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Intravenous bolus

Adenosine is produced by many tissues, mainly as a byproduct of ATP breakdown. It is released from neurons, glia and other cells, possibly through the operation of the membrane transport system. Its rate of production varies with the functional state of the tissue and it may play a role as an autocrine or paracrine mediator (e.g. controlling blood flow). The uptake of adenosine is blocked by dipyridamole, which has vasodilatory effects. The effects of adenosine are mediated by a group of G protein-coupled receptors (the Gi/o-coupled Ai- and A3 receptors, and the Gs-coupled A2a-/A2B receptors). Ai receptors can mediate vasoconstriction, block of cardiac atrioventricular conduction and reduction of force of contraction, bronchoconstriction, and inhibition of neurotransmitter release. A2 receptors mediate vasodilatation and are involved in the stimulation of nociceptive afferent neurons. A3 receptors mediate the release of mediators from mast cells. Methylxanthines (e.g. caffeine) function as antagonists of Ai and A2 receptors. Adenosine itself is used to terminate supraventricular tachycardia by intravenous bolus injection. [Pg.19]

The plasma half-life of 6-MP after intravenous bolus injection is 21 min in children and is twofold greater in adults. After oral intake peak levels are attained within 2 h. 6-MP is used for the treatment of ALL and has shown certain activity in chronic myelogenous leukemia. The major side effects involve myelosuppression, nausea, vomiting, and hepatic injury. [Pg.149]

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. [Pg.213]

The data for the use of GP Ilb/Illa inhibitors in conjunction with lAT are even more scant, and are limited to case reports. Intravenous abciximab has been successfully used as adjunctive therapy to lA rt-PA or UK in cases of acute stroke. Desh-mukh et al. reported on 21 patients with large vessel occlusion refractory to lAT with rt-PA who were treated with IV and/or lA abciximab, eptifibatide, or tirofiban. Twelve patients also received IV rt-PA and 18 patients underwent balloon angioplasty. Complete or partial recanalization was achieved in 17 of 21 patients. Three patients (14%) had asymptomatic ICH, but there were no cases of symptomatic ICH. Mangiafico et al. described 21 stroke patients treated with an intravenous bolus of tirofiban and heparin followed by lA urokinase. Nineteen of these patients also underwent balloon angioplasty. TIMI 2-3 flow was achieved in 17 of 21 patients. ICH occurred in 5 of 21 patients (3 symptomatic ICH and 2 SAH), and was fatal in 3... [Pg.79]

One compound from this series, (10), has been tested in vitro in human myometrium tissue obtained at term following caesarean section and shown to inhibit contractions induced by oxytocin [44] with a pA2 of 7.6. This is one of the first direct indications that the use of an oxytocin antagonist may be of benefit in the treatment of preterm labour in humans. This compound has been extensively studied in the near-term baboon and has been shown to inhibit nocturnal and near-term contractions following an intravenous bolus injection [45]. Further studies on the effect of oxytocin antagonism in the weeks leading up to delivery in the baboon have also been published [46]. [Pg.342]

FIGURE 1. Change in the apparent volume of distribution of PCP as a function of time following administration of an intravenous bolus dose of 3H-PCP (6.4 pg) in a male dog (19.5 kg)... [Pg.127]

Use a crystalloid (normal saline or lactated Ringer s solution) or a colloid (hydroxyethyl starch or albumin 5%) intravenous boluses... [Pg.66]

Magnesium sulfate 4-6 mg intravenous bolus over 20 minutes, then 2-3 g per hour intravenous drip Generally not favored... [Pg.729]

Mannitol is an agent that may be used in patients with I impending cerebral herniation. Mannitol is an osmotic diuretic that shifts brain osmolarity from the brain to the blood. Doses of 100 g (1-2 g/kg) as an intravenous bolus should be used. Repeated doses typically are not recommended because mannitol may diffuse into damaged brain tissue, leading to rebound increased ICP.21... [Pg.1478]

In vivo Release of Desmopressin and Somatostatin. The in vivo release of Desmopressin and Somatostatin after subcutaneous and intramuscular injections of the peptide in the cubic or the lamellar phase has been studied in the rabbit. Blood was sampled at regular intervals, and systemically absorbed Desmopressin and Somatostatin were determined as the specific immunoreactitvity in plasma of the actual peptide. For details of the analyses with dDAVP, consult ref. 9. For comparison, Desmopressin-like and Somatostatin-like immunoreactitvity (dDAVP-LI and SRIF-LI) in plasma after intravenous bolus injections of the two peptides were determined as well. [Pg.255]

Fig. 22 (A) Plasma concentration of SMA-NCS and NCS in human after an intravenous bolus injection. (B) Intratumor concentration of SMA-NCS, NCS, and mitomycin (MMC). SMA-NCS exhibits a much higher and more prolonged tumor concentration than MMC and NCS. All drugs were given as an intravenous bolus at 10 mg/kg to rabbits bearing VX-2 tumor in... Fig. 22 (A) Plasma concentration of SMA-NCS and NCS in human after an intravenous bolus injection. (B) Intratumor concentration of SMA-NCS, NCS, and mitomycin (MMC). SMA-NCS exhibits a much higher and more prolonged tumor concentration than MMC and NCS. All drugs were given as an intravenous bolus at 10 mg/kg to rabbits bearing VX-2 tumor in...
Equation (9) is most often associated with intravenous bolus administration, although proper definition of A, allows this equation to apply to extravascular and intravenous infusion administrations. [Pg.79]

Chen and Gross [48] derived equations to calculate partition coefficients for blood flow-limited compartments from either constant rate infusion (i.e., steady-state conditions) or intravenous bolus regimens. For a noneliminating organ under steady-state conditions,... [Pg.93]

Following intravenous bolus administration, the partition coefficients for a noneliminating blood flow-limited compartment is... [Pg.94]

A 36-year-old male is seen in the ED with tachycardia, a respiratory rate of 26 breaths per minute (BPM), and EKG evidence of an arrhythmia. An intravenous bolus dose of an antiarrhythmic agent is administered, and within 30 s, he has a respiratory rate of 43 BPM and complains of a burning sensation in his chest. [Pg.113]

The answer is a. (Katzung, p 240.) Older therapies—all designed to favor parasympathetic control of rhythm—include digoxin, propranolol, edrophonium, and vasoconstrictors. The vasoconstrictor phenylephrine (given by intravenous bolus) causes stimulation of the carotid sinus and reflex vagal stimulation of the atria. More recently, adenosine has been favored over verapamil, which is also very effective but slower acting... [Pg.126]

The plasma concentration of a drug immediately following a 50-mg intravenous bolus dose of the drug was found to be 0.84 mcg/mL. What is the apparent volume of distribution of the drug ... [Pg.249]

Intravenous bolus dose of a 500-mg dose of an antibiotic every six hours in a patient produces minimum steady-state concentration of 10 meg/ mL. If the desired minimum steady-state concentration in this patient is 16 mcg/mL, calculate the size of dose needed to change this concentration. Assume that the drug follows linear kinetics. [Pg.285]

Intravenous bolus dose in a rat efficacy model measuring potency, duration of action, and plasma levels for effect... [Pg.63]

LD50 acute toxicity assessed in CDl male mice after a single intravenous bolus injection. Values are calculated from the number of mice surviving the injection. [Pg.103]

The most sensitive technique for measuring brain uptake is the intravenous bolus administration or infusion and subsequent measurement of brain concentrations (Figure 2.4). Depending on the pharmacokinetics of the test compound in plasma, brain sampling may be performed after suitable circulation times ranging from minutes to hours or days. [Pg.34]

Animal experiments have shown (A3) that equilibration of lignocaine between blood and brain occurs relatively slowly. This may explain why plasma levels of lignocaine that can readily be tolerated, without cerebral side effects, after intravenous bolus injection nevertheless are associated with serious toxic symptoms when produced by constant intravenous infusion or when resulting from impaired metabolic degradation. [Pg.84]

The human intravenous bolus dose of oximes in nerve agent treatment ranges between 250 and 500 mg ". Side effects of oxime treatment in humans were monitored in 750 volunteers, and the main adverse effects reported were changes in blood pressure, pulse rate, dizziness, nausea and blurred vision . Oral administration of oximes produces gastrointestinal distress. ... [Pg.644]

Again we will take blood samples at intervals after dosing, measure plasma drug concentrations, and plot the results on a linear graph (Fig. 11). The first and obvious thing to note is that the plasma concentrations rise to a maximum at around 1 h, whereas, of course, the early plasma concentrations taken soon after the intravenous bolus were the highest. The time to reach the peak plasma concentration after an oral dose is often abbreviated to Tmax, and the concentration itself to Cmax - the maximum concentration achieved after that dose. [Pg.136]

Even if a medication is available in multiple formulations and dosage forms, the prescriber must consider the absorption and distribution differences between adult and pediatric patients. Blood supply at injection or infusion site, available blood supply for unit muscle mass, and skeletal muscle mass relative to body mass vary with patient age and size, causing drug absorption to vary, as well. A rapid intravenous bolus in a pediatric patient might result in acute toxicity a slow intravenous infusion, often required in neonates, can cause erratic, unreliable drug delivery in an older child. In addition, the volume of fluid tolerated for intravenous delivery varies significantly with the age and size of the patient. The blood supply and blood flow to and from the injection site are of prime importance since a gradual decrease in blood supply per unit muscle mass is seen with maturation. In addition, the skeletal muscle mass relative to... [Pg.196]

When the cardiac electrical activity is maintained, but there is no mechanical output (pulseless electrical activity, electromechanical dissociation), then hypovolaemia, tension pneumothorax, pulmonary embolism, cardiac tamponade, and various forms of metabolic or pharmacological disturbance may be responsible. In asystole or pulseless electrical activity (with an underlying rate of less than 60 beats per minute) a single intravenous bolus of 3 mg atropine is recommended. [Pg.508]


See other pages where Intravenous bolus is mentioned: [Pg.228]    [Pg.194]    [Pg.178]    [Pg.146]    [Pg.126]    [Pg.157]    [Pg.55]    [Pg.315]    [Pg.465]    [Pg.1298]    [Pg.131]    [Pg.136]    [Pg.93]    [Pg.320]    [Pg.289]    [Pg.289]    [Pg.44]    [Pg.174]    [Pg.181]    [Pg.544]    [Pg.135]    [Pg.146]    [Pg.174]   
See also in sourсe #XX -- [ Pg.57 , Pg.155 , Pg.156 , Pg.157 , Pg.158 ]




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