Antiarrhythmic and arrhythmogenic action of inosine in experimental ventricular tachyarrhythmias.

OBJECTIVE: To study the possible action of inosine on experimental ventricular tachyarrhythmias. MATERIAL AND METHODS: We used 92 mongrel dogs weighing 13 kg-17 kg, anesthetized with 30 mg/kg sodium pentobarbital applied intravenously. Myocardial lesions were induced by injecting 1 ml-1.5 ml of 70% phenol in the free wall of the left ventricle. In 36 dogs, the ventricular arrhythmia (VT) was induced 30 min later with aconitine crystals inserted into the periphery of the damaged area; in 16, VT was due only to myocardial damage and in the other 13 VT was spontaneously originated. Twenty-nine animals constituted the control group; no inosine was administered to them. The possible effects of inosine were studied in 63 animals. Leads II, aVR or aVL, right and Left unipolar intraventricular leads and that on the wall of the superior vena cava were recorded under control conditions, once the myocardial damage had been induced, during the ventricular tachycardia, and following the injection of inosine. Of the 63 inosine-treated animals; in 34, VT was due to aconitine; in 16, it was produced only by the myocardial damage and, in 13, VT was presented spontaneously. RESULTS: Sinus rhythm was not reestablished in the animals of the control group. Inosine reestablished the sinus rhythm in 26 of 34 dogs (76%) that received phenol and aconitine, in 13 of the 16 (81%) presenting only the myocardial damage, and in 6 of the 13 (46%) with spontaneous ventricular tachycardia. In some experiments, inosine induced supraventricular tachycardias, ventricular-atrial blocks, and ventricular pre-excitation phenomena. CONCLUSIONS: In this experimental series, inosine showed antiarrhythmic and arrhythmogenic effects, similar to those of adenosine from which it derives.

Antiarrhythmic and cardioprotective effects of remifentanil in anesthetized dogs.

OBJECTIVE: To study the antiarrhythmic effect of remifentanil in experimental arrhythmias in dogs. METHODS: We used dogs weighing 12 kg-18 kg anesthetized with 30 mg/kg sodium pentobarbital given intravenously. Ventricular arrhythmia, ventricular fibrillation and death were induced with digoxin (9 microg/kg/min). In another model, two types of arrhythmia were induced in the right atrium, one of them with aconitine crystals placed on the right atrium and the other was induced in the basement of the right atrium by electrical stimulation. The potential antiarrhythmic action of remifentaniL was investigated in ventricular and atrial arrhythmias by the administration of an intravenous bolus after toxic signs were evident. Thus, two arrhythmias with different mechanisms were generated. Leads DII, unipolar left intraventricular and right atrial leads, and left ventricular pressure were used to record control tracings and tracings in presence of remifentanil, during ventricular arrhythmia. RESULTS: Remifentanil abolished toxic effects of digoxin, it eliminated the A-V dissociation and ventricular extrasystoles, reverting to sinus rhythm in each case. Remifentanil extended the time to reach lethal doses from 63.25 +/- 11.3 to 100 +/- 11.8 min. These effects were blocked by naloxone (0.01 microg/kg) applied before remifentanil. In the two arrhythmias model, remifentanil suppressed both, ectopic focus and atrial flutter. CONCLUSIONS: Remifentanil elicits antiarrhythmic and cardioprotective effects in experimental ventricular arrhythmias induced by digoxin and in a model of two atrial arrhythmias induced by aconitine and by electrical stimulation.

[Hypertension in women]. / Hipertensión arterial sistémica en la mujer.

The cardiovascular disease is a crucial cause of morbidity and mortality in the woman mainly when they arrive at menopause. The pathophysiology and neurohormonal mechanisms widely vary with respect to the man. This finding has given the support to think that the estrogens may be playing a protector role in cardiovascular disease. However, the associated risk factors like obesity, diabetes, dislipidemia, smoking and sedentary life are increasing in an exponential form. In Mexico the population age distribution establishes that 60% of the women with hypertension are aged < 54 years old. This is reason why as factor of independent cardiovascular risk is commonest. Nevertheless, after the menopause cardiovascular mortality is greater in the woman than in the man. In this review, the importance of the new pathophysiological mechanisms and the clinical-therapeutic approach are analyzed, making emphasis in the importance of the change in the life style and also in the nutritional aspects. In Mexico the woman still have a unique role in the nutritional culture.

[Therapeutic clinical approach for the elderly patient with hypertension: recommendations for clinical practice]. / Abordaje clínico terapéutico del paciente adulto mayor con hipertensión arterial sistémica: recomendaciones para la práctica clínica.

The incidence of hypertension in the geriatric population is very high and is a significant determinant of cardiovascular risk in this group. The tendency for blood pressure to increase with age in westernized societies such as the United States may depend on environmental factors such as diet, stress, and inactivity. Our population tends to become more obese; to consume relatively greater amounts of sodium and lesser amounts of potassium, calcium, and magnesium; and to decrease exercising with increasing age. Senescent changes in the cardiovascular system leading to decreased vascular compliance and decreased baroreceptor sensitivity contribute not only to rising blood pressure but also to an impairment of postural reflexes and orthostatic hypotension. The hallmark of hypertension in the elderly is increased vascular resistance. Greater vascular reactivity in the elderly hypertensive patients may reflect decreased membrane sodium pump activity and decreased beta-adrenergic receptor activity as well as age-related structural changes. Treatment of diastolic hypertension in the elderly is associated with decreased cardiovascular morbidity and mortality. Although treatment of systolic hypertension may not decrease immediate cardiovascular mortality, it appears to decrease the incidence of stroke. The initial therapeutic approach to the elderly hypertensive patient should generally consist of a reduction in salt and caloric intake and an increase in aerobic exercise, i.e., walking. Drug therapy should be initiated with lower doses of medication with a special concern about orthostatic hypotension.

[Prevention and treatment of hypertension and coronary heart disease]. / Prevención y tratamiento de la hipertensión arterial sistémica en el paciente con enfermedad arterial coronaria.

The association between arterial systemic hypertension arterial coronary disease has been demonstrated by cumulated evidence of several epidemiological studies. Hypertension is an important independent risk factor for the development of coronary artery disease, vascular cerebral disease and nephropathy. Important advances exist in the knowledge of neurohumoral and hemodynamic factors that come together in the pathophysiology of the hypertension and in the development of coronary disease that allow to establish better strategies not only of treatment, but also of prevention, with the purpose of diminishing the cardiovascular mortality. The spectrum of the coronary artery disease secondary to atherosclerosis is wide and the strategies of treatment of hypertension must be adapted to each particular case. The treatment of both conditions needs of specific limits of agreement to the conditions of the patient and the form of presentation of each one of these disease.

[Extreme elevation of the blood pressure (hypertensive crisis): recommendations for its clinical-therapeutic approach]. / Elevación extrema de la presión arterial (crisis hipertensiva): recomendaciones para su abordaje clínico-terapéutico.

From beginnings of last century the hypertensive emergency was defined as the association of acutely elevation from the arterial pressure and the appearance of damage to end organ. At present is recognized the effects of the hypertensive emergency, the aspects of its patophysiology in which are included phenomenon of vasomotricity and the participation of different substances with vasoactives properties. The clinical presentation includes not only the manifestations of the increase of the arterial pressure, the end organ damage too; for this reason the hypertensive emergency needs the immediate reduction of the arterial tension to prevent the damage to specific organs. The treatment in every case will have to be individualized, with a wide knowledge of the characteristics of every medicament to obtain the best results. The diagnosis and treatment of the hypertensive emergencies needs often of the attention of its complications if they have appeared and later, of a treatment of support for the arterial hypertension.

[Clinical guidelines for detection, prevention, diagnosis and treatment of systemic arterial hypertension in Mexico (2008)]. / Guías clínicas para la detección, prevención, diagnóstico y tratamiento de hipertensión arterial sistémica en México (2008).

The multidisciplinary Institutional Committee of experts in Systemic Arterial Hypertension from the National Institute of Cardiology "Ignacio Chávez" presents its update (2008) of "Guidelines and Recommendations" for the early detection, control, treatment and prevention of Hypertension. The boarding tries to be simple and realistic for all that physicians whom have to face the hypertensive population in their clinical practice. The information is based in the most recent scientific evidence. These guides are principally directed to hypertensive population of emergent countries like Mexico. It is emphasized preventive health measures, the importance of the no pharmacological actions, such as good nutrition, exercise and changes in life style, (which ideally it must begin from very early ages). "We suggest that the changes in the style of life must be vigorous, continuous and systematized, with a real reinforcing by part of all the organisms related to the health education for all population (federal and private social organisms). It is the most important way to confront and prevent this pandemic of chronic diseases". In this new edition the authors amplifies the information and importance on the matter. The preventive cardiology must contribute in multidisciplinary entailment. Based mainly on national data and the international scientific publications, we developed our own system of classification and risk stratification for the carrying people with hypertension, Called HTM (Arterial Hypertension in Mexico) index. Its principal of purpose this index is to keep in mind that the current approach of hypertension must be always multidisciplinary. The institutional committee of experts reviewed with rigorous methodology under the principles of the evidence-based medicine, both, national and international medical literature, with the purpose of adapting the concepts and guidelines for a better control and treatment of hypertension in Mexico. This work group recognizes that hypertension is not an isolated disease; therefore its approach must be in the context of the prevalence and interaction with other cardiovascular risk factors such as obesity, diabetes, dislipidemia and smoking among others. The urgent necessity is emphasized to approach in a concatenated form the diverse cardiovascular risk factors, since independently of which they share common pathophysiological mechanisms, its suitable identification and control will affect without any doubt the natural history of the other concatenated risk factor. By all means that to greater participation of factors, greater it will be the global cardiovascular risk but never, however, the specific weight is due to avoid that each one has on the global cardiovascular risk. In this Second edition we try to amplify and give systematic forms for the clinical approach for the suspicion of secondary hypertension and we emphasizes that hypertension in the woman with or without menopause should be careful analyzed, and special recommendations are given for the hypertension in pregnancy. Also we have approached some aspects related to the hypertensive emergencies and other special situations. In this second version some recommendations are presented for boarding hypertension in children and adolescents.

Ionic basis of pharmacological therapy in Brugada syndrome.

An implantable cardioverter-defibrillator is considered the only effective therapy to terminate ventricular arrhythmias in symptomatic patients with Brugada syndrome. However, it does not prevent future arrhythmic episodes. Only antiarrhythmic drug therapy can prevent them. There have been several reports of a beneficial effect of oral quinidine in both asymptomatic and symptomatic patients. Other possible beneficial oral agents could be I(to) blockers. Intravenous isoproterenol has been reported to be especially useful in abolishing arrhythmic storms in emergency situations. Also, isolated case reports on the usefulness of cilostazol, sotalol, and mexiletine have been described. The present article reviews the mechanisms by which these drugs may act and their possible role in the pharmacotherapy of this disease.

Is digitalis compound-induced cardiotoxicity, mediated through guinea-pig cardiomyocytes apoptosis?

Our aim in performing this study was to analyze in vivo the cell death mechanism induced by toxic doses of digitalis compounds on guinea-pig cardiomyocytes. We analyzed three study groups of five male guinea pigs each. Guinea pigs were intoxicated under anesthesia with ouabain or digoxin (at a 50-60% lethal dose); the control group did not receive digitalis. A 5-hours period elapsed before guinea pig hearts were extracted to obtain left ventricle tissue. We carried out isolation of mitochondria and cytosol, cytochrome c and caspase-3 and -9 determination, and electrophoretic analysis of nuclear DNA. TdT-mediated DUTP-X nick end labeling (TUNEL) reaction was performed in histologic preparations to identify in situ apoptotic cell death. Ultrastructural analysis was performed by electron microscopy. Electrophoretic analysis of DNA showed degradation into fragments of 200-400 base pairs in digitalis-treated groups. TUNEL reaction demonstrated the following: in the control group, <10 positive nuclei per field; in the digoxin-treated group, 2-14 positive nuclei per field, while in the ouabain-treated group counts ranged from 9-30 positive nuclei per field. Extracts from ouabain-treated hearts had an elevation of cytochrome c in cytosol and a corresponding decrease in mitochondria; this release of cytochrome c provoked activation of caspase-9 and -3. Electron microscopy revealed presence of autophagic vesicles in cytoplasm of treated hearts. Toxic dosages of digitalis at 50-60% of the lethal dose are capable of inducing cytochrome c release from mitochondria, processing of procaspase-9 and -3, and DNA fragmentation; these observations are mainly indicative of apoptosis, although a mixed mechanism of cell death cannot be ruled out.

Viscum album aqueous extract induces NOS-2 and NOS-3 overexpression in Guinea pig hearts.

Viscum album L. aqueous extract, on the Langendorff isolated and perfused heart model, decreases coronary vascular resistance, when compared to control group (36.00 +/- 2.00 vs. 15.80 +/- 1.96 dyn s cm-5). Our data support the fact that this mechanism involves NOS-2 and NOS-3 overexpression (4.65 and 7.89 times over control, respectively), which is correlated with increases in NO (6.24 +/- 2.49 vs. 147.95 +/- 2.79 pmol) and cGMP production (43.94 +/- 2.00 vs. 74.81 +/- 1.96 pmol mg-1 of tissue), compared to control values. Such an effect is antagonized by gadolinium(III) chloride, L-NAME and ODQ. Therefore, coronary vasodilator effect elicited by V. album L. aqueous extract is mediated by the NO/sGC pathway.

Effect of the digitoxigenin derivative, INCICH-D7, on Na+, K+-ATPase.

Compound 14beta,17beta-cycloketoester-3beta-OH androstane (INCICH-D7) is a semisynthetic product of a structural modification of the digitoxigenin molecule. INCICH-D7 has a heterocyclic ketoester type fusion between positions C14 and C17 of the steroid nucleus, which confers this molecule stronger electronegativity than that of digitoxigenin. INCICH-D7 retained positive inotropic effect, with a greater safety margin, when compared to digitoxigenin and ouabain. In this study we have examinated the INCICH-D7 effect on Na+, K+-dependent adenosinetriphosphatase (Na+, K+-ATPase) and compared these results with the ones observed with digitoxigenin and ouabain. The inhibitory effect of INCICH-D7 on Na+, K+-ATPase was five times lower (IC50=4 microM) than that of ouabain (IC50=0.8 microM) and 70 times lower than that of digitoxigenin (IC50=0.06 microM). The inhibitory effect of INCICH-D7 and ouabain on the enzyme was irreversible while digitoxigenin's one was reversible in up to an 80%. Our results indicate that inclusion of the heterocycle between positions C14 and C17 in the digitoxigenin molecule lowers significantly the inhibitory effect on Na+, K+-ATPase and renders the interaction between INCICH-D7 and enzyme irreversible under the studied reaction conditions.

Prevalance of proteinuria in Mexico: a conjunctive consolidation approach with other cardiovascular risk factors: the Mexican Health Survey 2000.

BACKGROUND: A number of cross-sectional or serial studies have demonstrated the clinical impact of microproteinuria and macroproteinuria by identifying individuals at risk of both end-stage renal disease and major cardiovascular events. This study focused on the prevalence of proteinuria in Mexico and its relationship with other cardiovascular risk factors such as hypertension, type 2 diabetes mellitus, body mass index, smoking, age, and gender. METHODS: The prevalence of proteinuria in Mexico was obtained from the probabilistic cross-sectional national health survey performed in the year 2000. The proportion of urine dipstick samples that tested positive for protein (defined as > or =1+) in adults from 20 to 69 years of age was determined. The analysis was performed using both algebraic and multicategorical models. Potential interactions between proteinuria and other major cardiovascular risk factors were investigated. RESULTS: A total of 46,523 adult survey participants were included in the analysis. In the general population, 9.2% had proteinuria. By univariate, multivariate, and multicategorical analysis, hypertension, diabetes, obesity, and age were strongly associated with the prevalence of proteinuria (P < 0.001). However, in Mexico, the specific distribution of age groups demonstrated that the absolute number of patients without hypertension that had proteinuria is not irrelevant. To identify 1 case of proteinuria, one would need to screen 3 persons with diabetes mellitus, 5 patients with hypertension without diabetes, or 6 persons over the age of 55 years. When proteinuria is present, the probability of having a noncommunicable chronic disease or other major cardiovascular risk factor is more than 85%. CONCLUSION: Proteinuria is prevalent. When considered together, dipstick-positive proteinuria, blood pressure level, body mass index > or =30 m(2)/kg, and abnormal fasting blood glucose measured on a single occasion identifies different segments of the population. Studies such as this may be a suitable initial clinical approach to general population screening for renal and cardiovascular risk stratification.

Drug therapy in Brugada syndrome.

Sudden cardiac death in healthy individuals with structurally normal hearts and a characteristic morphology of the QRS complex resembling a right bundle branch block with elevation of the ST segment in V1 to V3 is known as Brugada syndrome (BrS). Although placement of an implantable cardioverter-defibrillator is considered the only effective therapy for symptomatic patients, some authors have repeatedly reported a beneficial effect of quinidine and isoproterenol in patients with BrS. Also, isolated case reports on the usefulness of cilostazol, sotalol, and mexiletine have been described. The present article reviews the mechanisms by which these drugs may act and their role in the pharmacotherapy of BrS. Other possible agents, mainly I(2) blockers, are also reviewed.

[Early and late effects of adenosine in experimental ventricular tachycardia]. / Efectos tempranos y tardíos de la adenosina en taquicardias ventriculares experimentales.

INTRODUCTION AND OBJECTIVE: To study the action of adenosine in experimental ventricular tachycardia. MATERIAL AND METHOD: We studied 173 mongrel dogs weighing 13-17 kg anesthetized with 30 mg/kg sodium pentobarbital given intravenously. Myocardial lesions were provoked with the injection of 1-1.5 mL phenol in the free wall of the left ventricle. Ventricular arrhythmia was induced 30 min later with aconitine crystals inserted into the periphery of the damaged area. The potential early and delayed antiarrhythmic action of adenosine was systematically investigated in 85 animals. Leads DII, aVR and aVL, unipolar right and left intraventricular leads, and one unipolar lead on the wall of the superior vena cava were used to record control tracings and tracings in the presence of myocardial damage during ventricular tachycardia and after injection of the drug. RESULTS: Sinus rhythm did not reappear in 72 control animals that did not receive adenosine. In the 63 animals with aconitine-induced ventricular tachycardia associated to myocardial damage, the optimal response to 6 mg adenosine-early and fleeting sinus rhythm-was seen in 45% of the dogs; delayed sinus rhythm was seen in 5%. In 67% of the 18 animals with ventricular tachycardia due only to myocardial damage, early and late sinus rhythm appeared with doses of 6 and 12 mg, and late sinus rhythm was seen with a dose of 12 mg. CONCLUSIONS: The antiarrhythmic action of adenosine was seen not only in ventricular tachycardia due to aconitine (triggered activity), but also in tachycardia induced by the myocardial damage (microreentries).

[Hypercholesterolemia and hypertension in Mexico: urban conjunctive consolidation with obesity, diabetes and smoking]. / Hipercolesterolemia e hipertensión arterial en México. consolidación urbana actual con obesidad, diabetes y tabaquismo.

AIMS: To know the prevalence and the interaction among the principal cardiovascular risk factors such as hypercholesterolemia (HCL), hypertension (HTA), overweight, carbohydrates metabolism disturbances, and smoking, an urban survey was performed in the six Mexican Republic states, where the national population is more concentrated. METHODS: This survey was transversally designed using the WHO type-III model in 120,005 adults from 6 highly populated urban centers (Mexico City, Guadalajara, León, Puebla, Monterrey andTijuana) were included. A blood sample from each person was obtained to quantify fasting glucose and cholesterol. Blood pressure, height and weight were measured using daily validated systems. Data were analyzed by a multicategorical conjunctive consolidation model and by multiple regression models. RESULTS: HCL global prevalence showed to be 43.3% for a population with an average age of 44.1 years. Female gender showed a slightly but statistically significant greater prevalence of HCL than male gender (44% vs 42.2%). From whole women population 33.2% declared to be in menopause, and 59.7% of them had HCL. In addition, HCL was directly related to body mass index (BMI). Thus, in those subjects with BMI < 25 showed a HCL prevalence 34.1%; while those with BMI was between 25 and 29.9, the HCL prevalence was 45.9%, and in those subjects with BMI > or = 30 Kg/m2, ranked a HCL prevalence of 47.3%. The prevalence of hypertension was 30.2% and 52.5% of them had HCL prevalence. Type-2 diabetes mellitus prevalence (DM-2) was 10.7%, 55.2% of them had HCL. In the group aged between 20 to 34 years old, the obesity was the principal determinant for higher HCL prevalence. The HCL prevalence showed to be quite similar in population with and without smoking. In conclusion, HCL prevalence shows 4 progressively increasing gradients associated with age, HTA, DM-2 and BMI.

[Arrhythmic activity of the papillary muscle induced by high frequency stimulation: n1 rhythms,transition forms and hysteresis]. / Actividad rítmica del músculo papilar inducida por estimulación de alta frecuencia: ritmos n:1, formas de transición e histéresis.

Cardiac tissues are able to work within a wide range of frequencies to respond to the changing requirements an organism may have. However, during these frequency variations and under certain pathologic conditions arrhythmias such as blocks, tachycardia, fibrillation, etc, may arise some with fatal consequences. For this reason several experimental procedures have been developed that have shown to be useful in studying whole heart properties, or as an alternative from portions of it when changes in its work rate are imposed. This study reports different phenomena occurring in the papillary muscle of the guinea pig heart when stimulated at very high frequency, of several tens of pps, while analyzing its responses during gradual increments starting at 1 (pulses per second). We found that in our conditions papillary muscles display N:1 rhythms with progressive higher N; further more we found that between one and the next rhythm diverse transition patterns appear, among them a new one that we have named "burst pattern". Finally we show that our system exhibits a generalized process of hysteresis by frequency, being this the first report for guinea pig cardiac tissue and the first one to show also the presence of several hysteresis loops in the same experiment. Due to the large volume of generated data we used a faster and easier way to analyze and display them, based on the fast Fourier transform (FFT). The method is briefly described.

Aging in blood vessels. Medicinal agents FOR systemic arterial hypertension in the elderly.

Aging impairs blood vessel function and leads to cardiovascular disease. The mechanisms underlying the age-related endothelial, smooth muscle and extracellular matrix vascular dysfunction are discussed. Vascular dysfunction is caused by: (1) Oxidative stress enhancement. (2) Reduction of nitric oxide (NO) bioavailability, by diminished NO synthesis and/or augmented NO scavenging. (3) Production of vasoconstrictor/vasodilator factor imbalances. (4) Low-grade pro-inflammatory environment. (5) Impaired angiogenesis. (6) Endothelial cell senescence. The aging process in vascular smooth muscle is characterized by: (1) Altered replicating potential. (2) Change in cellular phenotype. (3) Changes in responsiveness to contracting and relaxing mediators. (4) Changes in intracellular signaling functions. Systemic arterial hypertension is an age-dependent disorder, and almost half of the elderly human population is hypertensive. The influence of hypertension on the aging cardiovascular system has been studied in models of hypertensive rats. Treatment for hypertension is recommended in the elderly. Lifestyle modifications, natural compounds and hormone therapies are useful for initial stages and as supporting treatment with medication but evidence from clinical trials in this population is needed. Since all antihypertensive agents can lower blood pressure in the elderly, therapy should be based on its potential side effects and drug interactions.

Endothelial nitric oxide synthase impairment is restored by clofibrate treatment in an animal model of hypertension.

Adequate production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS) requires eNOS coupling promoted by tetrahydrobiopterin (BH(4)). Under pathological conditions such as hypertension, BH(4) is diminished, avoiding eNOS coupling. When eNOS is "uncoupled", it yields a superoxide anion instead of NO. Peroxisome proliferator activated receptors (NR1C) are a family of nuclear receptors activated by ligand. Clofibrate, a member of a hypolipidemic class of drugs, acts by activating the alpha isoform of NR1C. To determine the participation of NR1C1 activation in BH(4) and dihydrobiopterin (BH(2)) metabolism and its implications on eNOS coupling in hypertension, we performed aortic coarctation (AoCo) at inter-renal level on male Wistar rats in order to have a hypertensive model. Rats were divided into the following groups: Sham+vehicle (Sham-V); AoCo+vehicle (AoCo-V); Sham+clofibrate (Sham-C), and AoCo+clofibrate (AoCo-C). Clofibrate (7 days) increased eNOS coupling in the AoCo-C group compared with AoCo-V. Clofibrate also recovered the BH(4):BH(2) ratio in control values and prevented the rise in superoxide anion production, lipoperoxidation, and reactive oxygen species production. In addition, clofibrate increased GTP cyclohydrolase-1 (GTPCH-1) protein expression, which is related with BH(4) recovered production. NR1C1 stimulation re-establishes eNOS coupling, apparently through recovering the BH(4):BH(2) equilibrium and diminishing oxidative stress. Both can contribute to high blood pressure attenuation in hypertension secondary to AoCo.

Myocardial postconditioning: anaesthetic considerations.

"Recently, it has been shown that the heart can be protected against the ischemia-reperfusion injury if brief coronary occlusions are performed just at the beginning of the reperfusion. This procedure has been called postconditioning (PostC). It can also be elicited by pharmacological interventions, which are named pharmacological PostC. In general, PostC reduces the reperfusion- induced injury, blunts oxidant-mediated damages and attenuates the local inflammatory response to reperfusion, decreases infarct size, diminishes apoptosis, neutrophil activation, and endothelial dysfunction. The mechanisms that participate in PostC are still not completely understood. In this regard, adenosine, glycine, bradykinin, ciclosporin A are involved in PostC triggering. Similar to ischemic preconditioning, PostC triggers several signaling pathways and molecular components, including nitric oxide (NO), protein kinase C, adenosine triphosphate-sensitive potassium channels, the Reperfusion Injury Salvage Kinases (RISK) pathway, which comprises phosphatidylinositol-3-OH kinase (PI3K) and extracellular signal-regulated kinase (ERK 1/2), and, finally, the Survivor Activating Factor Enhancement (SAFE) pathway. In this review, we describe the mechanisms of reperfusion-induced injury as well as the proposed protective pathways activated by PostC, which seem to converge in inhibition of mitochondrial permeability transition pores opening. On the other hand, experimental evidence indicates that volatile anesthetics and opioids are capable of exerting cardioprotective effects under certain conditions, constituting a very useful pharmacological PostC. Thus, the first minutes of reperfusion represent a window of opportunity for triggering the aforementioned mediators, which acting in concert lead to protection of the myocardium against reperfusion injury. Pharmacological, especially anesthetic, PostC may have a promising future in the clinical scenarios in the operating room."