infusion of nitroglycerine. The patient eventually recovered through high-dose nicorandil intravenous infusion without ST elevation of his inferior leads. Therefore, intravenous infusion of a high dose of nicorandil must be considered a treatment option for cardiac arrest caused by refractory coronary vasospasm.

Suspected Anaphylactic Reaction Associated with Microemulsion Propofol during Anesthesia Induction

Although rare, intraoperative anaphylaxis can lead to significant morbidity and mortality. Aquafol® (Daewon Pharmaceutical Co. Ltd., Seoul, Korea), a microemulsion propofol, was developed to eliminate lipid solvent-related adverse events, and was used in clinical anesthesia since 2009 with little data about severe side effects such as anaphylaxis. A healthy 16-yr-old male patient who had past medical history with two previous operations of no complications developed cardiovascular shock with generalized erythema following administration of microemulsion propofol during anesthesia induction. Intravenous injection of epinephrine and steroid rescued him. He remained in a stable state without any problems postoperatively and was discharged. Clinicians should consider this rare but serious complication during induction of anesthesia with propofol.

The significance of an isoprenaline-like metabolite in the interpretation of the responses of blood vessels in skeletal muscle to adrenaline.

Abstract A depressor substance, which resembled isoprenaline in Rf value, was demonstrated after chromatography of plasma collected from chloralose-anaesthetised cats during the blood pressure responses to intravenous injections of adrenaline, but the results obtained did not substantiate the hypothesis of a functional metabolite. The amount of vasodilatation that the “metabolite” would have caused in the skeletal muscles of the hind limb could not, for example, be correlated with the increases in blood flow produced by the original intravenous doses of adrenaline. The fact that adrenaline was largely vasoconstrictor in acutely denervated hind limbs was taken to indicate that the original vasodilator effects were of reflex nervous origin. It is suggested that the afferent source of this and related reflexes involves the stimulation of chemoreceptors as opposed to mechanoreceptors and that increases in flow through denervated muscles in response to adrenaline are caused by a direct action on the walls of the blood vessels.

Relationship between the milk yield response to short-term bovine somatotropin treatment and the lipolytic response to adrenaline in dairy cows

The aim of this experiment was to determine if the milk yield response of dairy cows to short-term treatment with bovine somatotropin (bST) was correlated with the non-esterified fatty-acid (NEFA) response to an adrenaline challenge. Twenty-six multiparous Holstein cows (58 ± 5.4 days postpartum) received daily sub-cutaneous injections of saline for 7 days followed by sub-cutaneous injections of 20 mg/day of bST for 14 days. On day 7 of the saline treatment and day 14 of the bST treatment the cows were given an intravenous injection of adrenaline (1.4 μg/kg body weight). Blood samples were taken before and after the adrenaline challenge. The difference in milk yield between the saline and the second week of bST treatment (MYR) varied considerably between animals (from −0.4 to +8.0 kg/day). MYR was positively correlated with the change in the basal concentration of NEFA between the saline and second week of bST treatment, as well as with the change in the area under the profile of NEFA above basal values following the adrenaline challenge. It remains to be established whether the greater lipolytic responses to adrenaline of the cows with the greater MYR reflects the deeper negative energy that these animals also experienced or a fundamental difference in the physiology of their adipose tissue.

Cardiovascular collapse developing during thoracoscopic thoracic sympathectomy in a patient with essential palmar hyperhidrosis - A case report -

Thoracoscopic thoracic sympathectomy (TTS) is usually a safe and uncomplicated procedure for treating essential palmar hyperhidrosis. However, we report a case of cardiovascular collapse that developed in a healthy patient undergoing TTS. The surgeon performed the left sympathectomy without incident. However, scarcely had an incision been made in the skin of the right chest when the patient developed sinus bradycardia and sudden, severe hypotension. Pulseless ventricular tachycardia occurred immediately thereafter, which rapidly progressed to ventricular fibrillation and cardiovascular collapse. The patient required resuscitation with 200 J of direct current shock defibrillation along with an intravenous injection of epinephrine 1 mg. She recovered without sequelae. We believe the Bezold-Jarisch reflex was triggered by pooling of venous blood and surgical stimuli, and the patient developed cardiovascular collapse as a result.