Abstract

Summary The hemodynamic effects of hypertonic saline solution (hss) resuscitation on endotoxic shock were examined in pentoharhital-anesthetized calves (8 to 20 days old). Escherichia coli (055:B5) endotoxin was infused iv at dosage of 0.1 μg/kg of body weight for 30 minutes. Endotoxin induced large decreases in cardiac index, stroke volume, maximal rate of change of left ventricular pressure (+ dP/dtmax), femoral and mesenteric arterial blood flow, glomerular filtration rate, urine production, and mean aortic pressure. Severe pulmonary arterial hypertension and increased pulmonary vascular resistance were evident at the end of endotoxin infusion. Treatment with hss (2,400 mosm of NaCl/L, 4 ml/kg) or an equivalent sodium load of isotonic saline solution (iss: 300 mosm of NaCl/L, 32 ml/kg) was administered 90 minutes after the end of endotoxin administration. Both solutions were infused iv over a 4- to 6-minute period. Administration of hss induced immediate and significant (P < 0.05) increase in stroke volume and central venous pressure, as well as significant decrease in pulmonary vascular resistance. These effects were sustained for 60 minutes, after which all variables returned toward preinfusion values. The hemodynamic response to hss administration was suggestive of rapid plasma volume expansion and redistribution of cardiac output toward splanchnic circulation. Plasma volume expansion by hss was minimal 60 minutes after resuscitation. Administration of iss induced significant increase in cardiac index, stroke volume, femoral arterial blood flow, and urine production. These effects were sustained for 120 minutes, at which time, calves were euthanatized. Compared with hss, iss induced sustained increase in mean pulmonary arterial pressure and only a small increase in mesenteric arterial blood flow. The rapid administration of large-volume iss appears superior to small-volume hss for initial resuscitation of acutely endotoxemic, anesthetized calves. At this time, we do not advocate rapid infusion of iss to septicemic calves because exacerbation of pulmonary hypertension may potentially depress respiratory function, and rapid increase in preload may hemodynamically compromise calves with depressed cardiac contractility.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.