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Endotracheal and intravenous administration of atropine were compared in two groups of 10 children. No differences were found between the groups in effect on heart rate or speed of onset of the effect. We conclude that the two methods are equally effective.
Intravenous administration of plasmin as distinct from thrombin inhibited or did not provide a secretion of endogenous heparin into circulation. In these conditions non-enzymatic fibrinolysis was not observed both in fraction of euglobulins and in fibrinogen-heparin complex, isolated from euglobulins, due to insufficiency of heparin. Exogenous heparin, injected into circulation or added to corresponding fractions, enabled to produce the active heparin complexes. About 70% of total fibrinolytic activity was due to fibrinogen-heparin complex in euglobulin fraction of blood plasma, isolated from blood of animals intravenously administered with thrombin.
Theoretically, continuous intravenous administration of beta-lactam antibiotics has advantages over intermittent administration because of the close relationship between efficacy and the time the plasma concentration remains above the minimal inhibitory concentration that has been found in vitro. The aim of the present study was to establish the pharmacokinetic parameters of benzylpenicillin and cloxacillin administration in patients receiving high-dose benzylpenicillin or cloxacillin therapy by continuous infusion. A major part of the interindividual variation in the plasma concentrations at steady-state was attributable to variation in renal function, as estimated by the creatinine clearance. On the basis of these results, a nomogram was constructed that can be used to determine on an individualized basis the total daily dose of benzylpenicillin or cloxacillin necessary for each patient to obtain therapeutic plasma concentrations.
After the intravenous administration to the intact rat of triglyceride carried in either intestinal lipoproteins or in an artificial fat emulsion, the enzymatic activities of microsomal beta-hydroxy-beta-methylglutaryl-CoA reductase activity in the liver assayed in vitro became markedly elevated. This elevation of enzyme activity was not associated with a corresponding change in the overall rate of cholesterol synthesis in the rat liver slice as measured by the incorporation of either [3H]water or [1-14C]octanoate into nonsaponifiable lipids or into digitonin-precipitable sterols. The degree of dissociation of hydroxymethylglutaryl-CoA reductase activity from the overall rate of cholesterol synthesis correlated closely with the amount of lipid administered to the animal, the level of circulating lipids, and the level of ketone synthesis manifest in the liver cell suggesting that this phenomenon might be the consequence of a detergent effect of elevated cellular levels of fatty acids. In any event, under these experimental circumstances hydroxymethylglutaryl-CoA redutase activity no longer reflects the rate at which the liver cell is synthesizing cholesterol.
Intravenous administration of endotoxin into humans causes transient fever, alteration in the number of circulating neutrophils, and transient release into plasma of cytokines, cytokine antagonists, and other cellular products. The release can be temporally differentiated, and the extent of release is dose-dependent. By 1 h after endotoxin challenge, levels of tumor necrosis factor (TNF)-alpha and soluble TNF receptor increase; interleukin (IL)-6 and IL-8 increase by 1.5 h, and IL-1 receptor antagonist, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor, and lactoferrin increase by 2 h. Increased G-CSF is temporally associated with neutrophilia and the appearance of band neutrophils. Increased plasma lactoferrin and altered neutrophil surface antigen expression suggest that intravascular activation of neutrophils has occurred. The level of soluble E-selectin (sE-sel), an adhesion molecule released from endothelial cells, is elevated at 4 h and remains elevated at 24 h. sE-sel levels increase with higher doses of endotoxin at 4, 6, and 24 h.
Pharmacokinetic parameters of ipriflavone and its main metabolites, M1 and M5, after intravenous administration of spray-dried ipriflavone, SIP (10, 20, and 30 mg/kg as ipriflavone) and tissue distribution of ipriflavone, M1, and M5 after intravenous administration of SIP (20 mg/kg as ipriflavone) were evaluated in rabbits. Saturable metabolism of ipriflavone were observed after intravenous administration; at an ipriflavone dose of 30 mg/kg, the dose-normalized (based on 10 mg/kg) AUC was significantly greater (72.4 and 64.0 versus 103 microg min/mL), Cl was significantly slower (138 and 156 versus 97.6 mL/min/kg), and terminal half-life (94.8 and 129 versus 211 min) and mean residence time (91.3 and 116 versus 186 min) were significantly longer than those at 10 and 20 mg/kg. The AUC of M1 was also significantly greater at ipriflavone dose of 30 mg/kg. The terminal half-life, AUC, and renal clearance of M5 were also significantly different at ipriflavone dose of 30 mg/kg than those at 10 and 20 mg/kg. Ipriflavone was widely distributed in most rabbit tissues studied and the tissue-to-plasma (T/P) ratios of ipriflavone were greater than unity in all tissues (or organs) studied except spleen, indicating that ipriflavone has high affinity to rabbit tissues studied, and this could be supported by considerably high values of the apparent volume of distribution of ipriflavone at steady state (11 400-16 900 mL/kg). M1 and M5 were also detected in most rabbit tissues with considerable amount of M1 (T/P ratio of 9.43) and M5 (T/P ratio of 4.66) in the kidney.
Intravenous administration of a bolus of ethanol (40 mg/100 g b.w.) to rats induced bradycardia, hypotension and apnea. Bradycardia was dose dependent (r = -0.78, p less than 0.001). Acute bilateral vagotomy blocked bradycardia and hypotension. Apnea, however, persisted in all cases but was of short duration and occurred after a significant delay as compared to an untreated group. Atropine (0.1 mg/100 g b.w.) and hexamethonium (0.75 mg/100 g b.w.) blocked bradycardia and early hypotension. Pretreatment with reserpine (0.25 mg/100 g b.w. IP 24 and 48 hours before the experiment) significantly increased bradycardia induced by ethanol as compared to untreated animals. In rats pretreated with reserpine and vagotomized, IV ethanol did not induce bradycardia, early hypotension or apnea. A bolus of ethanol (20 mg/100 g b.w.) given directly into the left ventricle did not induce reflex changes in heart rate or respiration, while the same dose of alcohol given IV decreased heart rate by 53 +/- 8.9%. Thus, the ethanol effect seems to be initiated in pulmonary J receptors. Bradycardia appeared to be mediated both by increase in vagal tone, and to a lesser extent, by sympathetic withdrawal. Hypotension was due mainly to bradycardia, and apnea might be caused by a dual mechanism, reflex (early) and direct on the respiratory center (late).
Oral and intravenous challenge paradigms with the direct 5-HT agonist meta-chlorophenylpiperazine (m-CPP) in panic disorder (PD) have shown only moderate sensitivity or selectivity of the panicogenic effects in PD. However, the results of a study examining the effects of rapid intravenous administration of 0.1 mg/kg of m-CPP in healthy volunteers suggested that this approach may be a more selective and sensitive panicogenic paradigm in PD. We therefore compared the behavioural, neuroendocrine and physiological effects of rapid intravenous administration of 0.1 mg/kg of m-CPP in 10 patients with PD and 10 healthy controls. Panic attacks were significantly more provoked in patients with PD (90%) compared to healthy controls (0%). Effects on the behavioural, but not on the neuroendocrine and physiological parameters, were significantly greater in patients. Our data suggests that the behavioural effects of rapid intravenous administration of 0.1 mg/kg of m-CPP in patients with PD indeed show a unique combination of high sensitivity and selectivity.
BACKGROUND AND OBJECTIVES: In this study, we evaluated the efficacy and safety of prophylactic administration of intravenous caffeine sodium benzoate for postdural puncture headaches (PDPH) on patients administered spinal anesthesia. METHODS: Sixty ASA I and II patients undergoing lower abdominal or lower extremity surgery were included in this study. Patients were randomized by double-blind, placebo-controlled design to receive either 1,000 mL normal saline with 500 mg caffeine sodium benzoate (group C) or 1,000 mL normal saline (group S) during the first 90 minutes after spinal anesthesia administration. The patient's electrocardiogram, non-invasive blood pressure, and pulse oximetry were monitored and recorded. The patients' headaches were evaluated by using the visual analog scale (VAS). At the end of the fifth day, the severity of the headache was classified as follows: no headache = 0; mild headache = 1; moderate headache = 2; severe headache = 3. Analgesic requirements were recorded for 5 days. RESULTS: Visual analog scale scores were significantly lower in group C than in group S. The incidence of moderate and severe headache was significantly higher in group S (11 patients) when compared with group C (3 patients). Analgesic demand was significantly lower in group C than in group S for 4 days. CONCLUSION: Intravenous caffeine sodium benzoate administration during spinal anesthesia is a simple and safe way to minimize PDPH.
PURPOSE: Penetration of ceftazidime, a third generation cephalosporin, into the vitreous cavity after intravenous administration was investigated. METHODS: Because antimicrobial penetration varies with surgical status of the eye and with inflammation, studies were conducted in phakic, aphakic, and aphakic, vitrectomized eyes in both normal and inflamed conditions. Ceftazidime 50 mg/kg was administered every 8 hours and vitreous cavity concentrations were tested at intervals from 2 to 72 hours after the initial dose. RESULTS: No penetration was found into control phakic and aphakic eyes, but drug concentrations were detected in inflamed eyes at 24 hours. Vitreous concentrations of ceftazidime in aphakic, vitrectomized eyes reached levels well above the minimal inhibitory concentration (MIC) for Pseudomonas organisms within 2 hours of intravenous administration in control eyes (8.5 micrograms/ml) and inflamed eyes (35.4 micrograms/ml). Inflammation and removal of the lens and vitreous significantly enhanced ceftazidime penetration at all time periods tested. CONCLUSION: Ceftazidime penetrates into the vitreous cavity of inflamed eyes after intravenous administration and achieves concentrations above the MIC for Pseudomonas organisms. Penetration is greatest in aphakic, vitrectomized eyes.
BACKGROUND: The purpose of this initiative was to compare erythropoietin-alpha doses in hemodialysis patients who changed from subcutaneous to intravenous administration. The Manitoba Renal Program switched routes due to concern about erythropoietin-associated pure red cell aplasia. METHODS: We compared the erythropoietin-alpha dosage requirements during subcutaneous administration (3 months pre-switch) and intravenous administration (months 4-6 post-switch). We also compared: hemoglobin, transferrin saturation (Tsat%), ferritin, and percent of patients receiving intravenous iron. The same erythropoietin-alpha regimen was initially used when patients were switched. RESULTS: Of the 628 patients receiving erythropoietin-alpha, the data were complete for 400. The dose increased 26% (mean +/- SD, 10,425 +/- 7,330 vs. 13,125 +/- 8,638 IU/week; p < 0.0001), despite similar hemoglobin, (mean +/- SD, 11.5 +/- 1.1g/dl (114.9 +/- 11.2 g/l) vs. 11.3 +/- 1.0 g/dl (113.5 +/- 10.4 g/l); p = 0.0450) and iron parameters (Tsat 30.9%, ferritin 464 ng/ml (microg/l) vs. Tsat 28.7%, ferritin 538 ng/ml (microg/l)). For the subgroup of 84 patients who maintained target hemoglobin (10-11 g/dl or 110-120 g/l) for both periods, the dose increased 26% (mean +/- SD, 8,393 +/- 6,242 vs. 10,589 +/- 7,049 IU/week; p < 0.0001) without a change in hemoglobin, (mean +/- SD, 11.5 +/- 0.3 g/dl (115.2 +/- 3.0 g/l) vs. 11.5 +/- 0.3 g/dl (114.9 +/- 3.3 g/l); p = 0.5789). When stratified by subcutaneous dose, patients with the lowest dose (<5,000 IU/week) demonstrated the greatest increase (89%), and those with the highest dose (>20,000 IU/week) experienced no increase (-3%). CONCLUSION: Overall, erythropoietin-alpha doses increased by 26% when patients were converted from subcutaneous to intravenous administration.
The behavioral effects of oral versus intravenous administration of diazepam were studied in 50 volunteers using a battery of memory, cognitive, mood and psychomotor tests repeated over a 4.5 hr period. Subjects received diazepam 0.2 mg/kg or placebo as capsules, commercial tablets or intravenous solution in a randomized double blind manner. While a quick onset of effects occurred with intravenous administration followed by the capsule and tablet oral administrations in that order, the recovery rate was similar for the 3 methods of administration. Contrary to many claims in the literature the effects of oral administration were substantial. Behavioral impairment was directly related to the magnitude of the memory component of the task. On many of the tasks the pattern of diazepam impairment was one of delayed improvement of performance, a pattern which would only be apparent with repeated testing. Subjects who received diazepam showed a paradoxical enhancement of recall for material learned before the drug.
The pharmacokinetics of butorphanol tartrate were investigated following intravenous administration of 0.25 mg/kg of body weight to six healthy non-lactating Jersey cows. Three lactating Holstein cows also received 0.045 mg of butorphanol/kg of body weight intravenously to determine the extent and duration of drug transfer into milk. A radioimmunoassay technique was used to measure butorphanol concentrations in plasma and milk. The disposition of butorphanol following intravenous administration was characterized by rapid and extensive distribution followed by a slower elimination phase. Apparent volume of distribution was 4.178 +/- 1.145 (mean +/- SD) 1/kg, mean elimination half-life was 82 min, and clearance was 34.6 +/- 7.7 ml/min/kg. Trace quantities of butorphanol were detected in the cow's milk for up to 36 h following administration. These pharmacokinetic data were compared with pharmacokinetic and pharmacodynamic data for butorphanol in other species and for three other potent opioids in related ruminant species.
To study adverse reactions associated with intravenous administration of fusidic acid 6 patients were treated with fusidic acid intravenously in association with a major large bowl operation, and 9 patients were treated in the same way because of staphylococcal infections. The main adverse reaction was thrombophlebitis, which occurred in as many as 12 of 14 patients who were treated for 2 days or longer. Three surgical patients developed postoperative hyperbilirubinaemia, but studies of liver function before and during treatment in 6 of the patients with staphylococcal disease revealed no adverse liver reactions. Intravenous administration of fusidic acid into a peripheral vein for 24 h or more involves an extremely high risk of developing thrombophlebitis.
STUDY OBJECTIVE: We sought to compare the rate of akathisia after administration of intravenous prochlorperazine as a 2-minute bolus or 15-minute infusion. METHODS: We conducted a prospective, randomized, double-blind study in the emergency department of a central-city teaching hospital. Patients aged 18 years or older treated with prochlorperazine for headache, nausea, or vomiting were eligible for inclusion. Study participants were randomized to receive 10 mg of prochlorperazine administered intravenously by means of 2-minute push (bolus group) or 10 mg diluted in 50 mL of normal saline solution administered by means of intravenous infusion during a 15-minute period (infusion group). The main outcome was the number of study participants experiencing akathisia within 60 minutes of administration. Akathisia was defined as either a spontaneous report of restlessness or agitation or a change of 2 or more in the patient-reported akathisia rating scale and a change of at least 1 in the investigator-observed akathisia rating scale. The intensity of headache and nausea was measured with a 100-mm visual analog scale. RESULTS: One hundred patients were enrolled. One study participant was excluded after protocol violation. Seventy-three percent (73/99) of the study participants were treated for headache and 70% (70/99) for nausea. In the bolus group, 26.0% (13/50) had akathisia compared with 32.7% (16/49) in the infusion group (Delta=-6.7%; 95% confidence interval [CI] -24.6% to 11.2%). The difference between the bolus and infusion groups in the percentage of participants who saw a 50% reduction in their headache intensity within 30 minutes was 11.8% (95% CI -9.6% to 33.3%). The difference in the percentage of patients with a 50% reduction in their nausea was 12.6% (95% CI -4.6% to 29.8%). CONCLUSION: A 50% reduction in the incidence of akathisia when prochlorperazine was administered by means of 15-minute intravenous infusion versus a 2-minute intravenous push was not detected. The efficacy of prochlorperazine in the treatment of headache and nausea likewise did not appear to be affected by the rate of administration, although no formal statistical comparisons were made.
The acute and chronic effects of lithium carbonate administration at therapeutic blood levels on peripheral noradrenergic activity and sympathetic responses to alpha2 adrenoceptor blockade were examined in 10 medically and psychiatrically healthy volunteers. Supine resting levels of plasma norepinephrine and the increases in norepinephrine following intravenous infusion of 200 microg/kg of idazoxan, a selective alpha2 adrenoceptor antagonist, were determined before lithium (Li+) administration and after 5 days and after 4 weeks of daily Li+ treatment. Chronic Li+ treatment significantly increased mean resting plasma norepinephrine levels by 53.6%. The noradrenergic responses to infusions of idazoxan were slightly enhanced after 5 days of Li+ administration and significantly increased following 4 weeks of Li+ treatment. The possibility that Li+ produces functional alpha2 subsensitivity causing enhanced peripheral noradrenergic activity in humans is supported by the findings of increased mean resting plasma norepinephrine and increased response to idazoxan following chronic Li+ administration. Alteration of regulatory mechanisms in the noradrenergic system may be relevant to understanding the clinical effects of Li+ in manic-depressive illness.
We have compared the effects of intravenous administration of cimetidine and ranetidine on some cardiovascular parameters. Five healthy volunteers received both cimetidine (3, 5 mg/Kg) and ranetidine (1, 5 mg/Kg). Heart rate, blood pressure and PEP/LVET were recorded at baseline and 5, 10, 30, 45 minutes after administration of both drugs. Intravenous administration of cimetidine and ranetidine did not induce any significant alterations in cardiovascular variables.
The aim of the present study was to establish the effect of intravenous administration of indomethacin (10 mg/kg), potent inhibitor of prostaglandin synthesis, on hemodynamic parametrs after intravenous administration of propranolol (0.3 mg/kg) and enalaprilat (0.5 mg/kg) in rabbits. The following parameters were estimated: mean arterial blood pressure, heart rate, cardiac output and total peripheral resistance. Blood pressure was measured directly in the carotid artery, heart rate was counted according to ECG, cardiac output and total peripheral resistance were calculated using the method of human 125J albumin dilution. For statistical analysis, the average change in the examined parametres was calculated. Indomethacin significantly increased mean arterial pressure without altering other hemodynamic parameters. Combined intravenous administration of indomethacin with enalaprilat or propranolol abolished hypotensive effect of both drugs. Indomethacin magnified the effect of propranolol on total peripheral resistance and abolished the effect of enalaprilat on this parameter. Co-administration of indomethacin with propranolol or enalaprilat did not influence significantly heart rate and cardiac output in comparison with the effect of both antihypertensive drugs alone. This may indicate the predominant role of the influence of indomethacin on vascular tone in the observed interaction.