Differential effects of saturated and unsaturated fatty acids on vascular reactivity in isolated mesenteric and femoral arteries of rats

Free fatty acid (FFA) intake regulates blood pressure and vascular reactivity but its direct effect on contractility of systemic arteries is not well understood. We investigated the effects of saturated fatty acid (SFA, palmitic acid), polyunsaturated fatty acid (PUFA, linoleic acid), and monounsaturated fatty acid (MUFA, oleic acid) on the contractility of isolated mesenteric (MA) and deep femoral arteries (DFA) of Sprague–Dawley rats. Isolated MA and DFA were mounted on a dual wire myograph and phenylephrine (PhE, 1–10 µM) concentration-dependent contraction was obtained with or without FFAs. Incubation with 100 µM of palmitic acid significantly increased PhE-induced contraction in both arteries. In MA, treatment with 100 µM of linoleic acid decreased 1 µM PhE-induced contraction while increasing the response to higher PhE concentrations. In DFA, linoleic acid slightly decreased PhE-induced contraction while 200 µM oleic acid significantly decreased it. In MA, oleic acid reduced contraction at low PhE concentration (1 and 2 µM) while increasing it at 10 µM PhE. Perplexingly, depolarization by 40 mM KCl-induced contraction of MA was commonly enhanced by the three fatty acids. The 40 mM KCl-contraction of DFA was also augmented by linoleic and oleic acids while not affected by palmitic acid. SFA persistently increased alpha-adrenergic contraction of systemic arteries whereas PUFA and MUFA attenuated PhE-induced contraction of skeletal arteries. PUFA and MUFA concentration-dependent dual effects on MA suggest differential mechanisms depending on the types of arteries. Further studies are needed to elucidate underlying mechanisms of the various effects of FFA on systemic arteries.

Participation of hepatic α/β-adrenoceptors and AT1 receptors in glucose release and portal hypertensive response induced by adrenaline or angiotensin II

It has been previously demonstrated that the hemodynamic effect induced by angiotensin II (AII) in the liver was completely abolished by losartan while glucose release was partially affected by losartan. Angiotensin II type 1 (AT1) and adrenergic (∝1- and β-) receptors (AR) belong to the G-proteins superfamily, which signaling promote glycogen breakdown and glucose release. Interactive relationship between AR and AT1-R was shown after blockade of these receptors with specific antagonists. The isolated perfused rat liver was used to study hemodynamic and metabolic responses induced by AII and adrenaline (Adr) in the presence of AT1 (losartan) and ∝1-AR and β-AR antagonists (prazosin and propranolol). All antagonists diminished the hemodynamic response induced by Adr. Losartan abolished hemodynamic response induced by AII, and AR antagonists had no effect when used alone. When combined, the antagonists caused a decrease in the hemodynamic response. The metabolic response induced by Adr was mainly mediated by ∝1-AR. A significant decrease in the hemodynamic response induced by Adr caused by losartan confirmed the participation of AT1-R. The metabolic response induced by AII was impaired by propranolol, indicating the participation of β-AR. When both ARs were blocked, the hemodynamic and metabolic responses were impaired in a cumulative effect. These results suggested that both ARs might be responsible for AII effects. This possible cross-talk between β-AR and AT1-R signaling in the hepatocytes has yet to be investigated and should be considered in the design of specific drugs.

Síndrome coronario agudo con supradesnivel del ST asociado al feocromocitoma con las catecolaminas inicialmente normales / Acute coronary syndrome with ST elevation associated with pheochromocytoma with initially normal catecholamine values

Los feocromocitomas son tumores secretores de catecolaminas que cursan con paroxismos de hipertensión o hipotensión arterial y palpitaciones. Son una causa rara del síndrome coronario agudo. Presentamos el caso de una paciente con síndrome coronario agudo secundario a feocromocitoma que inicialmente tenía valores normales de catecolaminas.

Pheochromocytomas are catecholamine-secreting tumors that involve paroxysmal hypertension or hypotension and palpitations. They are a rare cause of acute coronary syndrome. We present the case of a patient with acute coronary syndrome secondary to a pheochromocytoma with initially normal catecholamine values.

Tapentadol: Can It Kill Two Birds with One Stone without Breaking Windows?

Tapentadol is a novel oral analgesic with a dual mode of action as an agonist of the µ-opioid receptor (MOR), and as a norepinephrine reuptake inhibitor (NRI) all in a single molecule. Immediate release (IR) tapentadol shows its analgesic effect quickly, at around 30 minutes. Its MOR agonistic action produces acute nociceptive pain relief; its role as an NRI brings about chronic neuropathic pain relief. Absorption is rapid, with a mean maximal serum concentration at 1.25-1.5 h after oral intake. It is present primarily in the form of conjugated metabolites after glucuronidation, and excretes rapidly and completely via the kidneys. The most common adverse reactions are nausea, dizziness, vomiting, and somnolence. Constipation is more common in use of the ER formulation. Precautions against concomitant use of central nervous system depressants, including sedatives, hypnotics, tranquilizers, general anesthetics, phenothiazines, other opioids, and alcohol, or use of tapentadol within 14 days of the cessation of monoamine oxidase inhibitors, are advised. The safety and efficacy have not been established for use during pregnancy, labor, and delivery, or for nursing mothers, pediatric patients less than 18 years of age, and cases of severe renal impairment and severe hepatic impairment. The major concerns for tapentadol are abuse, addiction, seeking behavior, withdrawal, and physical dependence. The presumed problem for use of tapentadol is to control the ratio of MOR agonist and NRI. In conclusion, tapentadol produces both nociceptive and neuropathic pain relief, but with worries about abuse and dependence.

Alpha adrenergic receptors in renal pelvis and calyces: can rat models be used?

We aimed, in this study, to determine the distribution of α-1 AR subtypes in rat and human pelvis and calyces, and to evaluate, by comparing these two species, the possibility of rats to be used as models for humans. Twenty patients with renal carcinoma were included into the study. The patients underwent radical nephrectomy for renal cell carcinoma (RCC). After nephrectomy, specimens were evaluated and excisional biopsies from healthy pelvis and calyces tissues were performed. When pathology confirmed the non-invasion of RCC, specimen was included into the study. A total of 7 adult Wistar Albino (250-300 g) female rats were used in this study. Specimens included renal pelvis and calyces. All specimens were evaluated under light microscope histopathologically. The concentrations of the receptor densities did not differ between the two groups. With the demonstration of the α receptors in rat kidneys and calyces, many receptor-based studies concerning both humans and rats can take place. Novel medication targeting these subtypes -in this matter α1A and α1D for renal pelvis and calyces- may be helpful for expulsive therapy and/or pain relief. With the demonstration of similar receptor densities between human and rat tissues, rat model may be useful for α-receptor trials for renal pelvis and calyces.

Uso de dexmedetomidina en anestesia total intravenosa (TIVA): [revisión] / Use of dexmedetomidine in total intravenous anesthesia (TIVA): [review]

La dexmedetomidina se usó para sedación inicialmente en unidades de cuidados intensivos. Sin embargo, sus efectos sedantes, analgésicos y ansiolíticos sin alteración de la función ventilatoria, permiten ampliar su uso en cirugía como anestésico intravenoso. La literatura reporta su utilidad en poblaciones quirúrgicas definidas, pero aún faltan estudios que respalden su utilización en todos los escenarios de la anestesia total intravenosa (TIVA). El propósito de la actual revisión es describir el papel de la exmedetomidina en la misma. Materiales y métodos. Se realizó la búsqueda de literatura en las bases de datos referenciales de PubMed, Medline, EMBASE, Cochrane y LILACS. Fue ampliada según la bibliografía encontrada en los artículos inicialmente revisados y analizados por los autores; la búsqueda fue hecha bajo los términos MeSH incluidos en las palabras claves.

Dexmedetomidine was used initially for sedation in intensive care units. However, because of its sedative, analgesic and anti-anxiety effects and the fact that it does not alter ventilatory function, its use may be expanded as an intravenous agent in surgery. There are reports in the literature about its effective use in specific surgical populations, although further studies are required in order to support its use in all situations where total intravenous anesthesia (TIVA) is applied. The purpose of this review is to describe the role of dexmedetomidine in this form of anesthesia.Materials y methods. A literature search was conducted in PubMed, Medline, EMBASE, Cochrane and LILACS. The search was expanded based on the references found in the articles reviewed initially and analyzed by the authors; the search was conducted under the MeSH included as key words below.

Modulation of Alpha 1 Adrenergic Receptors on Urinary Bladder in Rat Spinal Cord Injury Model / 대한배뇨장애요실금학회지

PURPOSE: Whereas many studies have focused on the vesical changes of the alpha1 adrenergic receptor (AR) subtypes in partial outlet obstruction, few studies have addressed the modulation of the alpha1 AR subtypes after spinal cord injury (SCI). Therefore, we studied the modulation of the alpha1 ARs in urinary bladder in a rat SCI model. METHODS: Four weeks after a SCI, the whole vesical bodies from eight female Sprague-Dawley rats and from eight controls were harvested. The total RNA was extracted from the samples and was used to prepare cDNA. We developed standard plasmid constructs of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and three alpha1 ARs (alpha1a, alpha1b, and alpha1d) to convert the cycle threshold (Ct) values from real-time polymerase chain reaction (RT-PCR) into subtype mRNA concentrations. The detected Ct values of 16 samples from RT-PCR were interpolated into the standard plasmid curves. RESULTS: All serially diluted standard samples showed very good linearity. The mRNA expression of GAPDH was higher in the SCI group, whereas the mRNA expression of all alpha1 ARs was lower in the SCI group than in the control animals. The alpha1a, alpha1b, and alpha1d mRNA expression in the controls was 81.7%, 3.3%, and 15.1%, respectively, whereas the alpha1a, alpha1b, and alpha1d mRNA expression in the SCI group was 33.5%, 5.2%, and 60.9%, respectively. CONCLUSIONS: SCI moderates the alpha1 AR mRNA subtypes in the urinary bladder. The relatively increased alpha1d or decreased alpha1a AR mRNA expression may be a therapeutic candidate for controlling the symptoms of neurogenic bladder after SCI.

A Case of Hemodynamically Unstable Bradycardia after Risperidone Overdose

Risperidone is an atypical antipsychotic medication commonly used to treat psychotic illness, such as schizophrenia. It has strong serotonin and dopamine receptor antagonism and antagonist activity at alpha-adrenergic receptors and histamine receptors. An overdose of risperidone can cause tachycardia, hypertension, hypotension, prolonged QT interval, and bradycardia. Risperidone overdose is rare,but life-threatening. Here, we present the rare case of a 33- year-old woman who ingested risperidone overdose for the purposes of suicide, developing hemodynamically unstable bradycardia with trifascicular block, leading to fatality. Lessons from our case report are of urgent consideration for temporary pacemaker insertion, and use of alpha-1 agonist, such as phenylephrine in cases of hemodynamically unstable bradycardia by risperidone overdose. Prompt and appropriate identification and interventions are essential for the successful management of risperidone overdose.

Dynamic changes of alpha-AR, beta1-AR and beta2-AR expression during hepatic fibrogenesis / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the dynamic changes of a-AR, b1-AR and b2-AR expression in hepatic fibrosis.</p><p><b>METHODS</b>Rat hepatic fibrosis model was established by bile duct ligation (BDL). HE and Masson staining were used to determine hepatic fibrosis levels. Immunohistochemistry was applied to detect alpha -smooth muscle actin (alpha -SMA), a marker of hepatic stellate cell (HSC) activation; Western blot and real-time RT-PCR were used to measure the dynamic changes of alpha -AR, beta(1)-AR, beta(2)-AR expression on protein and mRNA levels, respectively, during the development of hepatic fibrosis.</p><p><b>RESULTS</b>(1) HE and Masson trichrome staining showed that the liver fibrosis models were established successfully. (2) At 1, 2, 3, 4 wk after BDL, alpha -SMA positive area density of the model group (10.58% +/- 1.75%, 24.14% +/- 2.02%, 29.74% +/- 2.59%, 34.28% +/- 2.01%) was significantly higher than that of the sham operation group (4.12% +/- 1.51%), P less than 0.01. (3) The expression of alpha -AR, beta(1)-AR, beta(2)-AR protein and mRNA was increased with the development of the hepatic fibrosis (P less than 0.05). (4) alpha -SMA expression was positively associated with alpha -AR, beta(1)-AR, beta(2)-AR, r values were 0.564, 0.753 and 0.606, respectively.</p><p><b>CONCLUSION</b>The expression of alpha -SMA is increased dramatically during the fibrosis, and is positively associated with the expression of alpha -AR, beta(1)-AR and beta(2)-AR.</p>

[Analgesic effects of extremely low frequency electromagnetic fields in mice]

Environmental factors such as electromagnetic fields influence the pain sensation. To investigate the possible analgesic effect of extremely low frequency electromagnetic fields [ELF-EMFs] exposure and possible interaction between ELF-EMFs and opioid, alpha and beta adrenergic systems. This was an experimental study in which the effect of 60 Hz magnetic field [100mT] on the pain threshold of 80 male albino mice was investigated. Pain threshold was assessed by the tail immersion technique using water with a temperature of 52 C. The mean pain threshold was significantly increased in case group [5.85 +/- 0.69 sec] compared to control group [3.77 +/- 0.55 sec] following ELF-EMF exposure [p<0.0001]. Pretreatment of animals with naloxane [2 mg/kg] and phentolamine [10 mg/kg] significantly reduced the effect to [3.97 +/- 0.7 sec and 4.01 +/- 0.49 sec], respectively [p<0.0001]. There was no change in the value of mean pain threshold [5.77 +/- 0.68 sec] when propranolol [10 mg/kg] was administered [p<0.0001]. Based on our data, exposure to ELF-EMFs could induce analgesic behavior in mice and the associated effect is related to opioid and alpha-adrenergic systems

Increased autoantibody production against AT(1)-receptors and alpha(1)-adrenergic receptors in hypertensive patients / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe autoantibodies production against AT(1)-receptors and alpha(1)-adrenergic receptors and association to risk factors, such as sex, age, family history, course of hypertension and other cardiovascular diseases in hypertensive patients.</p><p><b>METHODS</b>A total of 690 patients with essential hypertension admitted to our hospital were selected and autoantibodies against AT(1)-receptors and alpha(1)-adrenergic receptors were detected by ELISA. Multiple logistic regression analysis was performed based on obtained data.</p><p><b>RESULTS</b>Positive rates for antibody against AT(1)-receptors and alpha(1)-adrenergic receptors were 47.1% (325/690) and 36.4% (251/690) respectively in this group of patients. Duration of hypertension history was significantly longer in the antibody against AT(1)-receptors and alpha(1)-adrenergic receptors positive groups [(9.3 +/- 11.0) year, (9.9 +/- 11.1) year] compared to the negative groups [(7.3 +/- 9.3) year, (7.2 +/- 9.5) year, all P < 0.01]. The ratio of family history with hypertension was also significantly higher in antibody positive groups than negative ones (47.69% vs 39.18%, P < 0.01). Regression analysis demonstrated that 5 risk factors were related to positive production of autoantibody against AT(1)-receptors including female gender, age, family history, duration of hypertension history and diabetes. However, just age, family history, duration of hypertension history were main factors responsible to the production of autoantibody against alpha(1)-adrenergic receptors (all P < 0.05).</p><p><b>CONCLUSION</b>The environmental and genetic factors contributed to the autoantibody production in patients with essential hypertension.</p>

Common approach to managing lower urinary tract symptoms and erectile dysfunction / 亚洲男科学杂志(英文版)

The present paper serves as a review of the associations between lower urinary tract symptoms (LUTS) and erectile dysfunction (ED), with a focus on common and combined pathways for treatment. LUTS and ED are common conditions seen in general urologic practice. Research has started to establish epidemiologic and pathophysiologic links between the two conditions and a strong association confirmed across multiple studies. Men seeking care for one condition should always be interviewed for complaints of the other condition. Proposed common pathways include alpha-1 adrenergic receptor imbalance, Rho-kinase overactivity, endothelial cell dysfunction and atherosclerosis-induced ischemia. Medical therapy has replaced surgery as the first-line treatment for LUTS in most patients, with the incorporation of alpha-adrenergic receptor antagonists (alpha-ARAs) and 5-alpha-reductase inhibitors (5-ARIs) into everyday practice. Treatment with alpha-ARAs contributes to some improvement in ED, whereas use of 5-ARIs results in worsened sexual function in some patients. Phosphodiesterase-5 (PDE-5) inhibitors have revolutionized the treatment of ED with a simple oral regimen, and new insights demonstrate a benefit of combined use of PDE-5 inhibitors and alpha-ARAs. The mechanisms of action of these medications support these observed benefits, and they are being studied in the basic science and clinical settings. In addition, novel mechanisms for therapy have been proposed based on clinical and research observations. The minimally invasive and surgical treatments for LUTS are known to have adverse effects on ejaculatory function, while their effects on erectile function are still debated. Much remains to be investigated, but it is clear that the associations between LUTS and ED lay the foundation for future therapies and possible preventative strategies.

alpha1-adrenergic receptors activate AMP-activated protein kinase in rat hearts / 生理学报

To test the hypothesis that AMP-activated protein kinase (AMPK) is possibly the downstream signaling molecule of certain subtypes of adrenergic receptor (AR) in the heart, we evaluated AMPK activation mediated by ARs in H9C2 cells, a rat cardiac source cell line, and rat hearts. The AMPK-alpha subunit and the phosphorylation level of Thr(172)-AMPK-alpha subunit were subjected to Western blot analysis. Osmotic minipumps filled with norepinephrine (NE), phenylephrine (PE) or vehicle [0.01% (W/V) vitamin C solution] were implanted into male Sprague-Dawley rats subcutaneously. The pumps delivered NE or PE continuously at the rate of 0.2 mg/kg per hour. After 7-day infusion, the activity of AMPK was examined following immunoprecipitation with anti-AMPK-alpha antibody. At the cellular level, we found that NE elevated AMPK phosphorylation level in a dose- and time-dependent manner, with the maximal effect at 10 micromol/L NE after 10-minute treatment. This effect was insensitive to propranolol, a specific beta-AR antagonist, but abolished by prazosin, an alpha(1)-AR antagonist, suggesting that alpha(1)-AR but not beta-AR mediated the phosphorylation of AMPK. Moreover, the results from rat models of 7-day-infusion of AR agonists demonstrated that the activity of AMPK was significantly higher in NE (7.4-fold) and PE (6.0-fold) infusion groups than that in the vehicle group (P<0.05, n=6). On the other hand, no obvious cardiac hypertrophy and tissue fibrosis changes were observed in PE-infused rats. Taken together, our results demonstrate that alpha(1)-AR stimulation enhances the activity of AMPK, indicating an important role of alpha(1)-AR stimulation in the regulation of AMPK in the heart. Understanding the activation of AMPK mediated by alpha(1)-AR might have clinical implications in the therapy of heart failure.

The role of adrenergic receptor polymorphisms in heart failure

The main function of the cardiac adrenergic system is to regulate cardiac work both in physiologic and pathologic states. A better understanding of this system has permitted the elucidation of its role in the development and progression of heart failure. Regardless of the initial insult, depressed cardiac output results in sympathetic activation. Adrenergic receptors provide a limiting step to this activation and their sustained recruitment in chronic heart failure has proven to be deleterious to the failing heart. This concept has been confirmed by examining the effect of ß-blockers on the progression of heart failure. Studies of adrenergic receptor polymorphisms have recently focused on their impact on the adrenergic system regarding its adaptive mechanisms, susceptibilities and pharmacological responses. In this article, we review the function of the adrenergic system and its maladaptive responses in heart failure. Next, we discuss major adrenergic receptor polymorphisms and their consequences for heart failure risk, progression and prognosis. Finally, we discuss possible therapeutic implications resulting from the understanding of polymorphisms and the identification of individual genetic characteristics.

Hypersensitization of alpha-adrenoreceptor of artery smooth muscle in hypertensive rats and hypertensive patients / 药学学报

<p><b>AIM</b>To investigate the hypersensitization of alpha-adrenoreceptor of artery smooth muscle in hypertensive patients and rats and the mechanisms concerned.</p><p><b>METHODS</b>Isometric tension of artery ring segments was recorded by a sensitive myograph system in vitro and the relative amount of alpha-adrenoreceptor mRNA was quantified by a real-time PCR.</p><p><b>RESULTS</b>Noradrenaline (NA)-induced concentration-contraction curve of mesenteric artery segments in spontaneously hypertensive rats (SHR) was more potent than that in Wistar-Kyoto (WKY) rats. The E(max) of NA in SHR was 1.82 times of that of WKY. The concentration-contractile curve induced by NA in great omental arteries of hypertensives significantly shifted toward left and the pD2 value of NA was larger than that of normotensives. After organ culture, the concentration-contractile curves of SD rat mesenteric artery induced by NA shifted toward left with significantly increased E(max). The relative amounts of mRNA for alpha1-adrenoreceptor was increased, but mRNA level for alpha2-adrenoreceptor did not change.</p><p><b>CONCLUSION</b>The sensitivity of alpha1-adrenoreceptor of artery smooth muscle in hypertensive man and rat is enhanced, suggesting alpha1-adrenoreceptor is upregulated.</p>

Electrophysiological effects of neurotransmitters on pacemaker cells in guinea pig left ventricular outflow tract / 生理学报

This study was designed to explore the innervation of autonomic nervous system and the distribution of receptors on pacemaker cell membrane in guinea pig left ventricular outflow tract (aortic vestibule). By using conventional intracellular microelectrode technique to record action potentials, autonomic neurotransmitters and antagonists were used to investigate the electrophysiological features and regularities of spontaneous activity of left ventricular outflow tract cells. Electrophysiological parameters examined were: maximal diastolic potential (MDP), amplitude of action potential (APA), maximal rate of depolarization (V(max)), velocity of diastolic depolarization (VDD), rate of pacemaker firing (RPF), 50% and 90% of duration of action potential (APD(50) and APD(90)). The results are listed below: (1) Perfusion with 100 mumol/L isoprenaline (Iso) resulted in a significant increase in V(max) (P <0.05), VDD, RPF, and APA (P <0.01), a notable decrease in MDP (P<0.05), and also a marked shortening in APD(50) (P<0.01). Pretreatment with Iso (100 mumol/L), propranolol (5 mumol/L) significantly decreased RPF and VDD (P<0.01), decreased APA, MDP and V(max) (P<0.01) notably, prolonged APD(50) (P<0.01) and APD(90) (P<0.05) markedly. (2) Application of 100 mumol/L epinephrine (E) resulted in a significant increase in VDD (P<0.05), RPF (P<0.001), V(max) (P<0.05) and APA (P<0.001), and a notable shortening in APD(50) and APD(90) (P<0.05). (3) Perfusion with 100 mumol/L norepinephrine (NE) led to a significant increase in VDD, RPF, APA and V(max) (P<0.05), and a marked shortening in APD(50) (P<0.05). Pretreatment with NE (100 mumol/L), phentolamine (100 mumol/L) significantly decreased RPF and VDD, MDP and APA (P<0.01), decreased V(max) notably (P<0.05), prolonged APD(50) and APD(90) markedly (P<0.01). (4) During perfusion with 10 mmol/L acetylcholine (ACh), VDD and RPF slowed down notably (P<0.05), APA decreased significantly (P<0.001), V(max) slowed down notably (P<0.01), APD50 shortened markedly (P<0.05), Atropine (10 mmol/L) antagonized the effects of ACh (10 mumol/L) on APD(50) (P<0.05). These results suggest that there are probably alpha-adrenergic receptor (alpha-AR), beta-adrenergic receptor (beta-AR) and muscarinic receptor (MR) on pacemaker cell membrane of left ventricular outflow tract in guinea pig. The spontaneous activities of left ventricular outflow tract cells are likely regulated by sympathetic and parasympathetic nerves.

Study on the interactions between Ligusticum chuanxiong extract and cardiac muscle membrane receptors by CMSP chromatography / 中国中药杂志

<p><b>OBJECTIVE</b>To study the interactions between Ligusticum chuanxiong Hort extract and cardiac muscle membrane receptors.</p><p><b>METHOD</b>The cell membrane of rabbit cardiac muscle was fixed on silicon to make cell membrane stationary phase (CMSP), and then the interactions were studied by comparing the retention characteristics of the extracts from different solvents with those of the antagonists or activators corresponding to known receptors in cardiac muscle membrane, and by competition effect on the retention characteristics of extracts when adding the antagonists or activators into the mobile phase.</p><p><b>RESULT</b>Water extract and ethanol extract both had retentions on CMSP; the retention characteristics of water extract could be affected when water extract was in competition with the antagonists for alpha receptor, and could not be affected when with the activator beta1 receptor.</p><p><b>CONCLUSION</b>It is possible that some components in water extract may combine with alpha receptor and no component with beta1 receptor, and that some components in ethanol extract may combine with cardiac muscle cell membrane. The process between active components and receptors in vivo can be imitated through the interactions between drugs and CMSP. The method provides references for the resolution of two applications: to screen the active components from Chinese medicine, and to figure out the type of receptors involved.</p>

alpha-Adrenoceptor Antagonistic Effect of Palmatine on the Prostatic Urethral Pressure of the Rabbit / 대한비뇨기과학회지

PURPOSE: Palmatine is an isoquinoline alkaloid, with multiple pharmacological actions, including anti-inflammatory activity. The aim of this study was to examine the effect of palmatine on the prostatic urethral pressure in anesthetized rabbit. MATERIALS AND METHODS: 10-week-old male New Zealand White rabbits (3.0-3.5kg) were used in the experiment. After anesthetized with urethane (800mg/kg i.v.), a midline incision was made, and the urinary bladder completely drained. To prevent filling of the bladder, polyethylene tubes were inserted into the bilateral ureters. Using a 3-F MIKRO-TIP catheter transducer positioned in the prostatic urethra, urethral pressure was recorded continuously. To record the blood pressure, the left femoral artery was cannulated with an angiocatheter. After a stabilizing period, phenylephrine (1mug/kg) was intravenously administered two or three times. When the increase in the urethral pressure became stable, palmatine was administered intravenously (0.5-3.0mg/kg), followed by phenylephrine, with no time interval. RESULTS: In the anesthetized rabbits, an intravenous bolus injection of palmatine (0.5-3.0mg/kg) caused no significant change in the resting prostatic urethral pressure (p>0.05), but decreased the blood pressure (p<0.05). After administration of phenylephrine, the urethral pressure increased from 7.5 0.8 mmHg to 26.5 2.6 mmHg, with the difference in the pressure (19.0 3.1 mmHg) being statistically significant (p<0.01). The intravenously administered palmatine (0.5-3.0mg/kg) dose-dependently inhibited the phenylephrine-induced increases in the prostatic urethral pressure and mean blood pressure. The maximal inhibition was obtained when a palmatine dose of 3.0mg/kg was administered, at which point, the decrease in the urethral pressure was 73.1% (p<0.01). CONCLUSIONS: These results indicate that palmatine inhibits the phenylephrine-induced increases in the prostatic urethral pressure and blood pressure in the anesthetized rabbits.

Intoxicación inusual con amitraz / Unusual intoxication with amitraz

El amitraz (1,5 di-(2,4-dimetifenil)-1,3,5-triaza-penta-1,4 dieno) es una formamidina, miembro de la familia química de las amidinas, de uso externo en la medicina veterinaria y en la agricultura como insecticida, antiparasitario y acaricida. La documentación y la experiencia clínica con intoxicación por amitraz es escasa habiendo solo 33 casos de intoxicación humana previamente publicados en la literatura. El propósito de este trabajo fue reportar tres nuevos casos graves, siendo los primeros cinco años en nuestro Instituto, quienes sobrevivieron a pesar de ingerir gran cantidad de amitraz. Se revisan las manifestaciones clínicas observadas en los tres casos, caracterizadas por signos típicos de depresión del S.N.C y estimulación alfa 2-adrenergica, además de sus complicaciones y tratamiento

Medical Treatment of the Benign Prostatic Hyperplasia

The search for nonhormonal pharmacological agents capable of reducing out flow obstruction caused by benign prostatic hyperplasia (BPH) began in the 1970s when alpha adrenergic receptors were demonstrated within the smooth muscle element of prostatic adenomas, the prostatic capsule, and the bladder neck. Recently, many studies have confirmed that the alpha adrenoceptor blockade sub-jectively and objectively reduces symptoms and urodynamic parameters in bladder outflow obstruction. Very longterm effects of the alpha blockade upon the pro-state are not yet known. There is no direct evidence of a decrease in the stromal smooth muscle bulk or in the total prostate volume after longterm treatment with alpha adrenoceptor blockers in man. The endocrinebased therapies, such as stilbestrol, luteinizing hormonereleasing hormone analogues, antiandrogens flutamide, and cyproterone acetate, have sometimes been used to treat BPH, but with a limited efficacy and prominent sideeffects such as loss of libido, impotence, hot flushes, and gynecomastia. Although it has been shown that some of these therapies may shrink the prostate, the sideeffects are intolerable to most patient. On the other hand, new 5 alpha reductaseinhibiting agents are able to block the effects of androgen within the prostate without a systemic antiandrogen activity. Since the effects of androgens are particularly directed at the glandular element of the prostate rather than at the smooth muscle, the combined use of alphaadrenoceptor blockers and 5 alphareductase inhibitors could theoretically produce an additive effect in the treatment of BPH. The indications of medical treatment for BPH include patients with mild to moderate symptoms, especially if they are reluctant to undergo surgery, and those who are not medically eligible to surgery.