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[Pathogenetical features of the acute period of traumatic disease. Traumatic shock as a special manifestation of the acute period].

Clinico-pathogenetical features of the acute period of trauma disease due to a severe combined injury were studied in 644 patients. An analysis of clinical indices was made in 428 of them, clinico-laboratory indices--in 216 patients. The results have shown that the main form of the acute period of the trauma disease are traumatic shock (62.8%), traumatic coma (18.3%), acute respiratory insufficiency (5.7%). Dramatically decreased delivery and consumption of oxygen lower than the metabolic requirements of the tissues accompany the traumatic shock which results in the suppression of tissue metabolism. Pronounced endotoxicosis developing along with the traumatic shock results not from the degree of injured tissues only, but from the centralization of blood circulation. It is also supported by the insufficient detoxicating function of the kidneys. A severe degree of the traumatic shock causes disseminated intravascular coagulation (DIC) of the II-III degree. After helping out from shock the patient has normocoagulation or the I degree DIC. Traumatic shock with marked hypotension and metabolic acidosis is a significant factor of high risk of the development of acute lesion of the lungs.

Abdominal Injuries↗

Subclass opioid receptors associated with the cardiovascular depression after traumatic shock and the antishock effects of its specific receptor antagonists.

The present available opioid receptor antagonists such as naloxone and naltrexone are not highly receptor selective. They may antagonize mu opioid receptors to affect the pain threshold of the patients with traumatic shock while they exert antishock effects. Therefore, they are not suitable for traumatic shock. It is very important to elucidate the subclass of opioid receptors that are closely associated with cardiovascular depression of traumatic shock and then choose their specific receptor antagonists to treat it. Traumatic shock was used in pentobarbital-anesthetized Wistar rats by right femur fracture plus hemorrhage (fixed hemorrhage at a rate of 20 mL/kg in experiment 1 or hemorrhage to 40 mmHg mean arterial blood pressure for 60 min in experiments 2 and 3), and the changes of myocardial and brain opioid receptors after traumatic shock, the antagonizing effects of mu, delta, and kappa opioid receptor antagonists on the cardiovascular depression of traumatic shock and the antishock effects of delta and kappa opioid receptor antagonists ICI174,864 and Nor-binaltorphimine (Nor-BNI) were observed. The results indicate that after traumatic shock, the number of myocardial and brain delta and kappa opioid receptors were significantly increased that were significantly associated with the decreased cardiovascular functions. mu Opioid receptors in the heart and brain did not change significantly. Intracerebral ventricular administration of ICI174,864 and Nor-BNI significantly antagonized the decreased cardiovascular function after traumatic shock and increased the survival rate of traumatic shock rats, but mu opioid receptor antagonist beta-funaltrexamine did not. Meanwhile, intravenous administration of delta and kappa opioid receptor antagonists ICI174,864 and Nor-BNI also significantly increased the mean arterial blood pressure, improved the hemodynamic parameters, and prolonged the survival rate of traumatic shock rats. These findings suggest that opioid receptors are involved in the cardiovascular depression of traumatic shock, and the subclass receptors are mainly delta and kappa opioid receptors. delta and kappa opioid receptor antagonists have good beneficial effects on traumatic shock.

Animals↗