Influence Of Inereased Intra-abdominal Pressure On Organ After Traumatic Hemorrhagic Shock

Intra-abdominal pressure(IAP) sharply rises after resuscitation on patients of traumatic hemorrhagic shock ,which affects visceral bloodflow ang organ function ang result in a series of pathological and physiologic change.This induces abdominal compartment syndrome(ACS) at last,if it isn't controlled in time.It is a clinical remedy difficult that ACS after critical trauma and hemorrhangic shock results in organ secondary lesion.It is a important factor of causing death.Therefore early precaution and transaction is very important.Past empirical study of ACS model is often based on health animal through injecting gas or liquid to abdominal cavity. This is jug-handled,because this method is short of pathological foundation of disease or trauma. The experimental result is different from ACS clinical feature. To study mechanism of ACS all the more,we choosed wistar rats,and divided four groups: (1)control group (n=8) , (2)7mmHg group(n=8) , (3)15mmHg group(n=8) , (4)20mmHg group(n=8)。Medisect on all animal abdomen was 2cm.Peritoneum lacerated wound was posed at arteria mesenterica superior root.Arterial blood pressure kept 40mmHg for 2 hours by right femoral artery bloodletting. all animal was undertaken resuscitation for 5 hours.Then we observed histopathology change of lung,hepar and kidney,detected blood gas analysis and functional parameter of hepar and kidney,and detected intestine and mesentery vascular permeability.This ACS model is in line with clinical ACS regularity.So this experimental result objectively reveals ACS mechanism and influenc to organ physiologic function,provided reliable theoretical proof.1. The experiment model of secondary ACS includes following characteristic:①The experimental device is simple.,and the experimental management is easy. The abdominal pressure parameter is controlled easily and the model repeatability is nice.②Comparing the ahead model, this model is in line with clinical pathogenetic condition of resuscitation after traumatic hemorrhagic shock better.③Indicatrix of the model parameter is concise and dirct-viewing, such as 20mmHg abdominal pressure, oliguresis oranuresis, dyspneic respiration,and so on.④Basing on the model, it is the next step to study hemodynamic change, pathological change of hepar,kidney and lung, digestive canal dynamia change, resuscitation strategies, reperfusion injury and survival after decompression,and so on.⑤Providing pathological and physiological foundation for ACS study.2. There was no obviously distinction in hepar histopathology change in all animal.The basic change were hepar cellular swelling , slight degeneration and neutrophil infiltration in, but structure of hepatic lobules retained normal essentially.Lung histopathology change included critical oedema of lung cells,inflammatouy cell infiltration in interstitium, occasionally finding inflammatouy cell in pneumoangiogram. Kidney histopathology change was characterised by renal tubular epithelial cell granular degeneration,but no any neutrophil infiltration. Importantly the granular degeneration in 20mmHg guoup wasmore severity than others. It suggests that histopathology change of hepar and lung and kidney concerned with hemorrhagic shock and reperfusion injury. Kidney is incurred damage than hepar and lung.Change of hepar and renal function related time factor.3. At the point abdominal pressure got 20mmHg, arterial pressure rised significantly than control group,7mmHg and 15mmHg group(P<0.01). Not remaining a hour arterial pressure decreased strikingly.,but the others didn,t change(P>0.05).Urine volume at 20mmHg was least than control group,7mmHg and 15mmHg group(P<0.01), but there was no difference among control group,7mmHg and 15mmHg group(P>0.05).Detection result of hepar and renal function was no variance in the fourteen groups(P>0.05). Blood gas nanlysis displayed serum PH at 20mmHg was lowest than control group,7mmHg and 15mmHg group(P<0.05), moreover serum PH at 15mmHg was diminished than control group,7mmHg(P<0.05),but there was no difference between control group and 7mmHg group(P>0.05).The result indicated that the animal occurred respiratory acidosis when IAP got 15mmHg,and occurred hypotension and ologuresis or anuresis..4. mesentery vascular permeability at 7mmHg and 15mmHg was lower than control group and 20mmHg(P<0.01), but between control group and 20mmHg there was no obvious difference(P>0.05).Intestine vascular permeability decreased at 7mmHg(P<0.05), and increased at 15mmHg(P<0.05),and got a peak at 20mmHg(P<0.01). Intestine vascular permeability was higher than mesentery vascular permeability at the same abdominal pressure,and Intestine vascular permeability began to increase at 15mmHg. It is assumed that mesentery is thiner than intestine wall, more EB in mesentery organism flowed into abdominal cavity.Therefore vascular permeability increase of intestine and mesentery is one of mechanism of IAH.5. The result indicated vascular permeability at 7mmHg was lower than control group,15mmHg group and 20mmHg.Because lymph fluid recirculated more at 7mmHg than other groups,and blood vessel leakage reduced,protein deprived decreased,tissue oedema lessened.This finding hints we take the IAP at about 7mmHg better than at 0mmHgwhen we perform abdominal decompression of clinical ACS.This not only conduces to prevent haemodynamics decompensation after abdominal decompression of ACS.,but also conduces to cut down reperfusion injury and death rate after abdominal decompression of ACS.