OBJECTIVETo investigate the influence of myocardial inhibition on injury to liver, kidney and intestine and blood perfusion at early stage in rat with severe burn.

METHODSThirty-two healthy male Wistar rats were enrolled in the study and randomly divided into sham scald, propranolol, scald control and scald + propranolol groups, with 8 rats in each group. After intraperitoneal injection of 10 g/L pentobarbital sodium for anesthesia, rats of the former two groups were sham scalded in a water bath of 37 degrees C for 18 s, while the latter two groups were inflicted with 30% TBSA full-thickness scald in a 97 degrees C water bath for 18 s. Rats were resuscitated with Ringer's lactate solution (4 mL x kg(-1) x 1% TBSA(-1), i. p.) following the Parkland formula 30 mins after the injury. At the same time, rats in propranolol and scald + propranolol groups received propranolol 0.75 mg/kg intravenously. After 6 hours, parameters of myocardiac mechanics (SBP, DBP, MAP, LVSP, LVEDP, +/- dp/dt max) were recorded by the multiple channel physiological signal collecting and processing system; blood flow of liver, kidney and intestine were detected with the laser doppler flowmetry; the serum contents of cTnI, TBA, beta2-MG and DAO were determined for reflecting injuries to the heart, liver, kidney and intestine, respectively.

RESULTSMyocardiac mechanics parameters, with the exception of LVEDP, were decreased in propranolol group as compared with those in sham group (P <.05). All myocardiac mechanics parameters in burn control group were lower than those in sham group and higher than those in burn + propranolol group (P < 0.05). Blood flow of organs showed similar changes in above-mentioned 3 groups (P < 0.05). Organ damages as shown in burn control group [cTnI (4.86 +/- 0.29) microg/L, TBA (83.6 +/- 18.2) micromol/L, beta2-MG (2.75 +/- 0.19) mg/L, DAO (1.45 +/- 0.09) x 10(3) U/L] were more serious than those in sham control group [cTnI (1.73 +/- 0.09) microg/L, TBA (24.5 +/- 2.4) micromol/L, beta2-MG (1.15 +/- 0.18) mg/L, DAO (0.87 +/- 0.13) x 10(3) U/L], and less serious than those in scald + propranolol group [cTnI 5.95 +/- 0.42 microg/L, TBA 125.8 +/- 21.3 micromol/L, beta2-MG 3.25 +/- 0.17 mg/L, DAO (1.83 +/- 0.13) x 10(3) U/L] (P < 0.05).

CONCLUSIONSPropranolol can aggravate injury to the liver, kidney and intestine at early stage in rat with severe burn, suggesting that "shock heart" may be one of initial factors in lowering blood flow to the organs, thus inducing injury to them.

Animals ; Blood Pressure ; Burns ; metabolism ; physiopathology ; Intestines ; blood supply ; Kidney ; blood supply ; Liver ; blood supply ; Male ; Myocardium ; metabolism ; Propranolol ; adverse effects ; Rats ; Rats, Wistar ; Shock

OBJECTIVETo investigate the systemic influence after an island flap with venous congestion-reperfusion.

METHODSAn island flap was formed in a Rat model. The vein in the pedicle was clamped for 2 hours, 6 hours and 10 hours and released. The ear microcirculation, levels of TNF alpha and IL-10 were measured, and the neutrophils sequestration in tissues were counted. The vascular structure of the lung and intestine were evaluated.

RESULTSThere were significant changes in the ear microcirculation, neutrophils sequestration of the lung and the intestine in the 2 hours, 6 hours and 10 hours groups, and became more serious by the time increasing. The TNF alpha level reached in maximum at 1 hour after the reperfusion, while the IL-10 became to the lowest level at 3 hours after the reperfusion. However, the TNF alpha and IL-10 levels were significant high in the 6 hour and 10 hours groups, compared with the 2 hours group and the control, but there was no differences between the2 hours group and the control.

CONCLUSIONSVenous congestion-reperfusion of flap could injury the remote organs such as lung, intestinal etc. The injury could be more serious with the time increasing.

Animals ; Constriction ; Ear ; blood supply ; Hyperemia ; complications ; Interleukin-10 ; analysis ; Intestines ; blood supply ; Leukocyte Count ; Lung ; blood supply ; Microcirculation ; Neutrophils ; cytology ; Rats ; Reperfusion Injury ; etiology ; Surgical Flaps ; blood supply ; Time Factors ; Tumor Necrosis Factor-alpha ; analysis ; Veins

PURPOSE: We reviewed the cases of 33 patients from our clinic and 142 patients from the literature with congenital bronchopulmonary vascular malformations (BPVM), systematically analyzed the bronchopulmonary airways, pulmonary arterial supplies, and pulmonary venous drainages, and classified these patients by pulmonary malinosculation (PM). MATERIALS AND METHODS: From January 1990 to January 2007, a total of 33 patients (17 men or boys and 16 women or girls), aged 1 day to 24 years (median, 2.5 months), with congenital BPVM were included in this study. Profiles of clinical manifestations, chest radiographs, echocardiographs, esophagographs, computer tomography (CT), magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), cardiac catheterizations with angiography, contrast bronchographs, bronchoscopies, chromosomal studies, surgeries, and autopsies of these patients were analyzed to confirm the diagnosis of congenital BPVM. A total of 142 cases from the literature were also reviewed and classified similarly. RESULTS: The malformations of our 33 patients can be classified as type A isolated bronchial PM in 13 patients, type B isolated arterial PM in three, type C isolated venous PM in two, type D mixed bronchoarterial PM in five, type F mixed arteriovenous PM in one, and type G mixed bronchoarteriovenous PM in nine. CONCLUSION: Dysmorphogeneses of the primitive foregut system and the primitive aortic arch system may lead to haphazard malinosculations of the airways, arteries, and veins of the lung. A systematic classification of patients with congenital BPVM is clinically feasible by assessing the three basic bronchovascular systems of the lung independently.
Adolescent ; Adult ; Aorta, Thoracic/*abnormalities ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Infant, Newborn ; Intestines/*abnormalities/*blood supply ; Lung/*abnormalities/*blood supply ; Male ; Vascular Malformations/*classification

Animals ; Escin ; pharmacology ; Intestines ; blood supply ; Lipid Peroxidation ; drug effects ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; physiopathology ; prevention & control

The role of nuclear factor kappaB in intestine injury induced by hepatic ischemia reperfusion was investigated. Eighteen male Wistar rats were divided into 3 groups randomly: sham operation group (group A), hepatic ischemia reperfusion group (group B) and hepatic ischemia reperfusion plus pyrrolidine dithiocarbamate (PDTC) group (group C). The rats in group A were only subjected to laparotomy, those in group B underwent partial hepatic ischemia reperfusion (ischemia for 1 h and reperfusion for 2 h) and those in group C underwent the same procedure as that of group B but received PDTC 200 mg/kg i.v. before and after ischemia. After reperfusion, tissues of jejunum and venous blood were obtained for measurement of TNF-alpha, MDA and MPO. The levels of TNF-alpha in jejunum and venous blood, the levels of MPO in jejunum in group B were significantly higher than those in group A and group C (P<0.05). There was no significant different in the levels of MDA between group B and group C. The severity of histological intestinal injury in group B and group C was similar. Hepatic ischemia reperfusion caused intestine injury, NF-kappaB may play an important role in this course and the targeting of upstream components of the inflammatory response, such as NF-kappaB, may have important therapeutic applications.
Animals ; Intestines ; pathology ; Liver ; blood supply ; metabolism ; Male ; NF-kappa B ; biosynthesis ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism

AIMTo explore effects of Safflor (Chinese Tradional Medicine) on the intestine ultrastructure characteristics during intestine ischemia/ reperfusion injury (I/RI) in rabbits.

METHODSThirty rabbits were randomly divided into three groups: control group (group S), ischemia/reperfusion group (group I/R) and Safflor injection group (group SI). Morphological changes of intestine ischemia/reperfusion in rabbits and the protective effects of Safflor were observed under electric telescope.

RESULTSThe intestine ultrastructure was badly injured in group I/R. Mitochondria and intestinal mucosal cells were swellen and endoplasmic reticulum expanded, however, in the SI group the ultrastructural injury of the ischemia greatly ameliorated.

CONCLUSIONThe ultrastructure injury occurrted after intestine I/RI and Safflor has protective effects on the intestine ultrastructure.

Animals ; Carthamus tinctorius ; chemistry ; Drugs, Chinese Herbal ; pharmacology ; Female ; Intestines ; blood supply ; ultrastructure ; Male ; Rabbits ; Reperfusion Injury ; prevention & control

The role of nuclear factor kappaB in intestine injury induced by hepatic ischemia reperfusion was investigated. Eighteen male Wistar rats were divided into 3 groups randomly: sham operation group (group A), hepatic ischemia reperfusion group (group B) and hepatic ischemia reperfusion plus pyrrolidine dithiocarbamate (PDTC) group (group C). The rats in group A were only subjected to laparotomy, those in group B underwent partial hepatic ischemia reperfusion (ischemia for 1 h and reperfusion for 2 h) and those in group C underwent the same procedure as that of group B but received PDTC 200 mg/kg i.v. before and after ischemia. After reperfusion, tissues of jejunum and venous blood were obtained for measurement of TNF-alpha, MDA and MPO. The levels of TNF-alpha in jejunum and venous blood, the levels of MPO in jejunum in group B were significantly higher than those in group A and group C (P<0.05). There was no significant different in the levels of MDA between group B and group C. The severity of histological intestinal injury in group B and group C was similar. Hepatic ischemia reperfusion caused intestine injury, NF-kappaB may play an important role in this course and the targeting of upstream components of the inflammatory response, such as NF-kappaB, may have important therapeutic applications.
Intestines/*pathology ; Liver/*blood supply ; Liver/metabolism ; NF-kappa B/*biosynthesis ; Random Allocation ; Rats, Wistar ; Reperfusion Injury/*metabolism

We report on an exceptional vascular cause of gastrointestinal hemorrhage. A 30-yr-old man was admitted because of recurrent hematochezia. Colonoscopy showed circumferential, erythematous, and nodular vascular distensions with hematocystic spots in the terminal ileum resembling varicosis and subsequent computed tomography with 3-dimensional angiographic reconstruction revealed a vascular architecture around the terminal ileum. No other potential source of bleeding was identified. The patient was treated by ileocecectomy and the final diagnosis was of an arteriovenous malformation confined to the terminal ileum. He has been followedup without a further hemorrhagic episode.
Adult ; Arteriovenous Malformations/complications/*pathology ; Diagnosis, Differential ; Gastrointestinal Hemorrhage/etiology/*pathology ; Humans ; Ileum/*abnormalities ; Intestines/*blood supply ; Male ; Recurrence ; Varicose Veins/etiology/*pathology

OBJECTIVETo investigate the protective effect of limited fluid resuscitation against intestinal ischemia- reperfusion injury in postpartum rabbits with severe uncontrolled obstetrical hemorrhagic shock.

METHODSTwenty- four postpartum rabbits were randomly assigned into sham shock group (group P), shock group without interventions (group P0), conventional fluid resuscitation group (group PNL), and limited fluid resuscitation group (group PLH), and the model of severe uncontrolled hemorrhagic shock was established in the latter 3 groups. The rabbits were sacrificed 4 h later, and SOD activity and MDA content in the intestinal mucosa and the degree of injury to the intestinal mucosa were observed.

RESULTSIschemia-reperfusion injury of the intestine due to uncontrolled hemorrhagic shock resulted in decreased SOD activity and increased MDA content. The MDA content was significantly lower and SOD activity was significantly higher in group PLH than in group PNL (P<0.05), and the intestinal mucosal tissue morphology and intestinal mucosa barrier lesion increased in group PLH.

CONCLUSIONInitial limited fluid resuscitation can relieve intestinal ischemia-reperfusion injury in postpartum rabbits with severe uncontrolled obstetrical hemorrhagic shock.

Animals ; Disease Models, Animal ; Female ; Fluid Therapy ; methods ; Intestines ; blood supply ; Pregnancy ; Rabbits ; Reperfusion Injury ; etiology ; prevention & control ; Shock, Hemorrhagic ; complications

To investigate the changes of intestinal microcirculation in endotoxic shock and the effect of inducible nitric oxide synthase (iNOS) on intestinal microcirculation, endotoxic shock was induced by intravenous injection of lipopolysaccharide (LPS) in mice. Mean arterial pressure (MAP) was monitored throughout the experimental procedure. The velocity and flux of red blood cell (RBC) in villus tip arteriole and capillaries were measured by FITC-labeled erythrocytes and intravital microscopy. The effect of iNOS was determined by targeted disruption of mice iNOS-gene and administration of S-methylthiourea sulfate (SMT), a selective inhibitor of iNOS, before LPS injection. No significant differences in MAP, RBC velocity and flux at baseline were found among wild type mice, SMT pretreated mice and iNOS-gene knockout mice. LPS induced a dramatic fall of MAP in wild type mice. The decrease of MAP was significantly restored in iNOS-gene knockout mice and in wild type mice received SMT before LPS injection. The velocity and flux of RBC in villus tip arteriole and capillaries decreased markedly after LPS injection in wild type mice, while significantly higher velocity and flux of RBC were found in iNOS-gene knockout mice and SMT-pretreated mice both 60 and 120 min after LPS injection. The results demonstrate that iNOS plays an essential role in the intestinal microcirculation disturbance which occurs in endotoxic shock.
Animals ; Intestines ; blood supply ; Lipopolysaccharides ; Male ; Mice ; Mice, Knockout ; Microcirculation ; physiology ; Nitric Oxide Synthase Type II ; genetics ; physiology ; Shock, Septic ; chemically induced ; physiopathology