Adverse Effects of Resuscitation With Lactated Ringer Compared With Ringer Solution After Severe Hemorrhagic Shock in Rats

Abstract

Lactated Ringer (LR) is a widely used resuscitation fluid that is known to mediate beneficial effects on acid-base balance when compared with normal saline. We here compared LR with the more physiological Ringer solution (RS) regarding acid-base status, hemodynamics, survival, and organ injury following fluid resuscitation subsequent to severe hemorrhagic shock. Anesthetized rats were hemorrhaged to a mean arterial blood pressure of 25 to 30 mmHg within 30 min. After 60 min, they were resuscitated with either RS or LR (three times the shed blood volume) or with RS or LR plus blood (shed blood plus twice its volume) within 30 min. Subsequently, the animals were observed for further 150 min. When the rats were resuscitated with pure LR or RS, all animals of the shock/LR group, but only three of eight shock/RS group rats were dead 100 min later (median survival, 50 ± 13.1 vs. 120 ± 14.1 min; P < 0.05). Coadministration of the shed blood with RS or LR increased the survival rates to 100%. In these blood-resuscitated groups, organ injury, especially of the kidney, was diminished by the use of RS compared with LR. Time-matched acid-base parameters were not different in all shock groups until death of the animals or euthanasia at the end of experimental time. We conclude that, in severe hemorrhagic shock, resuscitation with RS leads to an improved outcome compared with resuscitation with LR, regardless whether blood is coadministered or not.

Volume replacement with Ringer-lactate is detrimental in severe hemorrhagic shock but protective in moderate hemorrhagic shock: studies in a rat model

“…Contrary to recently published results, our group has shown that Ringer-lactate (RL) may mediate toxic effects in rats with severe hemorrhagic shock (mean arterial blood pressure (MAP) 25 to 30 mmHg) [16]. However, whether this effect occurs exclusively in severe hemorrhagic shock remains unclear.…”

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

“…The immunological and metabolic alterations in response to hypoxia contribute to the damage within the microvascular and tubular components of the kidney, which can be seen histologically. In one study following HS, several blood-filled and shrunken glomeruli were present and tubular necrosis was demonstrated by detached basal lamina [42]. Similarly, while models of electrical burns (and associated rhabdomyolysis) may be of benefit in studying AKI, only histological changes (glomerular congestion, proximal tubule degeneration) were shown without evidencing any functional changes [43].…”

“…Renal malondialdehyde generation, reduction in superoxide dismutase (SOD) activity and induction of inducible nitric oxide synthase (iNOS) and subsequent nitric oxide (NO) production were shown after HS in rats [42]. ROS and NOS facilitate the translocation of the transcription factor nuclear factor κ-B (NF-κB) from the cytoplasm to the nucleus, which elicits the inflammatory cascade.…”

“…resuscitation [42]. iNOS and NO production are also generated during hypoxia in rat proximal tubules [58,61] .…”

Changes in Renal Tissue Proteome Induced by Mesenteric Lymph Drainage in Rats After Hemorrhagic Shock With Resuscitation

“…Based on the theory of microcirculation disturbance, fluid resuscitation significantly reduces the morbidity of acute kidney injury (AKI) directly that is induced by ischemia after hemorrhagic shock (2,3). However, the oxidative stress and inflammation response induced by ischemia or reperfusion, hormonal and neural reactions, and vascular hyporeactivity result in refractory hypotension, which consequently causes AKI or acute renal failure (4Y6).…”