Concentrated infusions

Infusion Final concentration Infusion volume- Procainamide to be added Infusion rate... 

The cardiovascular response to dopamine in humans depends on the concentration infused. Low rates of dopamine infusion can produce vasodilation in the renal, mesenteric, coronary, and intercerebral vascular beds with little effect on other blood vessels or on the heart. The vasodilation produced by dopamine is not antagonized by the p-adrenoceptor blocking agent propranolol but is antagonized by haloperidol and other dopamine receptor-blocking agents. 

Nau H (1985) Teratogenic valproic acid concentrations infusion by implanted minipumps vs. conventional injection Fegimen in the mouse. Toxicol Appl Pharmacol, 80 243-250. 

Usual parenteral dosage IV Push Initially 0.25 mg/kg actual body weight over 2 min may repeat in 15 min at dose of 0.35 mg/kg actual body weight subsequent doses individualized IV Infusion After initial bolus injection 5-10 mg/h may increase at 5 mg/h up to 15 mg/h. Maintain over 24 h. Note Refer to manufacturer s information for dose concentration/infusion rate. 

Factor VIE is a large molecule that remains in the intravascular space. Therefore the plasma volume, approximately 50 mL/kg, can be used to estimate the volume of distribution. In general, each unit of factor VIE concentrate infused per kilogram of body weight yields a 2% rise in plasma factor VIE levels. The following equation may be used to calculate an initial dose of factor VEI ... 

Avoid large doses during pregnancy. Concentrated infusions have caused abortion in rats, though weak teas are considered safe. The essential oil is never appropriate to take internally small doses cause acute renal insufficiency and death. Extensive overuse of the herb over years may result in central nervous system damage from the high levels of thujone (a narcotic poison) in the plant. 

You do not discover the error until you administer the same drug to another patient later that day. By this time the 42-year old patient has aheady received all of the high concentration infusion. You are aware that in the long term the drug may impair cardiac functioning. You realise that there is a significant risk that the patient s level of functioning will be diminished and that she probably won t be able to maintain her present work. 

We studied a further 24 infants less than 1300 g similarly in all other respects monitoring blood sugar and urine sugar carefully and modifying the glucose concentration infused accordingly. We obtained much more satisfactory results. 

Another group of natural flavoring ingredients comprises those obtained by extraction from certain plant products such as vanilla beans, Hcotice root, St. John s bread, orange and lemon peel, coffee, tea, kola nuts, catechu, cherry, elm bark, cocoa nibs, and gentian root. These products are used in the form of alcohohc infusions or tinctures, as concentrations in alcohol, or alcohol—water extractions termed fluid or soHd extracts. Official methods for their preparation and specifications for all products used in pharmaceuticals are described (54,55). There are many flavor extracts for food use for which no official standards exist the properties of these are solely based on suitabiUty for commercial appHcations (56). 

Infusion. Infusion botanical extracts are tinctures that have been concentrated by either total or partial removal of the alcohol by distillation. 

The principal arninoglycoside toxicides are neuromuscular paralysis, ototoxicity, and nephrotoxicity. Neuromuscular paralysis is a relatively rare complication resulting from high aminoglycoside concentrations at the neuromuscular junctions following, for example, rapid bolus intravenous injection or peritoneal instillation, rather than the normal intravenous infusion. The mechanism apparentiy involves an inhibition of both the presynaptic release of acetylcholine and the acetylcholine postsynaptic receptors (51). 

Calcitonin is secreted when abnormally high calcium levels occur in plasma. Although plasma concentrations are normally minute (<100 pg/mL), they increase two- to threefold after calcium infusion. Calcitonin has a short plasma half-life (ca 10 min). Certain thyroid tumors are the result of CT concentrations 50—500 times normal. The mechanism of action is a direct inhibition of bone resorption. Calcitonin is used clinically in various diseases in which hypercalcemia is present, eg, Paget s disease (46). 

Pitches can be transformed to a mesophase state by further chemical and physical operations. Heat treatment of conventional pitches results in additional aromatic polymeriza tion and the distillation of low molecular weight components. This results in an increase in size and concentration of large planar aromatic molecular species whereupon the precursor pitch is transformed to a mesophase state exhibiting the characteristics of nematic Hquid crystals (1). Additional heat treatment converts the mesophase pitch to an infusible aromatic hydrocarbon polymer designated as coke. 

Coal-Tar Pitch Coke. Coal-tar pitch is used to produce needle coke primarily in Japan. Processes for producing needle coke from pitch have also been developed in Germany (4). The key to producing needle coke from coal tar or coal-tar pitch is the removal of the high concentrations of infusible sohds, or material insoluble in quinoline (QI), which are present in the original tar. The QI inhibits the growth of mesophase and results in an isotropic, high CTE coke from coal-tar pitch. After removal of the QI, very anisotropic and low CTE cokes are obtained from coal-tar-based materials. 

Time to peak plasma concentration depends on the rate of IV dosing but is usually achieved in 45—90 seconds. Therapeutic plasma concentrations are 1.5—5.0 )J.g/mL, and concentrations above 5 )J.g/mL maybe toxic. The elimination half-life after a bolus iv dose is 8 min the elimination half-life after a 24 h iv infusion is about 100 min. The dmg is eliminated by the kidneys. Ten percent is unchanged and the remainder is in the form of inactive metabolites... 

Esmolol is iv adrninistered. Maximal P-adrenoceptor blockade occurs in 1 min. Its elimination half-life is about 9 min. EuU recovery from P-adrenoceptor blockade is within 30 min after stopping the infusion. The therapeutic plasma concentrations are 0.4—1.2 lg/mL. It is metabolized by hydrolysis in whole blood by red blood cell esterases resulting in the formation of a primary acid metabohte and free methanol. The metabohte is pharmacologically inactive. The resulting methanol levels are not toxic. Esmolol is 55% bound to plasma protein, the acid metabohte only 10%. Less than 2% of parent dmg and the acid metabohte are excreted by the kidneys. Plasma levels may be elevated and elimination half-hves prolonged in patients with renal disease (41). 

After po dosing, verapamil s absorption is rapid and almost complete (>90%). There is extensive first-pass hepatic metabolism and only 10—35% of the po dose is bioavahable. About 90% of the dmg is bound to plasma proteins. Peak plasma concentrations are achieved in 1—2 h, although effects on AV nodal conduction may be apparent in 30 min (1—2 min after iv adrninistration). Therapeutic plasma concentrations are 0.125—0.400 p.g/mL. Verapamil is metabolized in the liver and 12 metabolites have been identified. The principal metabolite, norverapamil, has about 20% of the antiarrhythmic activity of verapamil (3). The plasma half-life after iv infusion is 2—5 h whereas after repeated po doses it is 4.5—12 h. In patients with liver disease the elimination half-life may be increased to 13 h. Approximately 50% of a po dose is excreted as metabolites in the urine in 24 h and 70% within five days. About 16% is excreted in the feces and about 3—4% is excreted as unchanged dmg (1,2). 

In normal human subjects, ANP infusion for one hour causes increased absolute and fractional sodium excretion, urine flow, GFR, and water clearance (53—55). As shown in many in vitro and in vivo animal studies, ANP achieves this by direct effect on the sodium reabsorption in the inner medullary collecting duct, ie, by reducing vasopressin-dependent free-water and sodium reabsorption leading to diuresis and by indirect effect through increased hemodynamic force upon the kidney. ANP inhibits the release of renin and aldosterone resulting in the decreased plasma renin activity and aldosterone concentration (56,57). 

The horizontal dispersion of a plume has been modeled by the use of expanding cells well mixed vertically, with the chemistry calculated for each cell (31). The resulting simulation of transformation of NO to NO2 in a power plant plume by infusion of atmospheric ozone is a peaked distribution of NO2 that resembles a plume of the primary pollutants, SO2 and NO. The ozone distribution shows depletion across the plume, with maximum depletion in the center at 20 min travel time from the source, but relatively uniform ozone concentrations back to initial levels at travel distances 1 h from the source. 

By using a low concentration of NH3 and with no NH4+ initially present, the amide [Hg(NH2)Cl], infusible white precipitate is... 

Little is known regarding the pharmacokinetic properties of volatile nitrites in humans, particularly isobutyl nitrite and its primary metabolite, isobutyl alcohol. In rodents, after an intravenous infusion of isobutyl nitrite, blood concentrations peaked rapidly and then declined, with a half-life of 1.4 minutes and blood clearance rate of 2.9 L/min/kg (Kielbasa and Fung 2000). Approximately 98% of isobutyl nitrite is metabolized rapidly to isobutyl alcohol, concentrations of which also decline rapidly, with a half-life of 5.3 minutes. Bioavailability of inhaled isobutyl nitrite at a concentration of 300-900 ppm is estimated to be 43%. 

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