Abstract:Purpose:The comparison after 6h of hemorrhagic shock (HS) treatment with NaCl 7.5% (Hypertonic Saline Solution -SSH) or Ringer Lactate (RL) on liver function and integrity. Methods: Male Wistar rats were submitted to HS (Mean Arterial Pressure -MAP= 45 mmHg) during 60 min and then treated with NaCl 7.5% (SSH, 10% of blood loss, n=8) or Ringer Lactate (RL, 400% of blood loss, n=8). After 6h rats were anesthetized, hepatic function was assessed by bile flow measurement and liver integrity evaluated by determinat… Show more
“…Previous study had shown that hypertonic saline with a colloid solution improved myocardial circulation in sepsis [25]. Hypertonic perfusion was also reported to reduce myocardial injury by reducing edema and diminishing calcium accumulation via decreasing Na/Ca exchange-mediated pathway during hypoxia [19,26]. Therefore, the enhanced myocardial anti-oxidative capacity in hyperosmolarityperfused hearts and enhanced coronary vasodilation may act in concert to reduce myocardial injury.…”
Background: Hyperosmotic solutions have been used successfully in different shock resuscitations with cardioprotection. This study was to examine the effects of hyperosmotic sodium chloride on isolated heart function and heart responses to ischemia/reperfusion in normotensive and hypertensive rats. The roles of hyperosmolarity-induced antioxidants including hyperosmolarity-relevant heat shock proteins as well as vasodilating endothelial nitric oxide synthase (eNOS) and vasoactive catecholamines were investigated.Methods: Hearts of normal rats and stroke-prone spontaneously hypertensive rats were isolated and perfused for 30 min with control Krebs-Henseleit buffer (osmolarity 300 mOsm/L) or hyperosmotic buffer of different sodium chloride concentrations (320, 350 and 400 mOsm/L) before subjected to 40-min global ischemia followed by 10-min hyperosmotic reperfusion and 30-min normal buffer reperfusion. Heart function, creatine phosphokinase leakage and myocardial antioxidants were examined. Myocardial antioxidants after hyperosmotic perfusion with different osmolytes were assayed with Western blotting.Results: Pre-ischemic hyperosmotic sodium chloride perfusion enhanced heart contractility and diastole function and reduced coronary vascular resistance in both normal and hypertensive hearts. Post-ischemic recoveries of heart function were improved in hyperosmotic perfused hearts, associated with lower creatine phosphokinase leakage, higher coronary flow, reduced coronary resistance and lower norepinephrine overflow. At the end of reperfusion, the myocardial activities of total superoxide dismutase and catalase, glutathione content as well as osmosis-relevant heat shock protein 32 and 90 were increased in hyperosmotic hearts. In addition to sodium chloride, in vitro hyperosmotic mannitol, glucose and raffinose also increased protein expressions of antioxidants including superoxide dismutase, catalase, heat shock protein 32 and 90 and vasodilating eNOS.
Conclusion:Hyperosmotic perfusion enhanced heart function and preconditioned normal and hypertensive hearts against ischemia/reperfusion injury. The hyperosmolarity-induced up-regulations in myocardial antioxidants including heat shock proteins and eNOS may play an important role in the hyperosmolarity-induced cardioprotection.
“…Previous study had shown that hypertonic saline with a colloid solution improved myocardial circulation in sepsis [25]. Hypertonic perfusion was also reported to reduce myocardial injury by reducing edema and diminishing calcium accumulation via decreasing Na/Ca exchange-mediated pathway during hypoxia [19,26]. Therefore, the enhanced myocardial anti-oxidative capacity in hyperosmolarityperfused hearts and enhanced coronary vasodilation may act in concert to reduce myocardial injury.…”
Background: Hyperosmotic solutions have been used successfully in different shock resuscitations with cardioprotection. This study was to examine the effects of hyperosmotic sodium chloride on isolated heart function and heart responses to ischemia/reperfusion in normotensive and hypertensive rats. The roles of hyperosmolarity-induced antioxidants including hyperosmolarity-relevant heat shock proteins as well as vasodilating endothelial nitric oxide synthase (eNOS) and vasoactive catecholamines were investigated.Methods: Hearts of normal rats and stroke-prone spontaneously hypertensive rats were isolated and perfused for 30 min with control Krebs-Henseleit buffer (osmolarity 300 mOsm/L) or hyperosmotic buffer of different sodium chloride concentrations (320, 350 and 400 mOsm/L) before subjected to 40-min global ischemia followed by 10-min hyperosmotic reperfusion and 30-min normal buffer reperfusion. Heart function, creatine phosphokinase leakage and myocardial antioxidants were examined. Myocardial antioxidants after hyperosmotic perfusion with different osmolytes were assayed with Western blotting.Results: Pre-ischemic hyperosmotic sodium chloride perfusion enhanced heart contractility and diastole function and reduced coronary vascular resistance in both normal and hypertensive hearts. Post-ischemic recoveries of heart function were improved in hyperosmotic perfused hearts, associated with lower creatine phosphokinase leakage, higher coronary flow, reduced coronary resistance and lower norepinephrine overflow. At the end of reperfusion, the myocardial activities of total superoxide dismutase and catalase, glutathione content as well as osmosis-relevant heat shock protein 32 and 90 were increased in hyperosmotic hearts. In addition to sodium chloride, in vitro hyperosmotic mannitol, glucose and raffinose also increased protein expressions of antioxidants including superoxide dismutase, catalase, heat shock protein 32 and 90 and vasodilating eNOS.
Conclusion:Hyperosmotic perfusion enhanced heart function and preconditioned normal and hypertensive hearts against ischemia/reperfusion injury. The hyperosmolarity-induced up-regulations in myocardial antioxidants including heat shock proteins and eNOS may play an important role in the hyperosmolarity-induced cardioprotection.
“…It was soon realized that the physiological vasodilator property of hypertonicity was a useful byproduct of small volume resuscitation in that it induced reperfusion of previously ischemic territories. Subsequently, a number of researches disclosed previously unsuspected properties of HTS resuscitation, amongst them the correction of endothelial and red cell edema accompanying significant consequences in capillary blood flow (Victorino et al, 2003;Homma et al, 2005;Hoppen et al, 2005;Cruz et al, 2006).…”
Abstract:Objective: To investigate the potential and early effect of hypertonic saline resuscitation on T-lymphocyte subpopulations in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock was established in 18 Sprague-Dawley (SD) rats. The rats were randomly divided into Sham group, HTS group (hypertonic saline resuscitation group) and NS group (normal saline resuscitation group). Each group contained 6 rats. The CD4 + and CD8 + subpopulations of T-lymphocytes in peripheral blood were detected respectively before shock and after resuscitation by double antibody labelling and flow cytometry. Results: In the early stage after hemorrhagic shock, fluid resuscitation and emergency treatment, the CD4 + lymphocytes of peripheral blood in HTS and NS groups markedly increased. Small volume resuscitation with HTS also induced peripheral CD8 + lymphocytes to a certain extent, whereas NS resuscitation showed no effect in this respect. Consequently, compared with Sham and HTS groups, CD4 + /CD8+ ratio of peripheral blood in NS group was obviously increased, and showed statistically differences. Conclusion: In this model of rat with severe hemorrhagic shock, small volume resuscitation with HTS is more effective than NS in reducing immunologic disorders and promoting a more balanced profile of T-lymphocyte subpopulations regulating network.
“…Firstly, HTS resuscitation effectively ameliorates the cellular metabolisms by inducing a considerable microcirculatory improvement and restoring intestinal perfusion, which can reduce abnormal apoptosis of small intestinal mucosa (Murao et al, 2003;Shires et al, 2005). This positive effect of HTS is related to the correction of endothelial or red cell edema and selective vasodilation of the precapillary arteriole, accompanying significant consequences in capillary blood flow (Victorino et al, 2003;Vajda et al, 2004;Homma et al, 2005;Hoppen et al, 2005;Zakaria et al, 2006). Secondly, hemorrhagic shock causes a whole body ischemiareperfusion injury, leading to multiple organ dysfunctions.…”
Abstract:Objective: To investigate the early effects of hypertonic and isotonic saline solutions on apoptosis of intestinal mucosa in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock was established in 21 Sprague-Dawley (SD) rats. The rats were randomly divided into the sham group, normal saline resuscitation (NS) group, and hypertonic saline resuscitation (HTS) group, with 7 in each group. We detected and compared the apoptosis in small intestinal mucosa of rats after hemorrhagic shock and resuscitation by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), FITC (fluorescein-iso-thiocyanate)-Annexin V/PI (propidium iodide) double staining method, and flow cytometry. Results: In the early stage of hemorrhagic shock and resuscitation, marked apoptosis of small intestinal mucosa in the rats of both NS and HTS groups was observed. The numbers of apoptotic cells in these two groups were significantly greater than that in the sham group (P<0.01). In the HTS group, the apoptic cells significantly decreased, compared with the NS group (P<0.01). Conclusion: In this rat model of severe hemorrhagic shock, the HTS resuscitation of small volume is more effective than the NS resuscitation in reducing apoptosis of intestinal mucosa in rats, which may improve the prognosis of trauma.
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