The catecholamine content was examined in the myocardium of dogs subjected to hemorrhagic hypotension of 40mmHg for a duration of one to hive hours respectively. No marked changes were noticed within two hours after production of homorrhagic hypotension but a significant reduction was found at the end of three hours of hypotension. The reduction of myocardial catecholamines was progressively pronounced with the prolonging the hypotensive period over three hours. Dogs were bled rapidly to an arterial blood pressure of 40mmHg and maintained at this hypotensive level for four hours, followed by reinfusion of the withdrawn blood. Eight out of 11 dogs succumbed within l2 hours, showing a 73 per cent mortality. The myocardial catecholamines in the surviving dogs returned almost to the normal level within 12-15 hours after the blood reinfusion, while those in the dogs which succumbed showed the same low level which was produced during hemorrhagic hypotension. It was also shown that the reduced myocardial catecholamines resulting from the hypotension will not be restored immediately after the reinfusion of the withdrawn blood. When norepinephrine was infused at a rate of five to seven microgram/kg/min for an hour before the reinfusion of the withdrawn blood, five out of six dogs died within 12 hours, showing a 82 per cent mortality. This result appears to indicate that norepinephrine infusion during oligemic hypotension may hasten death or not decrease the mortality of the animals. On the other hand, when norepinephrine was infused at a rate of three microgramkg/min for an hour following reinfusion of the withdrawn blood five out of 15 dogs died, indicating a significant increase of survival rate from hemorrhagic shock. The myocardial catecholamines of surviving dogs and dogs which succumbed following the administration of norepinephrine after blood reinfusion were similar respectively to those of dogs which survived and of dogs which died after blood reinfusion without norepinephrine. When norepinephrine (3 microgramkg/min) was infused for hour following blood reinfusion in the dogs pretreated with either dibenzyline (3mg/kg) or dichloroisoproterenol (1mg/kg), the beneficial effect of norepinephrine on the survival rate from hemorrhagic shock appeared to be absent. The efficacy of norepinephrine on the survival from hemorrhagic shock was discussed on the basis of myocardial catecholamine depletion.
Animals ; Catecholamines/*metabolism ; Dogs ; Epiphyses/*embryology ; Myocardium/*metabolism ; Norepinephrine/*pharmacology ; Shock, Hemorrhagic/*drug therapy

Spontaneous rupture with internal bleeding of solid tumors has rarely been described at the time of diagnosis or during chemotherapy. This rare event must be regarded as a life threatening condition. In these emergency situations, control of hemorrhage, which is life-saving, can be achieved by transcatheter arterial embolization (TAE) and/or surgical resection. This report describes two infants presenting with acute hemorrhagic shock due to spontaneous tumor rupture of hepatoblastoma and neuroblastoma during chemotherapy. TAE successfully arrested the tumor bleeding and a visibly reduced the tumor size in both children. Spontaneous rupture of solid tumors occur infrequently in children, but is a life threatening situation. Careful monitoring for the occurrence of this rare event especially in very young children presenting with a large tumor mass.
Child ; Diagnosis ; Drug Therapy ; Emergencies ; Hemorrhage ; Hepatoblastoma ; Humans ; Infant ; Neuroblastoma ; Rupture ; Rupture, Spontaneous ; Shock, Hemorrhagic

BACKGROUNDHemorrhagic shock (HS) results in myocardial contractile dysfunction. Studies showed that 17β-estradiol protects the myocardium against contractile dysfunction. The study investigated the cardioprotective effects of treatment with 17β-estradiol before resuscitation following 1 h of HS and resuscitation.

METHODSMale Sprague-Dawley rats were assigned to 2 sets of experimental protocols: Ex vivo and in vivo treatment and resuscitation. Each set had three experimental groups (n = 6 per group): Normotensive (N), HS and resuscitation (HS-R) and HS rats treated with 17β-estradiol (E) and resuscitated (HS-E-R). Rats were hemorrhaged over 60-min to reach a mean arterial blood pressure of 40 mmHg. In the ex vivo group, hearts were resuscitated by perfusion in the Langendorff system. In the 17β-estradiol treated group, 17β-estradiol 280 µg/kg was added for thefirst 5 min. Cardiac function was measured. Left ventricular generated pressure (LVGP) and +dP/dt were calculated. In the in vivo group, rats were treated with 17β-estradiol 280 µg/kg s.c. after 60-min HS. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30-min to restore normotension.

RESULTSTreatment with 17β-estradiol before resuscitation in ex vivo treated and resuscitated isolated hearts and in the in vivo treated and resuscitated rats following HS improved myocardial contractile function. In the in vivo treated group, LVGP and +dP/dt max were significantly higher in 17β-estradiol treated rats compared to the untreated group (LVGP 136.40 ± 6.61 compared to 47.58 ± 17.55, and +dP/dt 661.85 ± 49.88 compared to 88.18 ± 0.85). Treatment with 17β-estradiol improved LVGP following HS.

CONCLUSIONSThe results indicate that treatment with 17β-estradiol before resuscitation following HS protects the myocardium against dysfunction.

Animals ; Estradiol ; therapeutic use ; Male ; Myocardial Contraction ; drug effects ; Myocardium ; pathology ; Rats ; Rats, Sprague-Dawley ; Resuscitation ; Shock, Hemorrhagic ; drug therapy

OBJECTIVETo study the protective effect of lidocaine against lung injury after hemorrhagic shock in rabbits.

METHODSEighteen healthy rabbits were randomly divided into 3 groups (n=6), namely lidocaine group (group L), hemorrhagic shock group (group H) and control group (group C). Hemorrhagic shock model was established in rabbits in groups L and H, and the venous blood samples were collected for measurement of plasma malondialdehyde (MDA) and superoxidedismutase (SOD) before phlebotomy (T0), 2 h after hemorrhagic shock (T1) and 2 h after resuscitation (T2). Blood samples were also taken for measurement of MDA and SOD at the same time points in group C. The wet to dry weight ratio of the lung (W/D) was measured at T2.

RESULTSMDA level was significantly lower while SOD level significantly higher in group L than in group H (P<0.05). The W/D ratio in group L was reduced significantly as compared with that in group H (P<0.05).

CONCLUSIONLidocaine can remarkably alleviate lung injury after hemorrhagic shock by inhibiting MDA production and increasing SOD content.

Animals ; Disease Models, Animal ; Lidocaine ; pharmacology ; Lung ; drug effects ; metabolism ; Lung Injury ; prevention & control ; Malondialdehyde ; blood ; Rabbits ; Shock, Hemorrhagic ; drug therapy ; Superoxide Dismutase ; blood

OBJECTIVETo introduce the concept, methods for calculation and application of "number needs to be exposed (NNE)" in Epidemiological studies.

METHODSData was analyzed from a study on the association between diaspirin cross-linked hemoglobin (DCLHb) with 28-day mortality in patients with severe traumatic hemorrhagic shock.

RESULTSThe crude "number needed to be exposed for one additional person to be harmed" (NNEH) was 3.7 (95% CI: 2.2-11.5) for the exposure to DCLHb. After controlling the confounding bias of the baseline mortality risk, the adjusted NNEH became 2.6 (95% CI: 1.6-8.0) id., on average, among 2.6 patients exposed to DCLHb, one additional case of death would have developed within 28 days after initial hospitalization if the distribution of baseline mortality risk in exposed group had been equal to that in the unexposed group.

CONCLUSIONNNE could be expressed as the estimated average number of persons needed to be exposed for contributing (either developing or preventing for) one additional case of disease or death in a prospective study when compared with the unexposed persons. As a new index for measuring the absolute effect of an exposure, NNE presented the results on epidemiological studies in a more intuitive and understandable manner. Consequently, this method could be favorably accepted by clinicians, health policy makers and the public.

Epidemiologic Studies ; Hemoglobins ; therapeutic use ; Humans ; Logistic Models ; Randomized Controlled Trials as Topic ; Risk ; Shock, Hemorrhagic ; complications ; drug therapy ; mortality ; pathology ; Software ; Wounds and Injuries ; complications

OBJECTIVETo study the effect of methylprednisolone (MP) on reperfusion injury in severe uncontrolled hemorrhagic shock and explore the possible mechanism involved.

METHODSTwelve dogs were randomly divided into two groups, control group (Group I, n=6) and MP group (Group II, n=6). The animals were bled continuously from a femoral artery catheter to produce uncontrolled hemorrhagic shock models. Resuscitation with lactated Ringer's (LR) solution was initiated when mean arterial pressure (MAP) decreased to 20 mm Hg, and MAP was maintained at 30-40 mm Hg. MP (4 mg/kg) was injected intravenously in Group II when resuscitation began. While in Group I, normal saline (NS) was injected instead. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured before exsanguination (T(1)), when MAP decreased to 20 mm Hg (T(2)), 60 min (T(3)) and 120 min (T(4)) after resuscitation. Heart rate, MAP and cardiac output (CO) levels were recorded concomitantly.

RESULTSInfusion volume and hemorrhage volume shed from the superior mesenteric artery in Group I were higher than those in Group II (P<0.01 and P<0.05). After reperfusion, blood SOD levels decreased progressively and MDA levels increased rapidly in Group I. In Group II, blood SOD levels at T(3) and T(4) decreased as compared with that at T(1) but a stepwise increase was present. At T(4), blood SOD level was significantly higher in Group II than in Group I (Plt;0.01). At T(3) and T(4), MDA levels were markedly lower in Group II than in Group I. During reperfusion, MAP was more steady in Group II than in Group I and survival rate after 120 min (at T(4)) was higher in Group II than in Group I (P<0.05).

CONCLUSIONSMP has a protective effect on severe uncontrolled hemorrhagic shock and subsequent reperfusion injury. The mechanism mainly involves the anti-lipid peroxidation activity of MP.

Analysis of Variance ; Animals ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Female ; Lipid Peroxidation ; Male ; Methylprednisolone ; pharmacology ; Probability ; Random Allocation ; Reference Values ; Reperfusion Injury ; drug therapy ; physiopathology ; Sensitivity and Specificity ; Shock, Hemorrhagic ; drug therapy ; physiopathology ; Survival Rate

AIMTo approach the relationship between lung injury induced by shock/reperfusion and nitric oxide as well as the beneficial effect of taurine.

METHODSTwenty four rabbits were divided randomly into 3 groups (n = 8): control group, shock group, taurine group. The model of lung injury induced by shock/reperfusion was used. The activities of nitric oxide synthase (NOS), superoxide dismutase (SOD), the contents of malondialdehyde (MDA), nitric oxide products (NO2-/NO3-) in plasma and lung homogenate, lung wet/dry weight, lung water content, lung permeability index, and protein content in the pulmonary alveolar lavage fluid were measured. Meanwhile, pathologic samples treated routinely.

RESULTS(1) At 3 hours after reperfusion, the activities of SOD in plasma and lung homogenate decreased markedly, but the other indexes above mentioned were increased significantly compared with the control group (P < 0.01). (2) A close correlation was shown between MDA content and NO2-/NO3- content in plasma and lung. Furthermore, the content of NO2-/NQ3- in lung homogenate showed strong positive correlation with the lung injury parameters. (3) Taurine (40 mg x kg(-1) i.v.) could attenuate all the changes above mentioned at the same time points of reperfusion.

CONCLUSIONNO may play an important role in lung injury induced by shock/reperfusion. Taurine can ameliorate the lung injury, mechanism of which may be related to decreasing the generation of NO and anti-lipoperoxidation.

Animals ; Lung ; drug effects ; metabolism ; Lung Injury ; etiology ; prevention & control ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Rabbits ; Reperfusion Injury ; complications ; drug therapy ; Shock, Hemorrhagic ; complications ; drug therapy ; Superoxide Dismutase ; metabolism ; Taurine ; pharmacology ; therapeutic use

OBJECTIVETo investigate the early effects of hypertonic and isotonic saline solutions on apoptosis of intestinal mucosa in rats with hemorrhagic shock.

METHODSA 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.

RESULTSIn 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).

CONCLUSIONIn 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.

Animals ; Apoptosis ; drug effects ; Disease Models, Animal ; Flow Cytometry ; Fluid Therapy ; methods ; In Situ Nick-End Labeling ; Intestinal Mucosa ; drug effects ; pathology ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Resuscitation ; methods ; Saline Solution, Hypertonic ; administration & dosage ; Shock, Hemorrhagic ; therapy

OBJECTIVETo observe the effect of hypertonic sodium chloride hydroxyethyl starch 40 injection (HSH) in treatment of acute intracranial hypertension complicated by hemorrhagic shock in dogs, and explore the mechanism of the effects of HSH.

METHODSTwenty dogs were randomized into 4 equal groups, namely the 7.5% NaCl (HS) group, Ringer-Lactates solution (RL) group, hydroxyethyl strarch (HES) group, and HSH group. Canine models of acute intracranial hypertension complicated by hemorrhagic shock were established by epidural balloon inflation with saline and rapid discharge of the arterial blood. One hour after the induced shock, the dogs were given HS (6 ml/kg), RL of 3-fold volume of blood loss, HES of equivalent volume of blood loss, and HSH 8 ml/kg in the 4 groups, respectively. During the shock and resuscitationperiod, the intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) of the dogs were monitored, and the serum sodium level and plasma osmolality were measured at 30 min, 1 h and 4 h after the resuscitation.

RESULTSAll dogs had similar MAP, CPP, and ICP before resuscitation (P>0.05). After resuscitation, the MAP was significantly improved (P<0.01), but the dogs in HSH group exhibited the fastest response; with the exception of the dogs in HS group to have significantly decreased MAP 2 h after resuscitation (P<0.01), all the other dogs maintained the MAP for 4 h. The CPP was also significantly increased after resuscitation (P<0.01), and in HS group, CPP decreased significantly after 2 h (P<0.01), and HSH group maintained the high CPP after 4 h. The ICP was increased significantly in RL and HES groups after resuscitation (P<0.01), reaching the peak level at 1 and 3 h, respectively, but in HS and HSH groups, the ICP decreased significantly to the lowest level at 1 h (P<0.01) which was maintained for 4 h. After resuscitation, the plasma sodium and plasma osmolality were significantly increased in HSH and HS groups.

CONCLUSIONIn dogs with acute intracranial hypertension and hemorrhagic shock, HSH can effectively resuscitate hemorrhagic shock and decrease ICP, and the effect is longer-lasting than that of HS.

Acute Disease ; Animals ; Dogs ; Female ; Hydroxyethyl Starch Derivatives ; administration & dosage ; therapeutic use ; Intracranial Hypertension ; drug therapy ; etiology ; Male ; Plasma Substitutes ; administration & dosage ; therapeutic use ; Random Allocation ; Saline Solution, Hypertonic ; administration & dosage ; therapeutic use ; Shock, Hemorrhagic ; complications ; drug therapy ; Treatment Outcome

OBJECTIVEGlutamine (Gln) is now considered as conditionally essential amino acid with many biological activities. This study aimed to investigate whether it has protective effects on the intestinal mucosal barrier in young rabbits under hemorrhagic shock.

METHODSEighteen young rabbits aged 26 +/- 3 days were randomly assigned into 3 groups: Control (no treatment), Low-dose Gln (L-Gln, 0.5 g/kg daily) and High-dose Gln (H-Gln, 1.0 g/kg daily) treatment groups. Gln was administered by gastric tube daily for 7 days and then hemorrhagic shock was induced by blood withdrawing from femoral artery. Plasma levels of diamine oxidase (DAO) and serum levels of interleukin-8 (IL-8) were measured before shock, and at 2, 6 and 24 hrs after resuscitation. Ileum tissues located approximately 5 cm away from the ileocecal valve was removed for histological examination, lymphocyte distribution, polymorphonuclear (PMN) count and assessing the height, width and surface area of the villi.

RESULTSPlasma levels of DAO and serum levels of IL-8 at 6 and 24 hrs after resuscitation in the L-Gln and the H-Gln groups decreased significantly compared with those of the Control group. L-Gln and H-Gln also resulted in a decrease in the PMN counts and the lymphocyte percentage in the ileum compared with the Control group. Exfoliation and atrophy of villous epithelial cells occurred and the height and surface area of villous were reduced in the Control group. The ileum morphology of the two Gln treatment groups was found to be nearly normal. There were no differences between the L-Gln and the H-Gln groups.

CONCLUSIONSGln within a therapeutic dose has protective effects on intestinal mucosal barrier in young rabbits under hemorrhagic shock.

Amine Oxidase (Copper-Containing) ; blood ; Animals ; Bacterial Translocation ; drug effects ; Female ; Glutamine ; therapeutic use ; Interleukin-8 ; blood ; Intestinal Mucosa ; drug effects ; immunology ; pathology ; Male ; Rabbits ; Shock, Hemorrhagic ; complications ; drug therapy ; immunology ; Systemic Inflammatory Response Syndrome ; prevention & control