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Bone marrow (BM) dysfunction after trauma and hemorrhagic shock (T/HS) results in a decrease in clonogenic growth of BM progenitors through a plasma-mediated process. Although sex hormones have been shown to modulate some end-organ injury after shock, post-T/HS BM dysfunction has only been studied in male animals. Therefore, the present study examines the effects of sex hormones on post-T/HS BM dysfunction by measuring clonogenic growth of BM progenitors in castrated male rats and in ovariectomized and proestrus female rats.Laboratory experiment.University surgical research laboratory.Castrated and noncastrated male and ovariectomized and proestrus female Sprague-Dawley rats.All rats were subjected to either T/HS or sham shock with laparotomy (n = 3-5 per group). At 3 hrs after resuscitation, the rats were killed and plasma and BM mononuclear cells from bilateral femurs were harvested.BM mononuclear cells were cultured for erythroid burst-forming unit and granulocyte-macrophage colony-forming unit colonies to assess the extent of progenitor BM dysfunction. BM from noncastrated male rats subjected to T/HS demonstrated a significant decrease in granulocyte-macrophage colony-forming unit and erythroid burst-forming unit colony formation compared with BM of all the sham shock groups and with the castrated male and both female rat groups subjected to T/HS. In addition, plasma from noncastrated shocked male rats incubated in vitro with BM cells from unmanipulated male rats caused a significant suppression of BM granulocyte-macrophage colony-forming unit and erythroid burst-forming unit colonies compared with plasma from castrated rats subjected to either sham shock with laparotomy or T/HS.The profound BM dysfunction observed in noncastrated male rats after T/HS is not observed in proestrus female rats and castrated male rats. In addition, the in vitro plasma-mediated BM suppression present in male rats after T/HS is also lost in castrated male rats. Sex hormones seem to play a significant role in BM dysfunction after T/HS.

Objective: To determine whether hemorrhagic shock-induced bone marrow failure is mediated by the gut through the production of toxic mesenteric lymph and whether shock-induced bone marrow failure could be prevented by division of the mesenteric lymphatics. Design: Prospective, controlled study. Setting: University surgical research laboratory. Subjects: Male Sprague-Dawley rats. Interventions: Rats were divided into five groups: unmanipulated controls (n = 12), hemorrhagic shock with laparotomy (n = 8), hemorrhagic shock with mesenteric lymph duct ligation (n = 10), sham shock with laparotomy (n = 6), and sham shock with mesenteric lymph duct ligation (n = 7). At either 3 or 6 hrs after resuscitation, bone marrow was obtained for determination of early (cobblestone forming cells) and late (granulocyte-macrophage colony forming unit and erythroid burst forming unit) hematopoietic progenitor cell growth. Parallel cultures were plated with plasma (1% and 2% v/v) from all groups to determine the effect of lymphatic ligation on hematopoiesis. Measurements and Main Results: Bone marrow cellularity, cobblestone forming cells, granulocyte-macrophage colony forming unit, and erythroid burst forming unit growth in rats subjected to hemorrhagic with lymph duct ligation were similar to those observed in sham-treated animals and significantly greater than in rats subjected to shock and laparotomy without lymphatic duct ligation. Plasma from rats subjected to shock without lymph ligation was inhibitory to hematopoietic progenitor cell growth. In contrast, this shock-induced inhibition was not observed with plasma obtained from shocked rats that underwent mesenteric lymph ligation. Conclusions: Hemorrhagic shock suppresses bone marrow hematopoiesis as measured by a decrease in early and late progenitor cell growth. This suppression appears mediated through mesenteric lymph as the effect is abrogated by mesenteric lymph duct ligation. These data clearly demonstrate a link between the gut and bone marrow failure after hemorrhagic shock.

The major physiological effects of hemorrhage are hypovolemia and anemia. The administration of an oxygen-carrying plasma expander, such as crystalline hemoglobin solution (CHb), can restore both of these deficits while avoiding many of the logistical problems entailed in the use of blood. The authors have used Chb to treat severe hypovolemia and anemia in separate canine models and found it to be highly effective. CHb acts as a colloid plasma expander to resuscitate intravascular volume in hypovolemia and supplements oxygen-carrying capacity in anemia. CHb can support oxygen transport essentially in the absence of red blood cells. Hemodynamic responses to low P50 CHb, however, suggest that oxygen offloading at the tissue level is compromised by the high oxygen affinity of unmodified CHb. Whereas such oxygen offloading deficits may be compensated for in the chronic situation, they may be of crucial importance in severe trauma where oxygen transport is often limited by arterial desaturation, low cardiac output, maldistribution of perfusion and interstitial water overload. The development of a lower-affinity CHb is, therefore, of the essence.

Periods of apnea or severe hypoventilation may occur during procedures which involve the airway or during thoracic operations. Routine vital signs and ECG monitoring of these situations are incapable of quantitating the severe tissue hypoxia and acidosis which develop under these circumstances; rather, they only reflect the morbid complications of hypoxia and acidosis (i.e., bradycardia, ectopy, and hypotension). Transcutaneous oxygen and carbon dioxide sensors directly measure tissue gas tensions with a short sensor response time. This report documents the efficacy of transcutaneous gas tension monitoring in the management of these high-risk situations.