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Updated: Jul 20, 2026
Standardized Hemorrhagic Shock Induction Guided by Cerebral Oximetry and Extended Hemodynamic Monitoring in Pigs
Published on: May 21, 2019
The immediate response to severe shock in a canine model with a combination of hypertonic-hyperoncotic solution with
David García-Martínez1, Eliseo Portilla-de Buen, Caridad Leal
1Surgical Research Division, Centro de Investigación Biomédica de Occidente, Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, México.
To evaluate the acute hemodynamic and acid-base balance effects of hypertonic-hyperoncotic solution (HHS) combined with naloxone in the treatment of hemorrhagic shock in 45 male splenectomized adult mongrel dogs, a severe controlled hemorrhagic shock (20 mmHg mean arterial pressure during 30 min) was established in the groups (n=6) no treatment, shed blood reinfusion, hypertonic-hyperoncotic (saline-dextran) solution alone, naloxone alone (NX), or combination. Interventions included propiopromazine-pentobarbital anesthesia and installation of Swan-Ganz, femoral arterial, and urethral catheters, and exsanguination at 20 mmHg mean arterial pressure during 30 min followed by treatment and observation for 160 min. Fifteen (33%) dogs died before completing the 30-min shock period. Another 33% from the no-treatment group died during the following 90 min. Shed blood improved the cardiac index, arterial pressure, and acid-base balance. NX restored the cardiac index to less than 60% of baseline and reduced vascular resistance. Additionally, NX produced no improvement in acidosis, with 1 dog dead at 95 min posttreatment. HHS restored the cardiac index for 45 min and increased vascular resistance and arterial pressure. Acidosis was not improved. Single-dose HHS combined with naloxone resulted in a high cardiac index, oxygen consumption, and urine output with low peripheral vascular resistance (and no acute mortality) compared with untreated or single-dose groups.
To evaluate the acute hemodynamic and acid-base balance effects of hypertonic-hyperoncotic solution (HHS) combined with naloxone in the treatment of hemorrhagic shock in 45 male splenectomized adult mongrel dogs, a severe controlled hemorrhagic shock (20 mmHg mean arterial pressure during 30 min) was established in the groups (n=6) no treatment, shed blood reinfusion, hypertonic-hyperoncotic (saline-dextran) solution alone, naloxone alone (NX), or combination. Interventions included propiopromazine-pentobarbital anesthesia and installation of Swan-Ganz, femoral arterial, and urethral catheters, and exsanguination at 20 mmHg mean arterial pressure during 30 min followed by treatment and observation for 160 min. Fifteen (33%) dogs died before completing the 30-min shock period. Another 33% from the no-treatment group died during the following 90 min. Shed blood improved the cardiac index, arterial pressure, and acid-base balance. NX restored the cardiac index to less than 60% of baseline and reduced vascular resistance. Additionally, NX produced no improvement in acidosis, with 1 dog dead at 95 min posttreatment. HHS restored the cardiac index for 45 min and increased vascular resistance and arterial pressure. Acidosis was not improved. Single-dose HHS combined with naloxone resulted in a high cardiac index, oxygen consumption, and urine output with low peripheral vascular resistance (and no acute mortality) compared with untreated or single-dose groups.
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