Cardiac arrhythmias during phenol face peeling

Thirty-nine percent of 54 phenol face peel patients treated rapidly developed some form of cardiac arrhythmia. When half the face was treated on consecutive days, only 22 percent of 100 patients developed cardiac arrhythmias and these were less severe. Serum phenol levels varied from 4.4 to 337.1 mg/L. Neither age, sex, nor previous cardiac history were accurate predictors of cardiac arrhythmia susceptibility. There was no predictable relationship between serum phenol level and the appearance of cardiac arrhythmia. The duration of the cardiac arrhythmias (2 to 19 minutes) suggests that the risk of cardiac arrhythmia in phenol peeling can be reduced by dividing the face into several units and spacing the application of phenol to each unit 20 minutes apart.     

The prevention of cardiac arrhythmias produced in an animal model by the topical application of a phenol preparation in common use for face peeling

We have shown in an animal model that complex ventricular arrhythmias produced by topical application of a phenol preparation that is used in face peeling can be prevented by a brisk diuresis at the time of application or by gradual application of the phenol preparation. We recommend that continuous cardiac monitoring and recording be performed in patients having topical phenol applications in order to determine the true incidence of cardiac arrhythmias and to ascertain if they are prevented by a forced diuresis, by the gradual application of the preparation, or by a combination of both.     

An examination of the phenol-croton oil peel: Part I. Dissecting the formula

This article investigates which ingredients are the active ones in the most popular peel formula. The benefits of the "phenol" peel have been attributed to the effects of phenol on the dermis. Baker published a simple peel formula in 1962 that became a classic that has been used since by almost all plastic surgeons and dermatologists. Brown et al., in 1960, passed along a set of dogmas: (1) phenol is the active ingredient; (2) phenol peels more deeply in lower concentrations; and (3) adding a surface tension-lowering agent increases the peel. This article seeks to dissect the Baker formula by removing the croton oil. A patient was peeled serially with 18% phenol, 35% phenol, and 50% phenol solutions containing Septisol (surface tension-lowering agent) but no croton oil. This showed that increasing concentrations of phenol caused more clinical tissue reaction as evidenced by edema and erythema, but no significant dermal injury was seen. USP 88% phenol without Septisol did cause injury to the dermis. To test the effect of croton oil in the formula, the patient's face was peeled with two variations: the perioral area was peeled with 50% phenol to which croton oil was added to a strength of 2.1% and the remainder with 50% phenol without croton oil. The perioral area showed vesiculation, slough, and dermal exposure characteristic of a deep peel requiring 11 days to heal. The remainder of the face treated with 50% phenol without croton oil showed only edema and erythema without significant dermal injury. This experiment shows that the main postulates of Brown et al.--that phenol in lesser concentrations peels more than in higher concentrations and that phenol is the sole agent--are not true. In a fourth peel, a 0.7% concentration of croton oil in 50% phenol was applied to the parts of the face not peeled with croton oil in the third peel. The areas peeled with 50% phenol with 0.7% croton oil healed in 7 days, whereas the treatment with 50% phenol with 2.1% croton oil required 11 days. Deconstructing the Baker formula reveals fallacies in the four-decade-long belief system regarding these peels. The serial peels performed in this study show that increasing concentrations of phenol without croton oil cause increasing skin reaction but insignificant peeling effect. The addition of croton oil to 50% phenol, however, causes a marked increase in the depth of peeling into the dermis. Lowering the concentration of croton oil caused a lesser burn, as evidenced by fewer days to heal. The depth of the peel, therefore, seems to be more dependent on the concentration of croton oil than phenol. This will be further explored in Parts II, III, and IV.     

Effect of Heparin on Serum Free-fatty-acids,Plasma Catecholamines,and the Incidence of Arrhythmias following Acute Myocardial Infarction

The effect of intravenous heparin in a therapeutic dosage on cardiac arrhythmias in patients with indubitable acute myocardial infarction was investigated. The value of serum free-fatty-acids (F.F.A.s) and plasma catecholamines in the prediction of patients vulnerable to serious arrhythmias was also studied.Heparin produced a significant rise in F.F.A., maximal within 10 minutes of injection, but did not increase the incidence of cardiac arrhythmias.No relationship was found between the incidence of arrhythmias and the initial levels of F.F.A. or adrenaline. No correlation was obtained between F.F.A. and plasma catecholamine levels. Heparin did not have a consistent effect on plasma catecholamines. Initial control plasma noradrenaline concentrations, however, were found to be significantly correlated with the incidence of subsequent arrhythmias. It is suggested that the level of plasma noradrenaline may be a valuable predictive guide to those patients likely to develop significant arrhythmias after acute myocardial infarction.     

Cardiac arrhythmias in myocardial infarction as an extension of lesions to the myocardium and the state of circulatory efficiency

The study involved 55 patients with the acute myocardial infarction aged between 34 and 69 years (mean 53 years) in whom the relation of cardiac arrhythmias incidence to the extension of myocardial involvement and circulatory efficiency was assessed. All patients were examined clinically, a 24-hour ECG with Holter technique (in the first day, 21st day and 6th months after myocardial infarction) and echocardiographic (Echo-2D) tests were registered. Echocardiography was performed during hospital phase and 6 months after myocardial infarction. Cardiac arrhythmias were evaluated with classification into classes described by Lown. Close relation of serious cardiac arrhythmias with extension of myocardial involvement was noted especially in the acute phase of myocardial infarction. High risk arrhythmias--class IVA, IVB and V were noted in nearly 100% of patients in this phase with cardiac aneurysm, extensive akinesis of apex and anterior wall of the heart. Mean value of the ejection fraction was 31% in this group. Incidence of cardiac arrhythmias did not exceed 40%, ejection fraction was 56% in the group of patients with limited lesions to the heart, e.g. akinesis of the lower wall. Incidence of late cardiac arrhythmias (6 months) did not differ significantly in particular groups of patients. The value of ejection fraction remained, however, on the same level as in the hospital phase of the myocardial infarction.     

Cardiac arrhythmias during rewarming of patients with accidental hypothermia.

Accidental hypothermia has a high mortality and is associated with cardiac arrhythmias. To determine the incidence of arrhythmias and their importance 22 patients with accidental hypothermia (core temperature less than 35 degrees C) were studied by 12 lead electrocardiography and continuous recording of cardiac rhythm. Although 14 of the patients died (64%), only six died while hypothermic. Prolongation of the Q-T interval and the presence of J waves were related to the severity of the hypothermia. Supraventricular arrhythmias, including atrial fibrillation, were common (nine cases) and benign. Ventricular extrasystoles were also common (10 cases), but ventricular tachycardia or fibrillation did not occur during rewarming. In eight patients who died while being monitored the terminal rhythm was asystole. There was no correlation between the severity of hypothermia or the rate of rewarming and the clinical outcome. In the absence of malignant arrhythmias there is no indication for using prophylactic antiarrhythmic treatment in patients with accidental hypothermia. The presence or absence of severe underlying disease is the main determinant of prognosis.     

An examination of the phenol-croton oil peel: part IV. Face peel results with different concentrations of phenol and croton oil

In Part IV of this examination of the phenol-croton oil peel, the author presents peeling solutions using phenol in concentrations between 16% and 50% as the carrier for croton oil. Previously, in Part I, the author showed that phenol alone in concentrations of less than 50% has no significant peeling effect on the skin in the absence of taping. All of these formulas are dependent on the addition of croton oil for their peeling action. A topographic map of the face is presented that divides the face into the zones that the author believes are best treated with different strengths of croton oil. Five patients peeled between late 1992 and late 1995 were chosen as examples to illustrate the effect of different strengths of croton oil between 0.25% and 2.78%. The author has documented their immediate postoperative course photographically to show the effect of the different concentrations. It is clinically apparent that peels using croton oil between 0.25% and 0.5% generally heal within 7 days; peels between 0.6% and 1.0% usually heal within 9 or 10 days, and peels using concentrations higher than 1% heal later and have some risk of pigmentation loss. Peels using croton oil concentrations at 2% and above almost always have pigmentation loss and have healing delays in areas other than the thick skin of the lower nose and perioral area. The practical clinical formulas distributed at the time of the presentation of this article at the 1996 Annual Meeting of the American Society for Aesthetic Plastic Surgery in Orlando, Florida, entitled "Heresy Phenol Formulas--1996," are provided here. These have been used in both the United States and Europe over the past few years. A metric standard for drop size is suggested at 0.04 ml. This relates to the drop size used clinically over the years to measure croton oil. The adoption of this unit will make formulas around the world easier to calculate and compare. The author has produced a metric formula using the suggested standard size drop for croton oil. This uses 35% phenol as the carrier and provides the same range of treatment dilutions as the 1996 "Heresy Phenol Formulas." The need for research into "carriers" and solvents for croton oil is pointed out. Despite what is not known about how it works, the combination of croton seed extract and phenol has been a success story in providing facial rejuvenation from the 1920s to the present. The croton oil-phenol peel in its many formulas still sets the standard for facial rejuvenation.     

Long-term histologic follow-up of phenol face peels

Deep phenol peels were done on 11 middle-aged white women with severe actinic damage. Subsequently, face lifts were carried out after periods of 1.5 to 20 years. This made it possible to obtain a full-thickness specimen extending several centimeters on either side of the border between peeled and unpeeled skin. In contrast to the markedly abnormal elastotic appearance of unpeeled skin, a new band of connective tissue 2 to 3 mm in width was laid down in the subepidermal region. Fine elastic fibers formed a dense network in the band of regenerated collagen. The disarray and cytologic abnormalities of sun-damaged epidermis were also largely corrected. Melanocytes were not eliminated, but melanin synthesis was evidently impaired, accounting for the bleaching effects. The effects of a phenol peel are very long lasting and adequately account for the effacement of wrinkles and obliteration of actinic keratoses, mottling, and freckling.     

Thromboxane A2-induced arrhythmias in the anesthetized rabbit

Experiments were conducted in the anesthetized rabbit to investigate mechanisms for arrhythmias that occur after left atrial injection of the thromboxane A(2) (TxA(2)) mimetic U-46619. Arrhythmias were primarily of ventricular origin, dose dependent in frequency, and TxA(2) receptor mediated. The response was receptor specific since arrhythmias were absent after pretreatment with a specific TxA(2) receptor antagonist (SQ-29548) and did not occur in response to another prostaglandin, PGF(2alpha). Alterations in coronary blood flow were unlikely the cause of these arrhythmias because coronary blood flow (as measured with fluorescent microspheres) was unchanged after U-46619, and there were no observable changes in the ECG-ST segment. In addition, arrhythmias did not occur after administration of another vasoconstrictor (phenylephrine). The potential involvement of autonomic cardiac efferent nerves in these arrhythmias was also investigated because TxA(2) has been shown to stimulate peripheral nerves. Pretreatment of animals with the beta-adrenergic receptor antagonist propranolol did not reduce the frequency of these arrhythmias. Pretreatment with atropine or bilateral vagotomy resulted in an increased frequency of arrhythmias, suggesting that parasympathetic nerves may actually inhibit the arrhythmogenic activity of TxA(2). These experiments demonstrate that left atrial injection of U-46619 elicits arrhythmias via a mechanism independent of a significant reduction in coronary blood flow or activation of the autonomic nervous system. It is possible that TxA(2) may have a direct effect on the electrical activity of the heart in vivo, which provides significant implications for cardiac events where TxA(2) is increased, e.g., after myocardial ischemia or administration of cyclooxygenase-2 inhibitors.     

Facial resurfacing in xeroderma pigmentosum with chemical peeling

We describe our experience with two patients with xeroderma pigmentosum who underwent multiple trichloroacetic acid chemical peels. Trichloroacetic acid and phenol were used in one case. Until now numerous treatment modalities have been reported. Deep chemical peeling has not been reported before in patients with xeroderma pigmentosum. Chemical peeling is a simple procedure with less associated morbidity.     

The actions of prostaglandins I2 and E2 on arrhythmias produced by coronary occlusion in the rat and dog.

Prostaglandins E2 and I2 were compared with known antiarrhythmics for their actions against arrhythmias produced by occlusion of the left anterior descending coronary artery in the anaesthetised rat while PGI2 was also examined in the dog. PGI2 in the dog suppressed early arrhythmias produced during occlusion but did not influence those produced by occlusion-release or those occurring 24 hours after a permanent occlusion; none of the A,B,C or D series prostaglandins tested markedly reduced 24 hour arrhythmias. In the rat PGE2 was antiarrhythmic against early occlusion arrhythmias (30 minutes occlusion) in a dose related manner (infusions of 1-4 microgram/kg/min) whereas PGI2 infusions potentiated the arrhythmogenic effect of occlusion. PGE2 was as effective an antiarrhythmic as 10mg/kg Org. 6001 which was more effective in this test situtation than dl-propranolol. No obvious mechanisms for the actions of PGE2 or PGI2 were apparent although both agents lowered blood pressure and reduced the size of the occluded zone produced by ligation.     

Prevention of ischemic and re-oxygenation arrhythmias and heart fibrillation using the antioxidant ionol

The effect of a synthetic antioxidant, ionol (2,4-ditrebutyl-4-methylphenol) on cardiac arrhythmias induced by 10-minute occlusion of the left coronary artery followed by 5 minutes of reperfusion (RP) was investigated. The study was performed on male Wistar rats, 250-300 g body weight. The animals were ventilated with room air under urethan anesthesia. RP induced more severe ventricular arrhythmias than ischemia (IS). During RP ventricular fibrillation developed in 12 and during IS in 2 out of 24 animals. Other types of arrhythmias--tachycardia and extrasystole--were also more pronounced during RP than during IS. Preadministration of animals with ionol (60 mg/kg, per os) abolished completely ventricular fibrillation during IS and RP. Ionol reduced considerably the incidence of tachycardia and extrasystole, shortening their duration 5-7-fold. The data suggest that the activation of lipid peroxidation may play an important role in the pathogenesis of cardiac fibrillation and open prospects for the prevention and treatment of cardiac arrhythmias with antioxidants.     

The automatic external cardioverter-defibrillator

In-hospital cardiac arrest remains a major problem but new technologies allowing fully automatic external defibrillation are available. These technologies allow the concept of "external therapeutic monitoring" of lethal arrhythmias. Since early defibrillation improves outcome by decreasing morbidity and mortality, the use of this device should improve the outcome of in-hospital cardiac arrest victims. Furthermore, the use of these devices could allow safe monitoring and treatment of patients at risk of cardiac arrest who not necessarily must be in conventional monitoring units (Intensive or Coronary Care Units) saving costs with a more meaningful use of resources. The capability to provide early defibrillation within any patient-care areas should be considered as an obligation ("standard of care") of the modern hospital.     

Left ventricular false tendons

Left ventricular false tendons (LVFTs) are fibromuscular structures, connecting the left ventricular free wall or papillary muscle and the ventricular septum.There is some discussion about safety issues during intense exercise in athletes with LVFTs, as these bands have been associated with ventricular arrhythmias and abnormal cardiac remodelling. However, presence of LVFTs appears to be much more common than previously noted as imaging techniques have improved and the association between LVFTs and abnormal remodelling could very well be explained by better visibility in a dilated left ventricular lumen.Although LVFTs may result in electrocardiographic abnormalities and could form a substrate for ventricular arrhythmias, it should be considered as a normal anatomic variant. Persons with LVFTs do not appear to have increased risk for ventricular arrhythmias or sudden cardiac death.     

柑橘叶片和果皮总蛋白质提取及双向电泳体系的建立

以春甜橘(Citrus reticulata Blanco‘Chuntianju’)果皮和叶片为材料,分别用Tris-HCl、尿素/硫脲(Thi/Urea)、三氯乙酸/丙酮(TCA)和酚(Phe)等4种方法提取柑橘总蛋白质,从蛋白质产量、单向SDS-PAGE和双向电泳等方面进行比较。结果表明,4种方法的分离效果存在较大差异,不论是以柑橘叶片还是果皮为材料,均以TCA法最好,且双向电泳图谱分辨率较好,蛋白点清晰、均匀、基本没有条纹,且蛋白点多。这说明TCA法不仅能很好地去除柑橘果皮、叶片中存在的大量干扰物质,而且还能得到稳定的蛋白点。     

Dietary fibre components and pectin chemical features of peels during ripening in banana and plantain varieties

The effects of the ripeness stage of banana (Musa AAA) and plantain (Musa AAB) peels on neutral detergent fibre, acid detergent fibre, cellulose, hemicelluloses, lignin, pectin contents, and pectin chemical features were studied. Plantain peels contained a higher amount of lignin but had a lower hemicellulose content than banana peels. A sequential extraction of pectins showed that acid extraction was the most efficient to isolate banana peel pectins, whereas an ammonium oxalate extraction was more appropriate for plantain peels. In all the stages of maturation, the pectin content in banana peels was higher compared to plantain peels. Moreover, the galacturonic acid and methoxy group contents in banana peels were higher than in plantain peels. The average molecular weights of the extracted pectins were in the range of 132.6-573.8 kDa and were not dependant on peel variety, while the stage of maturation did not affect the dietary fibre yields and the composition in pectic polysaccharides in a consistent manner. This study has showed that banana peels are a potential source of dietary fibres and pectins.     

The effect of lidocaine on lysophosphatidylcholine-induced cardiac arrhythmias and cellular disturbances

The production of arrhythmias in the isolated heart by perfusion with lysophosphatidylcholine has been well documented. However, the role of the lysophospholipid as a physiological factor in the generation of cardiac arrhythmias is not clear. In this study, a pharmacological approach was used to delineate the physiological significance of lysophosphatidylcholine during this cardiac dysfunction. Lidocaine (5-20 mg/L) was found to be effective in the protection of the isolated rat heart from the lysophospholipid-induced arrhythmias at pharmacological concentrations. The effect of lidocaine in the protection of lysophospholipid-induced membrane dysfunction was studied with red blood cells. Lidocaine (2 mg/mL) protected red blood cells from hemolysis in the presence of lysophosphatidylcholine. Lidocaine did not inhibit the binding of the lysophospholipid to the red cell membrane, but inhibited hemolysis in a manner similar to cholesterol. The results are consistent with the postulate that lysophosphatidylcholine is a physiological factor in the pathogenesis of cardiac arrhythmias during myocardial ischemia.     

Duration of Last Attack in 998 Fatal Cases of Coronary Artery Disease and its Relation to Possible Cardiac Resuscitation

All the deaths attributed to coronary artery disease and occurring in Belfast during one year were studied.The frequency distributions of the cases by interval of time between onset of the last attack and death are given for those not admitted to hospital, for those admitted to hospital, and for those already in hospital for some other cause of illness.Sixty per cent. of all the deaths occurred outside hospital. This indicates that the problem of cardiac resuscitation in coronary artery disease is to a considerable extent an extra-hospital one.Twenty-seven per cent. of the men and 22% of the women died within 15 minutes, but the median period of survival was 3 hours 30 minutes for men and 6 hours 18 minutes for women.The median time interval from the onset of the attack to sending for medical aid was 1 hour 17 minutes for men and 1 hour 6 minutes for women, and from summoning medical aid to sending for the ambulance 59 minutes for men and 1 hour 26 minutes for women. Ninety-six per cent. of the ambulance journeys to the patient were accomplished in less than 20 minutes.It was found among men, but not among women, that the duration of survival tended to be longer in older patients and in second or subsequent attacks.Of the 596 who did not gain admission to hospital 229 (23% of all the 998 patients) were known to have survived for more than half an hour after the onset of the fatal attack; 182 (18%) survived for more than one hour; and 143 (14%) survived for more than two hours. It is among these that there would appear to be special scope for the cardiac ambulance, providing that medical aid is sought and the ambulance is summoned without delay.     

Dynorphin A (1-13) in the brain suppresses epinephrine-induced ventricular premature complexes and ventricular tachyarrhythmias.

The objectives of this study were to test the hypothesis that dynorphin in the central nervous system modulates epinephrine-induced cardiac arrhythmias and that central cholinergic mechanisms are operative in this action of dynorphin. Cardiac arrhythmias were produced by continuous intravenous infusion of epinephrine, in Wistar rats, previously instrumented with catheters in the lateral cerebral ventricle, femoral vein and femoral artery. Epinephrine produced ventricular premature complexes and later the development of fatal ventricular fibrillation. Dynorphin A (1-13), 5 or 20 micrograms (3 or 12 nM) administered into the lateral cerebral ventricle (ICV), significantly (P less than 0.05) increased the threshold for development of cardiac arrhythmias. Dynorphin A (1-13), 20 micrograms, increased the epinephrine dose at the occurrence of ventricular premature beats to 171 +/- 8 (mean +/- 1 S.E.M.) compared to 120 +/- 5 micrograms epinephrine/kg in the control group and increased the dose at the onset of fatal arrhythmias to 186 +/- 8 compared to 141 +/- 10 micrograms epinephrine/kg in the control group. The action of dynorphin was significantly (P less than 0.05) antagonized by the kappa opioid antagonist MR2266. Atropine sulfate, administered ICV or intravenously, produced a dose dependent antagonism of this action of dynorphin A (1-13). This was not due to the peripheral effects of atropine, as atropine methylnitrate, which does not cross the blood brain barrier, did not oppose the effects of dynorphin A (1-13). These data indicate (i) dynorphin A (1-13) increases the threshold for or suppresses the manifestations of epinephrine-induced ventricular arrhythmias, (ii) dynorphin's action on cardiac arrhythmias is mediated through central cholinergic rather than peripheral parasympathetic mechanisms (iii) dynorphin may play a role as an endogenous opioid within the brain that modulates cardiac arrhythmias in circumstances of elevated circulating epinephrine concentration.     

Arrhythmia in patients with mitral valve prolapse]

An incidence of cardiac arrhythmias was evaluated in 119 patients with mitral valve prolapse. The disease was made basing on the results of clinical symptoms, echo-, angio- and phonocardiography. Electrocardiograms were recorded from the standard 12 lead and Holter technique for 24 hours in each patient to assess present arrhythmias. It was found that the most frequent cardiac arrhythmias accompanying mitral valve prolapse are ventricular extrasystolic contractions of Lown's class 1a and 1b. Only examination of strictly selected groups of patients (age groups with or without co-existing mitral valve insufficiency for adequate period of time) will facilitate precise evaluation of an incidence of different cardiac arrhythmias accompanying the underlying disease.