Vasoconstrictive properties of sympathomimetic drugs are the basis of their widespread use as decongestants and possible source of adverse responses. Insufficiently substantiated practice of combining decongestants in some marketed preparations, such are those containing phenylephrine and lerimazoline, may affect the overall contractile activity, and thus their therapeutic utility. This study aimed to examine the interaction between lerimazoline and phenylephrine in isolated rat aortic rings, and also to assess the substrate of the obtained lerimazoline-induced attenuation of phenylephrine contraction. Namely, while lower concentrations of lerimazoline (10⁻⁶ M and especially 10⁻⁷ M) expectedly tended to potentiate the phenylephrine-induced contractions, lerimazoline in higher concentrations (10⁻⁴ M and above) unexpectedly and profoundly depleted the phenylephrine concentration-response curve. Suppression of NO with NO synthase (NOS) inhibitor N(w)-nitro-L-arginine methyl ester (L-NAME; 10⁻⁴ M) or NO scavanger OHB₁₂ (10⁻³ M), as well as non-specific inhibition of K⁺-channels with tetraethylammonium (TEA; 10⁻³ M), have reversed lerimazoline-induced relaxation of phenylephrine contractions, while cyclooxygenase inhibitor indomethacin (10⁻⁵ M) did not affect the interaction between two vasoconstrictors. At the receptor level, non-selective 5-HT receptor antagonist methiothepin reversed the attenuating effect of lerimazoline on phenylephrine contraction when applied at 3×10⁻⁷ and 10⁻⁶ M, but not at the highest concentration (10⁻⁴ M). Neither the 5-HT1D-receptor selective antagonist BRL 15572 (10⁻⁶ M) nor 5-HT₇ receptor selective antagonist SB 269970 (10⁻⁶ M) affected the lerimazoline-induced attenuation of phenylephrine activity. The mechanism of lerimazoline-induced suppression of phenylephrine contractions may involve potentiation of activity of NO and K⁺-channels and activation of some methiothepin-sensitive receptors, possibly of the 5-HT(2B) subtype.
Animals ; Aorta* ; Indomethacin ; Methiothepin ; Nasal Decongestants ; Nitric Oxide Synthase ; Phenylephrine* ; Prostaglandin-Endoperoxide Synthases ; Rats* ; Relaxation ; Serotonin ; Sympathomimetics ; Tetraethylammonium ; Vasoconstrictor Agents

No abstract available.
Basilar Artery* ; Rabbits* ; Vasoconstrictor Agents* ; Vasodilator Agents*

Nasotracheal intubation is often the method of choice in oral or maxillofacial operations. During the insertion of endotracheal tube (ETT) through nostril, a considerable damage can be inflicted on the nasal mucosa by forcing ETT into the nasal cavity, and epistaxis may occur as a result of mucosal damage even when vasoconstrictors, a lubricated tube, and careful manipulation are employed. This study was conducted to observe whether balloon dilation technique(BDT) can help to minimize the expected problems during nasotracheal tube insertion and was to tried to get a data for further studies. In 30 patients in whom the nasotracheal tube was placed, smooth passage into the nasal cavity without using BDT occurred in 9 patients(30.0%). Of 21 patients(70.0%) who were come into the use of BDT when resistance to tube insertion due to anatomical structures of the nasal cavity was encountered, epistaxis was not developed. By the above results, The BDT appers to prevent epistaxis during nasotracheal tube insertion and to make an easy and smooth passage of the tube and then it suggest that the BDT should provide a basic data and an alternative to conventional techniques for a safe and atraumatic nasotracheal intubation.
Epistaxis ; Humans ; Intubation ; Nasal Cavity ; Nasal Mucosa ; Vasoconstrictor Agents

Hepatorenal Syndrome ; drug therapy ; Humans ; Vasoconstrictor Agents ; therapeutic use

Hepatorenal Syndrome ; therapy ; Humans ; Liver Transplantation ; Vasoconstrictor Agents ; therapeutic use

BACKGROUND: Septic shock causes life threatening organ dysfunction needing vasopressor despite adequate fluid resuscitation. Numerous studies and meta-analysis have proven norepinephrine as the initial vasopressor of choice in septic shock with vasopressin as add-on. Although guidelines have established the goal monitoring response in septic shock, optimal approach in discontinuation of the vasopressors in the recovery phase of septic shock remains limited. METHODS: A systematic review and meta-analysis was performed on randomized controlled trials (RCTs) and nonrandomized studies comparing incidence of hypotension within 24 hours of discontinuing norepinephrine first versus vasopressin. Three reviewers independently selected studies, assessed their quality, and extracted the following data: the number and characteristics of patients enrolled, inclusion and exclusion criteria for each study, the description of interventions (discontinuing norepinephrine first versus discontinuing vasopressin first) and outcomes (incidence of hypotension within 24 hours). RESULTS: Seven retrospective cohort studies and one prospective randomized control trial were included. Compared with norepinephrine, risk of hypotension is higher when vasopressin is discontinued first among patients in the recovery phase of septic shock (RR 2.06; 95% CI [1.11,3.82]; I 2 91%). Results were consistent in the subgroup analysis after excluding abstract-only and poor-quality studies (RR 1.73; 95% CI [0.74, 4.03]; I 2 93%). There is no difference in ICU (RR 0.97; 95% CI [0.71, 1.32]; I 2 38%) and in-hospital mortality (RR 0.88; 95% CI [0.66, 1.16]; I 2 41%) between the two vasopressor weaning strategies. Finally ICU length of stay was reported on 5 studies with no significant difference between the two strategies. CONCLUSION: Based on the results, there is increased risk of hypotension when vasopressin is discontinued first versus norepinephrine.
Norepinephrine ; Shock, Septic ; AVP protein, human ; Vasopressins ; Vasoconstrictor Agents ; Neurophysins

Portal hypertension is responsible for most of the complications associated with liver cirrhosis, including variceal hemorrhage, ascites, and hepatic encephalopathy. It has become clear that a decrease in portal pressure can prevent or manage these serious complications. Until now, the pharmacotherapy of portal hypertension has focused on agents that reduce splanchnic blood flow, such as non-selective beta blockers and splanchnic vasoconstrictors. However, recent advances in the knowledge of the pathophysiology of portal hypertension have directed future treatment towards modulating the increased intrahepatic vascular resistance, in addition to managing the splanchnic circulation. Consequently, agents that modulate either the hyperdynamic circulation or angiogenesis are new therapeutic targets for managing portal hypertension. Several have been developed or are under investigation. To incorporate these pharmacologic approaches into clinical practice, data on patient-oriented outcomes are needed.
Ascites ; Hemorrhage ; Hepatic Encephalopathy ; Hypertension, Portal ; Liver Cirrhosis ; Portal Pressure ; Splanchnic Circulation ; Vascular Resistance ; Vasoconstrictor Agents

BACKGROUND: After cardiopulmonary bypass (CPB), the radial arterial pressure is often lower than that of the femoral artery. If this difference is overlooked, the patients might be treated with unnecessary vasoconstrictors or inotropes. However, the exact etiology or mechanism of this discrepancy is not known. If a patients group with the risk of a high pressure gradient after CPB could be predicted, the femoral arterial pressure from pre-CPB period might be monitored in order to not be inadequately managed after weaning from CPB. We studied the predicting factors of this phenomenon in patients undergoing a valvular replacement. METHODS: One hundred patients undergoing valvular replacement were included in this study. The radial and femoral arterial pressures were measured in the same monitoring system during entire procedure of the operation. The radial to femoral arterial pressure ratio (R/F) was calculated. Demographic data and hemodynamic variables after induction of anesthesia were studied using correlation analysis to assess which data could be associated with R/F. A best predictive model was developed with stepwise multiple linear regression analysis. RESULTS: Correlation analysis showed that age, preoperative ejection fraction (EF), and cardiac index after induction were statistically significant. A predictive model was developed including age and preoperative EF. The regression equation is R/F = 86.249 - (0.294 X age) + (0.329 X preoperative EF). CONCLUSIONS: It could be predicted in the patients with old age or low preoperative ejection fraction that radial arterial pressure might be lower than that of femoral artery in a valvular replacement operation.
Anesthesia ; Arterial Pressure* ; Cardiopulmonary Bypass* ; Femoral Artery ; Hemodynamics ; Humans ; Linear Models ; Vasoconstrictor Agents ; Weaning

Epinephrine is one of the most widely-used vasoconstrictors in dental treatment including endodontic microsurgery. However, the systemic safety of epinephrine has been in debate for many years because of its potential risk to cause cardiovascular complications. The purpose of this review was to assess the cardiovascular effect of epinephrine use in endodontic microsurgery. Endodontic microsurgery directly applies epinephrine into the bone cavity, and the amount is reported to be much larger than other dental surgeries. Moreover, when considering that systemic potency of intraosseous application is reported to be comparable to intravenous application, the systemic influence of epinephrine could be increased in endodontic microsurgery. Besides, pre-existing cardiovascular complications or drug interactions can enhance its systemic influence, resulting in increased susceptibility to cardiovascular complications. Although clinical studies have not reported significant complications for patients without severe systemic complications, many epinephrine-induced emergency cases are warning the cardiovascular risk related with pre-existing systemic disease or drug interactions. Epinephrine is a dose-sensitive drug, and its hypersensitivity reaction can be fatal to patients when it is related to cardiovascular complications. Therefore, clinicians should recognize the risk, and the usage of pre-operative patient evaluation, dose control and patient monitoring are required to ensure patient's safety during endodontic microsurgery.
Cardiovascular Diseases ; Drug Interactions ; Emergencies ; Epinephrine* ; Hemostasis ; Humans ; Hypersensitivity ; Microsurgery* ; Monitoring, Physiologic ; Vasoconstrictor Agents

Vasoconstrictors such as epinephrine or phenylephrine have been used as an adjunct to local anesthetics to prolong the duration of spinal anesthesia. Recently, clonidine, an areceptor agonist, has been proved to have analgesic effect and to prolong epidural and spinal anesthesia. We used 0.3mg of epinephrine, 75 ug and 150 ug of clonidine in spinal anesthesia with 12 mg of T-Cain respectively and compared hemodynamic and analgesic effects of each drug. Heart rate and blood pressure were checked before, during and after anesthesia. Sensory level was checked by pin-prick method and motor blockade was measured by Bromages scale. The results were as follows. 1) Heart rate changed little in the epinephrine group and decreased significantly in all other groups.2) Systolic blood pressure decreased significantly in all groups except the epinephrine group. Both 75 ug and 150 ug of clonidine caused a significant fall in diastolic pressure. 3) The onset time for sensory and motor blockade varied little among all groups. 4) Sensory blockade was significantly higher in the 150 ug of clonidine group than the control group. Time to achieve the maximum level of sensory blockade was significantly faster in control group than 150 ug of clonidine group. 5) The duration of sensory and motor blockade was significantly prolonged in epinephrine and clonidine group than control group. The results indicate that clonidine, when used as an adjunct to T-Cain spinal anesthesia, is as effective as epinephrine in prolongation of motor and sensory blockade.
Anesthesia ; Anesthesia, Spinal* ; Anesthetics, Local ; Blood Pressure ; Clonidine* ; Epinephrine* ; Heart Rate ; Hemodynamics ; Phenylephrine ; Vasoconstrictor Agents