| Full text | |
| Author(s): |
Paulo Carnicelli
[1]
;
Denise Aya Otsuki
[2]
;
Adalberto Monteiro Filho
[3]
;
Marcia Aparecida Portela Kahvegian
[4]
;
Keila Kazue Ida
[5]
;
José Otavio Costa Auler-Jr
[6]
;
Jean-Jacques Rouby
[7]
;
Denise Tabacchi Fantoni
[8]
Total Authors: 8
|
| Affiliation: | [1] Universidade de São Paulo. Faculdade de Medicina Veterinária e Zootecnia. Surgery Department - Brasil
[2] Universidade de São Paulo. Hospital das Clínicas da Faculdade de Medicina. LIM08-Laboratory of Anesthesiology - Brasil
[3] Clínica Ufape. Veterinary Intensive Care Unit - Brasil
[4] All Care Vet - Brasil
[5] Texas A&M University. College of Veterinary Medicine and Biomedical Sciences. Department of Small Animal Clinical Sciences
[6] Universidade de São Paulo. Hospital das Clínicas da Faculdade de Medicina. Laboratory of Anesthesiology - Brasil
[7] Medicine Sorbonne University. La Pitié Salpêtrière Hospital. Department of Anaesthesiology and Critical Care - França
[8] Universidade de São Paulo. Faculdade de Medicina Veterinária e Zootecnia. Surgery Department - Brasil
Total Affiliations: 8
|
| Document type: | Journal article |
| Source: | Acta Cirurgica Brasileira; v. 37, n. 7 2022-11-11. |
| Abstract | |
ABSTRACT Purpose: To determine whether dexmedetomidine aggravates hemodynamic, metabolic variables, inflammatory markers, and microcirculation in experimental septic shock. Methods: Twenty-four pigs randomized into: Sham group (n = 8), received saline; Shock group (n = 8), received an intravenous infusion of Escherichia coli O55 (3 × 109 cells/mL, 0.75 mL/kg, 1 hour); Dex-Shock group (n = 8), received bacteria and intravenous dexmedetomidine (bolus 0.5 mcg/kg followed by 0.7 mcg/kg/h). Fluid therapy and/ornorepinephrine were administered to maintain a mean arterial pressure > 65 mmHg. Hemodynamic, metabolic, oxygenation, inflammatory markers, and microcirculation were assessed at baseline, at the end of bacterial infusion, and after 60, 120, 180, and 240 minutes. Results: Compared to Shock group, Dex-Shock group presented a significantly increased oxygen extraction ratio at T180 (23.1 ± 9.7 vs. 32.5 ± 9.2%, P = 0.0220), decreased central venous pressure at T120 (11.6 ± 1 vs. 9.61 ± 1.2 mmHg, P = 0.0214), mixed-venous oxygen saturation at T180 (72.9 ± 9.6 vs. 63.5 ± 9.2%, P = 0.026), and increased plasma lactate (3.7 ± 0.5 vs. 5.5 ± 1 mmol/L, P = 0.003). Despite the Dex-Shock group having a better sublingual vessel density at T240 (12.5 ± 0.4 vs. 14.4 ± 0.3 mL/m2; P = 0.0003), sublingual blood flow was not different from that in the Shock group (2.4 ± 0.2 vs. 2.4 ± 0.1 mL/kg, P = 0.4418). Conclusions: Dexmedetomidine did not worsen the hemodynamic, metabolic, inflammatory, or sublingual blood flow disorders resulting from septic shock. Despite inducing a better sublingual vessel density, dexmedetomidine initially and transitorily increased the mismatch between oxygen supply and demand. (AU) | |