Intravenous Catecholamine Administration Research Articles

Pulmonary CT perfusion robustly measures cardiac output in the context of multilevel pulmonary occlusion: a porcine study

BackgroundTo validate pulmonary computed tomography (CT) perfusion in a porcine model by invasive monitoring of cardiac output (CO) using thermodilution method.MethodsAnimals were studied at a single center, using a Swan-Ganz catheter for invasive CO monitoring as a reference. Fifteen pigs were included. Contrast-enhanced CT perfusion of the descending aorta and right and left pulmonary artery was performed. For variation purposes, a balloon catheter was inserted to block the contralateral pulmonary vascular bed; additionally, two increased CO settings were created by intravenous administration of catecholamines. Finally, stepwise capillary occlusion was performed by intrapulmonary arterial injection of 75-μm microspheres in four stages. A semiautomatic selection of AFs and a recirculation-aware tracer-kinetics model to extract the first-pass of AFs, estimating blood flow with the Stewart-Hamilton method, was implemented. Linear mixed models (LMM) were developed to calibrate blood flow calculations accounting with individual- and cohort-level effects.ResultsNine of 15 pigs had complete datasets. Strong correlations were observed between calibrated pulmonary (0.73, 95% confidence interval [CI] 0.6–0.82) and aortic blood flow measurements (0.82, 95% CI, 0.73–0.88) and the reference as well as agreements (± 2.24 L/min and ± 1.86 L/min, respectively) comparable to the state of the art, on a relatively wide range of right ventricle-CO measurements.ConclusionsCT perfusion validly measures CO using LMMs at both individual and cohort levels, as demonstrated by referencing the invasive CO.Relevance statementPossible clinical applications of CT perfusion for measuring CO could be in acute pulmonary thromboembolism or to assess right ventricular function to show impairment or mismatch to the left ventricle.Key points• CT perfusion measures flow in vessels.• CT perfusion measures cumulative cardiac output in the aorta and pulmonary vessels.• CT perfusion validly measures CO using LMMs at both individual and cohort levels, as demonstrated by using the invasive CO as a reference standard.Graphical

Risk Stratification for Acute Pulmonary Embolism in Patients with Atrial Fibrillation: Role of CHADS2 Score.

AbstractPulmonary embolism (PE) is associated with atrial fibrillation (AF). This study sought to explore if the CHADS2 score could predict the prognosis of PE in patients with AF. In a tertiary hospital, 4,288 consecutive patients with diagnosis of PE were screened. In total, 305 patients with PE had AF and were included in this retrospective study. In-hospital outcome was defined as at least one of the following: death from any cause, need for intravenous catecholamine administration, endotracheal intubation, cardiopulmonary resuscitation, or thrombolytic therapy. The in-hospital outcome occurred in 10.2% of the patients. Patients with adverse outcome had higher CHADS2 score, CHA2DS2-VASc score, and simplified pulmonary embolism severity index (sPESI) score. The area under the receiver operating characteristics curve was 0.66, 0.62, and 0.71 for CHADS2 score, CHA2DS2-VASc score, and sPESI score, respectively, in predicting in-hospital outcome. The incidence of in-hospital outcome was 3.4 and 14.4% in sPESI = 0 and sPESI ≥1 groups (p < 0.01). CHADS2 also had good predictive value with the incidence of in-hospital outcome, being 4.6% in CHADS2 < 2 and 14.3% in CHADS2 ≥ 2 groups (p < 0.01). The incidences of in-hospital outcome were 2.6, 4.8, 7.4, and 17.3% in patients with sPESI = 0 and CHADS2 < 2, sPESI = 0 and CHADS2 ≥ 2, sPESI ≥ 1 and CHADS2 < 2, and sPESI ≥ 1 and CHADS2 ≥ 2 (p < 0.01), respectively. In multivariable analysis, CHADS2 (odds ratio: 1.50; 95% confidence interval: 1.11–2.02; p < 0.01) was an independent predictor of in-hospital adverse outcome. High CHADS2 score could predict worse in-hospital outcome in patients with PE and AF.

Atypical or Variant stress cardiomyopathy

Sir, We would like to describe atypical or variant type of stress cardiomyopathy (SCM) wherein there is no involvement of the apical segment of the heart, in the background of recent publication in Indian Journal of Anaesthesia.[1] The prevalence of SCM is estimated to be 1.2-2.2%, and the atypical SCM constitutes 40% of these cases.[2] Intravenous administration of catecholamines and adenosine receptor antagonists has been reported in association with reverse SCM.[3] We hereby report a case of a young woman who developed atypical SCM postoperatively. A 23-year-old female with refractory chylous ascites was posted for surgical sealing of chylous leak. She had undergone diagnostic laparoscopy 1 week back, wherein 10 litres (L) of ascitic chylous fluid was removed. She was thin built, malnourished and had recurrence of ascites which was tense. She was given general anaesthesia combined with epidural analgesia (put on pre-induction, under local anaesthesia). On opening the abdomen, there were multiple sites of chylous leak, and the surgery took 7–8 h. She lost around 5–6 L of ascitic fluid, which was replaced with albumin (8 g/L loss). Central venous pressure was maintained between 6 and 10 mmHg. During the surgery, she developed hypotension, which did not respond to intravenous fluids. Noradrenaline, vasopressin and adrenaline were started subsequently. Intraoperatively, there were no electrocardiographic (ECG) changes. At the end of the surgery, she was on only adrenaline 0.16 μg/kg/min. She was extubated and shifted to the Intensive Care Unit. Her total input was 8000 ml of crystalloids and 1000 ml of colloids. Total urine output was 1050 ml and chylous tap was 5600 ml. On the post-operative day 1, she had an episode of sinus tachycardia which soon returned to normal without any intervention. After 2 h, her ECG showed ST elevation in I, aVL, V5-V6 leads and T inversion in V1–V2 [Figure 1]. Echocardiogram showed moderate left ventricular (LV) dysfunction and inferior wall hypokinesia. Troponin levels and emergency coronary angiogram done were normal; hence, a diagnosis of inverted SCM was made. She was treated with carvedilol, heparin and noradrenaline. She was discharged after 4 weeks with normal ECG, echocardiogram [Figure 2] and stable haemodynamics, with no chylous leak.Figure 1: Electrocardiograph 1Figure 2: Electrocardiograph 2Four types of atypical SCM have been described depending on the patterns of LV involvement:[45] (1) inverted/reverse (2) mid-ventricular (3) localised and (4) global type. The difference in the distribution, density and sensibility of adrenergic receptors over the myocardium determines the area of hypokinesis.[46] The area with a highest density of adrenergic receptors being the most affected. The most common of these forms is the inverted type with hyperdynamic apex and akinetic base of the LV.[6] This phenomenon explains why typical SCM occurs more often in older patients where adrenoreceptors density in the apex is reduced because of hormonal change, while atypical variant occurs in younger patients.[24] Inverted SCM is more often associated with either mental or physical stress. It presents with a lower prevalence of T-wave inversion.[4] Release of troponin is higher, which is the consequence of the larger muscle region involved. Natriuretic peptides are more elevated in apical and mid-ventricular patterns, which is evident by more severe symptoms. Younger patients with a poor general condition when undergoing major surgeries can develop SCM perioperatively. Refractory intra-operative hypotension treated with catecholamines might be the cause. This can be atypical in presentation. Increased awareness leads to timely use of intra-operative trans-oesophageal echocardiogram, early diagnosis and proper intervention. As recurrence rate is high, due care is required during future surgeries also. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest. Acknowledgement We sincerely thank the Department of Anaesthesiology, KIMS, for their support and technical help.

High Levels of Circulating Epinephrine Trigger Apical Cardiodepression in a β 2 -Adrenergic Receptor/G i –Dependent Manner

Background— Takotsubo cardiomyopathy is an acute heart failure syndrome characterized by myocardial hypocontractility from the mid left ventricle to the apex. It is precipitated by extreme stress and can be triggered by intravenous catecholamine administration, particularly epinephrine. Despite its grave presentation, Takotsubo cardiomyopathy is rapidly reversible, with generally good prognosis. We hypothesized that this represents switching of epinephrine signaling through the pleiotropic β 2 -adrenergic receptor (β 2 AR) from canonical stimulatory G-protein–activated cardiostimulant to inhibitory G-protein–activated cardiodepressant pathways. Methods and Results— We describe an in vivo rat model in which a high intravenous epinephrine, but not norepinephrine, bolus produces the characteristic reversible apical depression of myocardial contraction coupled with basal hypercontractility. The effect is prevented via G i inactivation by pertussis toxin pretreatment. β 2 AR number and functional responses were greater in isolated apical cardiomyocytes than in basal cardiomyocytes, which confirmed the higher apical sensitivity and response to circulating epinephrine. In vitro studies demonstrated high-dose epinephrine can induce direct cardiomyocyte cardiodepression and cardioprotection in a β 2 AR-Gi–dependent manner. Preventing epinephrine-G i effects increased mortality in the Takotsubo model, whereas β-blockers that activate β 2 AR-G i exacerbated the epinephrine-dependent negative inotropic effects without further deaths. In contrast, levosimendan rescued the acute cardiac dysfunction without increased mortality. Conclusions— We suggest that biased agonism of epinephrine for β 2 AR-G s at low concentrations and for G i at high concentrations underpins the acute apical cardiodepression observed in Takotsubo cardiomyopathy, with an apical-basal gradient in β 2 ARs explaining the differential regional responses. We suggest this epinephrine-specific β 2 AR-G i signaling may have evolved as a cardioprotective strategy to limit catecholamine-induced myocardial toxicity during acute stress.

Reverse Takotsubo Cardiomyopathy Associated With the Consumption of an Energy Drink

A 24-year-old man presented to the emergency room with chest pain, acute respiratory failure, and palpitations shortly after the ingestion of small amounts of an energy drink in little cups one after another. He was afebrile, with frequent runs of supraventricular and ventricular tachycardia and underlying sinus tachycardia. The patient was treated with fluids and metoprolol but required intubation because of progressive hypoxia. Chest x-ray revealed bilateral fluffy pulmonary infiltrates. His ECG was free of ischemic changes, and an echocardiogram at that time showed hypokinesis of all basal left ventricular segments with apical sparing and an ejection fraction of 35% (Figure 1 and Movie I in the online-only Data Supplement). His troponin was mildly increased and serially measured brain natriuretic peptide was elevated at 8000 pg/mL. Figure 1. ECG recorded at admission showing sinus tachycardia and nonspecific T-wave inversion in leads I and aVL. After treatment with furosemide, nitroglycerine, heparin, and aspirin, the patient responded with clinical improvement of vital signs and chest x-ray. Episodes of agitation and delirium ensued, delaying extubation. Computerized tomography brain scan and electroencephalogram were negative, and toxicological testing demonstrated no cocaine, cannabis, or …

Stress Cardiomyopathy After Intravenous Administration of Catecholamines and Beta-Receptor Agonists

The aim of this study was to report a series of patients with stress cardiomyopathy precipitated by the intravenous administration of catecholamines and beta-receptor agonists. Stress cardiomyopathy is a syndrome of transient cardiac dysfunction precipitated by intense emotional or physical stress. Excessive sympathetic stimulation is believed to be central to the pathogenesis of this disorder, but a causal link has not been convincingly demonstrated. We observed 9 cases of stress cardiomyopathy precipitated immediately by the intravenous administration of epinephrine (n = 6) or dobutamine (n = 3). Patients were evaluated with coronary angiography and with serial echocardiography, electrocardiography, and cardiac enzymes. The median age was 44 years (interquartile range [IQR]: 30 to 48 years), and 7 (78%) were woman. Troponin-I was mildly elevated (median 4.07 ng/ml, IQR: 0.47 to 5.63 ng/ml), but none of the patients undergoing angiography had obstructive coronary disease. All patients developed corrected QT interval (QTc interval) prolongation (median QTc interval 504 ms, IQR: 477 to 568 ms) within 24 h of receiving drug. All 3 previously described variants of left ventricular "ballooning" (apical, midventricular, and basal) were observed. The median ejection fraction on admission was 35% (IQR: 35% to 40%). During follow-up (median 7 days, IQR: 4 to 13 days) there was recovery of left ventricular systolic function in all patients (median ejection fraction 55%, IQR: 40% to 60%, p < 0.001 vs. admission). Exposure to catecholamines and beta-receptor agonists used routinely during procedures and diagnostic tests can precipitate all the features of stress cardiomyopathy, including cardiac isoenzyme elevation, QTc interval prolongation, and rapidly reversible cardiac dysfunction. These observations strongly implicate excessive sympathetic stimulation as central to the pathogenesis of this unique syndrome.

Apical and Non-Apical Variants of Stress Cardiomyopathy Following Intravenous Catecholamine Administration

Background: Stress cardiomyopathy (SCM) is a syndrome of transient left ventricular (LV) dysfunction precipitated by acute stress. While the majority of patients present with apical and mid-ventricular dysfunction with sparing of the base (apical ballooning), variants have been reported in which the apex is spared and only mid-ventricular or basal segments are affected. Excessive sympathetic stimulation is believed to underlie the pathogenesis of SCM, but it is unknown whether direct catecholamine infusion can reproduce the clinical features of this disorder.

Ｃａｒｏｔｉｄ ａｒｔｅｒｙ ｓｔｅｎｔｉｎｇにおける遷延性低血圧発生の予測因子の検討

We evaluated predictive factors for prolonged hypotension after carotid artery stenting by retrospectively analyzing 88 lesions of 77 consecutive patients (mean age: 69.9±8.0 years). Easy Wall stent was applied in 14 lesions, SMART stent in 35, Protégé stent in 15, Aurora stent in 11 and Precise stent in 13. We investigated correlations between the incidence of prolonged (≧3 hours) hypotension below 90 mmHg and clinical characteristics, angiographic findings and kind of deployed stents. Postprocedural hypotension occurred in 44 lesions (50%), and medical treatment (intravenous administration of catecholamines) was required in 21 lesions (23.9%). Although there was no permanent neurological deficits related with postprocedural hypotension, transient neurological deficits including consciousness disturbance were found in 5 patients. Predictive factors of prolonged hypotension were assessed by univariate and multivariate analyses. Among angiographic characteristics, calcifications at the carotid bifurcation (present vs. absent: p=0.004) were statistically significant on multivariate analysis. Although other variables including age, gender, side of lesion and degree of stenosis were not associated with postprocedural hypotension after carotid stenting, SMART (eR) stent and Protégé stent were accompanied with frequent occurrence of prolonged hypotension in this study. Among angiographic variables, the presence of calcification at the carotid bifurcation can be used to identify patients at risk for postprocedural hypotension after carotid stenting. Furthermore, such identification may help us prevent a perioperative complication of CAS for high-risk patients.

Risk Factors of Postprocedural Hypotension following Carotid Artery Stenting

This study is performed to investigate risk factors of hypotension in response to elective carotid stenting. Forty-four lesions of 40 consecutive patients (mean age 70.4 +/- 8.2 years) were retrospectively analyzed. Easy Wall stent was applied in 15 lesions and SMART stent in 29 lesions. We investigated correlations between the occurrence rate of postoperative hypotension below 90 mmHg and persisting over three hours and findings of preoperative angiograms, ultrasonograms and clinical characteristics. Postprocedural hypotension occurred in 19 patients (47.5%) and medical treatment (intravenous administration of catecholamines) was required in eleven patients (27.5%). Although there was no permanent neurological deficits related with postprocedural hypotension, transient neurological deficits were found in three patients. Risk factors of prolonged postprocedural hypotension were statistically analyzed. On angiographic characteristics; 1) distance between the carotid bifurcation and the lesion with maximum stenosis (</= 10 mm vs. > 10 mm: p=0.031), 2) type of stenosis (eccentric vs. concentric: p=0.014) On ultrasonographic characteristics; 1) calcifications at the carotid bifurcation (present vs. absent: p < 0.001). Other variables, including age and degree of stenosis, were not associated with postprocedural hypotension after carotid stenting. These angiographic and ultrasonographic variables can be used to identify patients at risk for postprocedural hypotension after carotid stenting. Such identification may help in selection of patients who will benefit from appropriate pharmacological treatment.

Intravenous catecholamine administration affects mouse intestinal lymphocyte number and apoptosis

The purposes of this study were to determine plasma and intestinal epinephrine (E) and norepinephrine (NE) concentrations in mice after exercise stress and, the effect of intravenous injection of E and NE (at concentrations during exercise) on viability of intestinal lymphocytes (IL). Exhaustive exercise significantly elevated plasma E and NE, and intestinal E, compared with sedentary animals. Twenty-four hours after intravenous NE administration, IL counts were higher (p<0.001) and % apoptotic IL were lower ( p<0.001) than saline conditions. E resulted in fewer apoptotic IL at 24 h compared to saline controls. E and NE differentially influence IL numbers at 24 h after injection although both result in fewer % apoptotic IL relative to mice given saline only.

Models of dilated cardiomyopathy in small animals and novel positive inotropic therapies.

Several randomized clinical trials of vesnarinone and milrinone in patients with heart failure left disappointing results in the 1990s. Thereafter, use of positive inotropic agents has been avoided. Exceptions are the use of digitalis glycosides to treat mild-moderate heart failure and the intravenous administration of catecholamines and phosphodiesterase inhibitors in patients with acute and/or refractory heart failure. It is not, however, exactly known whether chronic enhancement of cardiac contractility indeed has harmful effects, besides increased risk of arrhythmia and mortality. We investigated the potential chronic benefit of positive inotropic modification to treat progressive cardiomyopathy and associated heart failure using a genetic complementation strategy of muscle lim-protein and phospholamban (PLN) double mutagenesis in the mouse and found clear evidence of positive effects. Subsequent somatic modification of PLN function via gene transfer with recombinant adeno-associated virus vectors in small animal models of dilated cardiomyopathy further supported the chronic benefit of enhanced cardiac function achieved in an beta-adrenergic stimulus-independent manner. This study examines current small animal models of dilated cardiomyopathy and recent multiple attempts to use these models as novel gene-based inotropic therapies.

Surgical treatment of patients with psychiatric disorders: a review of 21 patients.

Between January 1985 and September 1994, 21 patients with psychiatric disorders underwent various forms of surgery at our hospital. There were 12 men and 9 women with an average age of 57.6 years. The coexisting psychiatric disorders were schizophrenia in 15 patients, depression in 2, dementia in 2, mental retardation with epilepsy in 1, and Parkinson's disease in 1. All the patients had been receiving neuroleptic medications for a long period. The indications for surgery were: cholelithiasis in 6 patients, acute appendicitis in 4, perforation of the small intestine in 3, incarceration of an inguinal hernia in 2, and esophageal cancer, stomach cancer, bleeding from a gastric ulcer, perforation of a duodenal ulcer, strangulating ileus, and burns in 1 patient each, respectively. All of the patients who underwent elective surgery were given epidural anesthesia with or without general anesthesia. Antipsychotic medications were given until just prior to surgery and recommenced concurrent with the first meal. Abnormal behavior was observed in 11 patients (52.4%) postoperatively, but all the patients were discharged in accordance with recovery from their surgical disorder. Intra- and postoperative hypotension resistant to intravenous catecholamine administration was recognized in 9 patients (42.9%), and this peculiar complication should be borne in mind when patients with psychiatric disorders require surgical management.

Risk Factors of Postprocedural Hypotension following Carotid Artery Stenting

This study is performed to investigate risk factors of hypotension in response to elective carotid stenting. Forty-four lesions of 40 consecutive patients (mean age 70.4 ± 8.2 years) were retrospectively analyzed. Easy Wall stent was applied in 15 lesions and SMART stent in 29 lesions. We investigated correlations between the occurrence rate of postoperative hypotension below 90 mmHg and persisting over three hours and findings of preoperative angiograms, ultrasonograms and clinical characteristics. Postprocedural hypotension occurred in 19 patients (47.5%) and medical treatment (intravenous administration of catecholamines) was required in eleven patients (27.5%). Although there was no permanent neurological deficits related with postprocedural hypotension, transient neurological deficits were found in three patients. Risk factors of prolonged postprocedural hypotension were statistically analyzed. On angiographic characteristics; 1) distance between the carotid bifurcation and the lesion with maximum stenosis (≦10 mm vs. &gt;10 mm: p = 0.031), 2) type of stenosis (eccentric vs. concentric: p = 0.014) On ultrasonographic characteristics; 1) calcifications at the carotid bifurcation (present vs. absent: p&lt;0.001). Other variables, including age and degree of stenosis, were not associated with postprocedural hypotension after carotid stenting. These angiographic and ultrasonographic variables can be used to identify patients at risk for postprocedural hypotension after carotid stenting. Such identification may help in selection of patients who will benefit from appropriate pharmacological treatment.

Antiadrenergic cardiovascular adverse effects of high-dose amiodarone loading regimen

A 55-year-old patient with inferior wall infarction was treated effectively for ventricular tachycardia with high-dose oral amiodarone loading regimen (5 g within 16 hours). Serial pharmacokinetic studies demonstrated a rapid temporary increase in amiodarone plasma concentration to a maximum of 3.40 μg/ml 17 hours after initiation of therapy followed by a return to normal plasma concentration within 8 hours. During fast drug evasion the patient developed acute low-output syndrome with syncope successfully controlled with intravenous catecholamine administration. Our findings suggest that the cardiovascular collapse was caused by the non-competitive adrenoceptor antagonism of amiodarone resulting in secondary autonomic insufficiency.

Inhibition of a peripheral sympathetic-cholinergic system by presynaptic alpha 2-adrenoceptors.

Intravenous administration of catecholamines produced dose-related inhibition of electrodermal responses (EDRs) evoked by electrical stimulation of the post-ganglionic sciatic nerve in anaesthetized rats, with relative potencies being (-)-adrenaline greater than (+/-)-adrenaline greater than (-)-noradrenaline = (+)-adrenaline. The suppression of EDRs by (+/-)-adrenaline and (-)-noradrenaline was blocked by pretreatment with yohimbine (0.75 mg/kg i.v.) but not by prazosin (0.3 mg/kg i.v.). The selective alpha 2-adrenoceptor agonist B-HT 920 also inhibited neurally evoked skin potential responses. This effect of B-HT 920 was antagonized by the selective alpha 2-adrenoceptor antagonist idazoxan (0.1 mg/kg i.v.) but was insensitive to prazosin. Idazoxan was more potent than yohimbine in blocking (+/-)-adrenaline-induced suppression of EDRs. Methacholine administered into the femoral artery evoked EDRs by an atropine-sensitive mechanism. Methacholine-induced EDRs were not suppressed by intravenous administration of (-)-adrenaline (1 microgram/kg or 3 micrograms/kg) whereas EDRs evoked by the sciatic nerve stimulation on the other hindpaw were inhibited. Increase in the endogenous catecholamines by asphyxia strongly inhibited EDRs by a mechanism which was also sensitive to yohimbine but not to prazosin. These results suggest that peripheral presynaptic alpha 2-adrenergic mechanisms are involved in inhibition of transmitter release in this sympathetic-cholinergic system.

Effects of catecholamines on hemodynamics and myocardial contractility in dog--especially the effects of norepinephrine, epinephrine and isoproterenol

Catecholamines play an important role in main-trance of circulatory function and are widely employed in treatment of shock states. There have been many experimental studies on cardiovascular effects of catecholamines. However, few has been reported on comprehensive observations of their hemodynamic effects in animals maintaining normal circulation. The purpose of the present study is to investigate the effects of catecholamines on hemodynamics and myocardial contractility in special reference to influence of different dosage and manners of administration. Methods Adult mongrel dogs anesthetized with intraperitoneal pentobarbital sodium (30 mg/kg) were subjected to thoracotomy under artificial respiration. The following six tracings were simultaneously recorded on an electromagnetic oscillograph; (1) aortic blood flow curves with the probe of an electromagnetic flowmeter fixed around the aortic root, (2) aortic blood pressure curves with a catheter tip lodged in the left common carotid artery, (3) left atrial pressure curves with a catheter inserted in the left atrial appendage, (4) left ventricular cavity through the apex, (5) the first derivatives of the left ventricular pressure using an R-C differentiating circuit whose time constant was 0.5 msec, and (6) unipolar left ventricular epicardial electrocardiogram. These simultaneous tracings were analyzed for the following parameters; the heart rate, aortic blood pressure and flow, stroke volume, mean left atrial pressure, left ventricular external power, stroke work, Isometric Time-Tension Index [(dp/dt)/IIT], and total peripheral vascular resistance. A catheter lodged in the femoral vein was used for intravenous administration of catecholamines. For evaluation of the effects of a single bolus dose of the drugs, each of eight dogs was subjected, at an interval of 5 to 8 minutes, to rapid intravenous injections of six different drug-dose combinations (0.1 and 0.8 μg/kg of ISP, EP and NE). The effects of sustained intravenous infusion of NE was also investigated. A constant flow pump was employed for intravenous infusion of 5% dextrose solution for 3 hours throughout the experiment. Control data was obtained during the first one hour when only the dextrose solution was infused. NE was given at a rate of 0.8 μg/kg/min for the next one hour. For the last one hour continuous observation was also made with the dextrose solution alone infused. A similar experiment was also performed in spinal dogs who had undergone ligation of the bilateral vertebral arteries and disconnection of the bilateral cervical vagus nerves and the spinal cord at the level of the second cervical vertebra.

Efect of adrenergic stimilation on ion transport across skin of living frogs

1. 1. The influence of the intravenous administration of catecholamines and a β adrenergic blocking agent on short-circuit current ( I s ) skin resitance and sodium flux was studied with living anesthetized frog. 2. 2. Epinephrine (α plus β adrenergic stimulation) adn isoproterenol (β stimulation) produced an increase of I s , which was not explained by sodium transport changes, and mucous release. 3. 3. In contrast to epinephrine, isoproterenol decreased skin resistance and increased sodium outflux. 4. 4. Pronethalol (a β adrenergic blocking agent) decreased I 3, net sodium flux, and increased skin resistance. 5. 5. The results indicate that ion transport across the skin, in vivo, is influenced by α and β adrenergic stimulation. They support the concept that the two stimuli produce opposing effects on sodium transport, i.e. α stimulation decreases and β stimulation increases sodium permeability of the skin.