Atropine 1mg/0.3ml / Adrenaline (base) 120micrograms/0.3ml / Procaine hydrochloride 6mg/0.3ml solution for injection ampoules

We have studied the responses to electrical and chemical stimulation of the ventrolateral medulla in the chloralose-anesthetized, paralyzed, artificially ventilated rat. Locations of most active pressor responses were compared to regions containing neurons labeled immunocytochemically for phenylethanolamine N-methyltransferase (PNMT), the enzyme catalyzing the synthesis of adrenaline. Elevations of arterial pressure (+81.6 +/- 2.5 mm Hg) and cardioacceleration (+73 +/- 13.6 bpm) were elicited with low current (5 times threshold of 9.5 +/- 1.1 microA) electrical stimulation in a region of rostral ventrolateral medullary reticular formation we have termed the nucleus reticularis rostroventrolateralis (RVL). Electrical stimulation of the RVL increased plasma catecholamines (16.8-fold for adrenaline, 5.3-fold for noradrenaline, and 1.9-fold for dopamine) and vasopressin (1.7-fold before spinal transection, 4.7-fold after). The location of the most active pressor region in the ventrolateral medulla corresponded closely with the location of C1 adrenaline-synthesizing (PNMT-containing) neurons. In addition, the location of the most active pressor region in the dorsomedial medulla corresponded with the location of a bundle of PNMT-containing axons. Unilateral injections into the RVL of the excitatory amino acid monosodium L-glutamate (50 pmol to 10 nmol), but not saline, caused transient dose-dependent and topographically specific elevations (maximum +71.6 +/- 4.9 mm Hg) of arterial blood pressure and tachycardia. Injections of the rigid structural analogue of glutamate, kainic acid, caused large, prolonged (at least 15 min) pressor responses and tachycardia. Unilateral injections of the inhibitory amino acid gamma-aminobutyric acid (GABA) into the RVL caused transient dose-dependent hypotension (maximum -40.8 +/- 6.6 mm Hg) and bradycardia, whereas the specific GABA antagonist bicuculline caused prolonged (10 to 20 min) elevations (+64.2 +/- 6.8 mm Hg) of arterial pressure and tachycardia. By contrast, injections of the glycine antagonist strychnine had no significant effect. Bilateral injections of the neurotoxin, tetrodotoxin, dropped arterial pressure to low levels (51.7 +/- 4.7) not changed by subsequent spinal cord transection at the first cervical segment (52.5 +/- 6.2). We propose the following. (1) Neurons within the RVL, most probably C1 adrenaline-synthesizing neurons, exert an excitatory influence on sympathetic vasomotor fibers, the adrenal medulla, and the posterior pituitary. (2) These neurons are tonically active and under tonic inhibitory control, in part via GABAergic mechanisms--perhaps via the nucleus of the solitary tract (NTS).(ABSTRACT TRUNCATED AT 400 WORDS)

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BackgroundSpinal anesthesia, as an effective approach, is widely performed in various surgeries with possible complications. To reduce the side effects, many adjuvants are used to maintain desirable sensory and motor blockades and increase the quality and prolong the analgesia.MethodsIn the current double-blind, randomized clinical trial, 105 participants aged 18 - 60 years with ASA class I or II who were candidate for lower limb surgery were randomly allocated to patients receiving bupivacaine 15 mg + normal saline 1 mL (B group), bupivacaine 15 mg + epinephrine 10 µg (BE group), and bupivacaine 15 mg + sufentanyl 5 µg (BS group). Onset of sensory blockade was determined bilaterally with the pinprick test. The maximum Bromage scale was assessed for the onset of motor blockage. Recovery from sensory and motor blockades was also evaluated. Pain score (visual analogue scale; VAS) was determined for all participants.ResultsOnset of sensory and motor blockades was statistically different among the groups. Intrathecal bupivacaine (the placebo group) had the lowest onset of sensory blockage, whereas the onset of motor blockade was significantly shorter with the administration of sufentanil + epinephrine (P = 0.001) (BS and BE groups). However, epinephrine (BE group) did not significantly prolong sensory and motor blockade. Recovery time from sensory and motor blockade was significantly lower with the bupivacaine alone (the placebo group).ConclusionsThe current study results suggested that the combination of 10 µg epinephrine and 5 µg sufentanil + bupivacaine did not prolong the sensory and motor blockades in spinal anesthesia for lower limb surgery, compared with bupivacaine alone.

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BackgroundPupil dilation and mydriasis maintenance throughout vitreoretinal surgeries are important to allow satisfactory fundus visualization and reduce risk of complications. The purpose of this study is to evaluate the role of subconjunctival epinephrine 0.1% injection in mydriasis maintenance during vitrectomy.MethodsNinety-nine consecutive patients undergoing vitrectomy were enrolled. All subjects were preoperatively dilated with tropicamide 1%. Each patient was randomly allocated either in the epinephrine or placebo group. In epinephrine group, patients were submitted to a 0.2 cc subconjunctival injection of a 0.1% epinephrine solution just before first incisions. In placebo group, the same procedure was performed with 0.2 cc of saline 0.9%. Horizontal pupil diameter was measured with calipers before and in the end of the procedure.ResultsPatients in the epinephrine group showed a significantly larger mean pupil diameter in the end of the surgery compared to placebo. There was a significant increase of mean pupil diameter from the beginning to the end of the surgery in such patients. Blood pressure was significantly higher in the epinephrine group than in placebo group. No other adverse effects were noted.ConclusionSubconjunctival epinephrine is effective for maintaining and increasing pupil size during vitrectomy, compared to placebo. Caution should be taken regarding intraoperative blood pressure levels.Trial registrationRBR; RBR-3qzhvg; Registered 8 May 2018-Retrospectively registered, http://www.ensaiosclinicos.gov.br/rg/RBR-3qzhvg/.

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Mast cell degranulation and other interacting and linked cells, including T-lymphocytes, macrophages, eosinophils, and platelets, as well as a range of inflammatory mediators produced during an anaphylactic or allergic reaction, constitute the main causes of Kounis syndrome. Acute ischemia episodes, coronary spasm, atheromatous plaque erosion/rupture, and platelet activation can all be caused by histamine, tryptase, arachidonic acid derivatives, and chymase in the Kounis syndrome cascade. Kounis syndrome can be triggered by a variety of factors, including medications, hymenopteran stings, metals, foods, environmental exposures, illnesses, and immunizations. In addition, some unusual, rare, intriguing, and significant causes of Kounis syndrome have been discovered recently, namely the “kiss of death”, where human kissing and pet kissing can induce fatal Kounis syndrome. Moreover, the clinical conundrum is that several of the main drugs and substances used to treat myocardial infarction and Kounis syndrome, such as adrenaline (epinephrine), aspirin, atropine, clopidogrel, corticosteroids, heparins, protamine sulfate, and hirudotherapy can also initiate it. Therefore, physicians should be aware of this clinical discrepancy to prevent catastrophic consequences.

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