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10.1111/j.1365-2125.1986.tb02876.x http://scihub22266oqcxt.onion/10.1111/j.1365-2125.1986.tb02876.x 3741724!1401074!3741724     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=3741724&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Br+J+Clin+Pharmacol 1986 ; 22 (1): 31-6 Nephropedia Template TP {{tp|p=3741724|t=1986. Cardiovascular toxicity and distribution kinetics of intravenous chloroquine |pdf=|usr=}}{{3741724}} gab.com Text Cardiovascular toxicity and distribution kinetics of intravenous chloroquine JO: Br J Clin Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=3741724 #FOAvip Chloroquine diphosphate (3 mg base kg-1) was given by constant rate intravenous injection over 10 min to 12 healthy adult male volunteers. Plasma concentrations of chloroquine and the principal metabolite desethylchloroquine, electrocardiograph intervals, and arterial blood pressure were measured at frequent intervals to determine the relationship between cardiovascular effects and plasma concentrations. Peak plasma concentrations ranged between 784 and 6649 (mean 2913) ng ml-1. The decline in plasma concentrations was multiexponential with an initial rapid distribution phase; mean (+/- s.d.) first order rate constant 0.65 +/- 0.14 min-1, and an estimated apparent volume of the central compartment of 0.18 +/- 0.15 l kg-1. There was no serious toxicity, but subjective side effects were reported in all patients and there was a significant fall in systolic blood pressure (110 +/- 9.5 to 101 +/- 12.5 mm Hg; P = 0.03) and rise in heart rate which paralleled the change in plasma chloroquine concentrations. Coincident with changes in blood pressure, there was a significant prolongation of the electrocardiograph QRS interval; 81 +/- 15 to 92 +/- 13 ms (P less than 0.01) but no change in the QTc interval. These findings suggest that the cardiovascular toxicity of parenteral chloroquine is related to transiently high plasma concentrations occurring early in the distribution phase. This results from incomplete distribution from a central compartment that is approximately one thousand times smaller than the eventual total apparent volume of distribution at steady state. Rate of administration is therefore a major determinant of toxicity. Twit Text FOAVip Cardiovascular toxicity and distribution kinetics of intravenous chloroquine ????Br J Clin Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=3741724 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=3741724 #FOAvip English Wikipedia <ref>{{Cite pmid|3741724}}</ref> Cardiovascular toxicity and distribution kinetics of intravenous chloroquine #MMPMID3741724 Looareesuwan S; White NJ; Chanthavanich P; Edwards G; Nicholl DD; Bunch C; Warrell DA Br J Clin Pharmacol 1986[Jul]; 22 (1): 31-6 PMID3741724show ga Chloroquine diphosphate (3 mg base kg-1) was given by constant rate intravenous injection over 10 min to 12 healthy adult male volunteers. Plasma concentrations of chloroquine and the principal metabolite desethylchloroquine, electrocardiograph intervals, and arterial blood pressure were measured at frequent intervals to determine the relationship between cardiovascular effects and plasma concentrations. Peak plasma concentrations ranged between 784 and 6649 (mean 2913) ng ml-1. The decline in plasma concentrations was multiexponential with an initial rapid distribution phase; mean (+/- s.d.) first order rate constant 0.65 +/- 0.14 min-1, and an estimated apparent volume of the central compartment of 0.18 +/- 0.15 l kg-1. There was no serious toxicity, but subjective side effects were reported in all patients and there was a significant fall in systolic blood pressure (110 +/- 9.5 to 101 +/- 12.5 mm Hg; P = 0.03) and rise in heart rate which paralleled the change in plasma chloroquine concentrations. Coincident with changes in blood pressure, there was a significant prolongation of the electrocardiograph QRS interval; 81 +/- 15 to 92 +/- 13 ms (P less than 0.01) but no change in the QTc interval. These findings suggest that the cardiovascular toxicity of parenteral chloroquine is related to transiently high plasma concentrations occurring early in the distribution phase. This results from incomplete distribution from a central compartment that is approximately one thousand times smaller than the eventual total apparent volume of distribution at steady state. Rate of administration is therefore a major determinant of toxicity. |Adolescent[MESH] |Adult[MESH] |Blood Pressure/drug effects[MESH] |Cardiovascular System/*drug effects[MESH] |Chloroquine/administration & dosage/adverse effects/*metabolism[MESH] |Electrocardiography[MESH] |Humans[MESH] |Injections, Intravenous[MESH] |Kinetics[MESH] |Male[MESH]Cardiovascular toxicity and distribution kinetics of intravenous chlor(epmc).pdf DeepDyve Pubget Overpricing