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Panminerva Medica 1999 December;41(4):323-30


lingua: Inglese

Effects of ATP-MgCl2 administration in hypovolemic dogs

Katircioglu S. F., Ulus A. T., Saritas Z., Gokçe P.*

From the Türkiye Yüksek Ihtisas Hospital - Ankara (Turkey) Cardiovascular Surgery Department * University of Study - Ankara (Turkey) Faculty of Veterinary Medicine Cardiovascular Research Center at Surgical Department


Back­ground. The aim of the ­study was to eval­u­ate the effi­ca­cy of ATP-­MgCl2 on myo­car­dial insuf­fi­cien­cy asso­ciat­ed ­with hypo­vo­lem­ic ­shock in ­dogs. We ­designed the ­study as a con­trolled ran­dom­ized ­study.
Meth­ods. Six ­mixed-­breed ­dogs weigh­ing 22±3 kg ­were includ­ed in the con­trol ­group and 20±3 kg in the ATP-­MgCl2 ­group. ­After the ani­mals ­were anes­the­tized 40 ml/kg of ­blood was with­drawn in 15 min­utes. Ani­mals ­were ­observed for 45 min­utes ­after remov­al of ­blood. Six ani­mals ­received 45 ml/kg of lac­tat­ed ­Ringer’s solu­tion and the oth­er ani­mals ­were treat­ed ­with 45 ml/kg of lac­tat­ed ­Ringer’s solu­tion and ATP-­MgCl2. All meas­ure­ments ­were ­made ­before remov­al of ­blood, 45 min ­after exsan­gui­na­tion and at 1 ­hour inter­vals for 3 ­hours. The fol­low­ing param­e­ters ­were meas­ured; system­ic and pul­mo­nary arte­ri­al pres­sures, pul­mo­nary cap­il­lary ­wedge pres­sure, cen­tral ­venous pres­sure, car­diac out­put, rec­tal tem­per­a­ture, arte­ri­al pH, PCO2 and PO2 and ­mixed ­venous hemo­glo­bin oxy­gen sat­u­ra­tion. In addi­tion ­blood sam­ples ­were col­lect­ed for the anal­y­sis of lac­tate and ­tumor necro­sis fac­tor (TNF) con­cen­tra­tions.
­Results. ­After hem­or­rhage, car­diac ­index (CI) ­decreased sig­nif­i­cant­ly ­from 122±9 to 52±9 ml/kg/min in the con­trol ­group (p<0.0001) and ­from 124±11 ml/kg/min to 50±6 ml/kg/min in the ATP-­MgCl2 ­group, respec­tive­ly (p<0.0001). ­After vol­ume replace­ment, Cl was 93±6 ml/kg/min in the con­trol ­group and 111±4 ml/kg/min in the ATP-­MgCl2 ­group 3 ­hours ­after the ­onset of rein­fu­sion, respec­tive­ly (p<0.05). TNF was 36±5 pg/ml in the con­trol ­group and 21±3 pg/ml in the ATP-­MgCl2 ­group (p<0.05). ­Three ­hours ­after the ­onset of hemor­rhag­ic ­shock, oxy­gen con­sump­tion and deliv­ery ­were 126±14 and 206±19 ml/min in the con­trol ­group and 198±16 and 305±27 ml/min in the ATP-­MgCl2 ­group, respec­tive­ly. At the ­same ­time ­point the oxy­gen extrac­tion ­ratio was 0.49±0.04 in the con­trol ­group and 0.61±0.03 in the ATP-­MgCl2 ­group (p<0.01).
Con­clu­sions. Hemor­rhag­ic ­shock caus­es TNF ­release ­which may ­cause mul­ti­ple ­organ fail­ure. ­Organ dys­func­tion ­still per­sists ­even ­after the appro­pri­ate treat­ment. ATP-­MgCl2 atten­u­ates the ­release of TNF ­which may ­improve the ­adverse ­effects of hemor­rhag­ic ­shock.

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