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PubMedDate not supplied

[Effect of synthetic analogs of enkephalins, morphine and their antagonists on the course of experimental traumatic shock].

Effects of naloxone, nalorphine, thyroliberin, morphine and two analogues of enkephalins (FK 33-824 and Tyr-D-Ala-Gly-Phe(NO2)-NH2) on the course of traumatic shock were studied in experiments on rabbits. It was found that antagonists of opioid peptides aggravated the course of traumatic shock and morphine and synthetic analogues of enkephalins exerted positive effects during its treatment. Endogenous opioid peptides are suggested to play the protective role in experimental traumatic shock.

Animals↗
PubMed1997

Beneficial effects of C1 esterase inhibitor in murine traumatic shock.

Activation of the complement system is an integral part of the initiation and maintenance of the inflammatory process such as that occurring in traumatic shock, and is considered responsible for much of the trauma-induced microvascular injury. We investigated the effects of early complement blockade induced by a C1 esterase inhibitor (C1 INH) in a rat model of traumatic shock. Pentobarbital-anesthetized rats subjected to Noble-Collip drum trauma developed a shock state characterized by marked hypotension and a 83.3% mortality rate with a mean survival time of 157.5 +/- 26 min. Accompanying these effects were significant endothelial dysfunction and elevated intestinal myeloperoxidase activity. Treatment with C1 INH 15 mg/kg administered intravenously 10 min post-trauma, increases survival rate to 66.7% (p < .05), and prolonged survival time to 248 +/- 27 min (p < .05). C1 INH significantly preserved the endothelium-dependent relaxation to acetylcholine and attenuated the increase in myeloperoxidase activity in C1 INH-treated rats compared with untreated trauma rats (p < .05). Our results suggest that complement activation plays an important role in tissue injury associated with trauma, and that its inhibition at an early step in the complement cascade through a C1 esterase inhibitor is beneficial in rats experiencing traumatic shock. The mechanisms of the protective effect of C1 INH involves preservation of vascular endothelial function and diminished neutrophil accumulation leading to reduced neutrophil-mediated tissue injury.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1987

The rise of blood sugar as an additional parameter in traumatic shock.

Besides the known cardiovascular effects of hemorrhagic shock, regular metabolic consequences can be demonstrated in the rabbit: 1. The rise in blood sugar in hemorrhagic shock increases with the amount of blood withdrawn per unit of time. 2. The characteristic rise in blood sugar lasts longer than the phase of the partial exsanguination. 3. In traumatic shock, the rise in blood sugar indicates the degree of severity of the injury earlier than the fall in blood pressure does. The rise in blood sugar is attributable to a reflex increase in glycogenolysis due to catecholamine secretion elicited via baroreceptors in hemorrhagic shock. For the pronounced rise in blood sugar in traumatic shock, an additional receptor is postulated. Supplementary investigation of the blood sugar may possibly enable the extent of the injury to be diagnosed earlier in traumatic shock, and the negative sequelae may be reduced by timely, adequate therapy.

Animals↗
PubMed1976

Coronary circulation in experimental traumatic shock, and effect of some vasoactive agents on its parameters.

On 35 heparinized cats with experimental traumatic shock induced according to Cannon, changes in the coronary blood flow, produced by intravenous injections of noradrenaline, angiotensin, hydrocortisone, histamine, and serotonin, were studied. Traumatic shock was characterized by decreases in the coronary blood flow and organic oxygen uptake, despite a simultaneous decrease in the regional vascular resistance. Injections of noradrenaline (14-18 mug/kg) and angiotensin (29 mug/kg) induced, both in the initial normal state and in shock, increases in the coronary blood flow rate and in the regional oxygen uptake; an injection of hydrocortisone (7.1 mg/ml) produced similar effects in the normal state, but did not elevate the oxygen uptake in shock; an injection of histamine (32 mug/kg) had no effect on the coronary blood flow rate, but reduced the regional oxygen uptake both in the normal state and in shock; an injection of serotonin (30 mug/kg) exerted no major effects on the blood flow. The results obtained might serve as guidelines for pharmacological regulation of coronary circulation in shock.

Angiotensin II↗
PubMed1976

[Field study on the therapeutic value of trasylol in traumatic shock].

A report of the results of a multicenter study including 4686 patients concerning the therapeutic value of Trasylol (Aprotinin) in traumatic shock. The group treated additionally with Trasylol showed, beside a reduced overall mortality, a statistically significant reduction of mortality in those treated within the first 30 min after the injury. Surgery performed in the posttraumatic stage showed a lower mortality in the Trasylol group. The importance of a time factor in shock treatment and the effects of Trasylol in traumatic shock are emphasized.

Aprotinin↗
PubMedDate not supplied

[Evaluation of the effectiveness of antishock suits at the early stages of the treatment of patients with traumatic shock].

The efficacy of the early use of antishock overalls (ASO) as part of intensive care for traumatic shock is assessed in the clinical study performed in 15 patients with severe mechanical trauma complicated with shock. Hemodynamic parameters were compared in groups where ASO was and was not used as part of antishock procedures. High efficacy of ASO use for stabilization of hemodynamic parameters in patients with severe trauma complicated with shock has been demonstrated and the advisability of its use in the complex of intensive care procedures in traumatic shock at prehospital stage has been proved.

Gravity Suits↗
PubMed1995

PASG: does it help in the management of traumatic shock?

A prospective, randomized study was designed to determine the efficacy of pneumatic antishock garment (PASG) in the treatment of traumatic shock in a medium-size urban community. A total of 291 traumatic shock patients were assigned to either the PASG or No-PASG treatment groups. Of these, data from 248 patients were analyzed in detail. Analysis of demographic factors--such as age, sex, and mechanism of injury--as well as prehospital evaluative tools--such as trauma and CRAMS scores, and injury severity scores--revealed that the two groups were well-matched. This study did not demonstrate significant differences in hospital stay or mortality between PASG and No-PASG patients. Similarly, in the subset of patients with blunt trauma, PASG was not found to be beneficial.

Adult↗
PubMed1986

[Effect of enkephalins on the energy potential of the rat liver and cerebral cortex during an early period of traumatic shock].

The experiments were performed on 86 white male rats, weighing 180-220 g. The animals with traumatic shock revealed a decrease in ATP concentration and a rise in ADP and AMP levels in the brain cortex and hepatic tissue, resulting in the energy charge reduction. The injection of synthetic leu-enkephalin analog D-ala2-arg6-leu-enkephalin to animals with traumatic shock led to energy charge normalization in the brain cortex and increase in hepatic tissue. The mechanisms of enkephalin effect on the energy metabolism during shock are discussed.

Adenine Nucleotides↗
PubMed1982

Post-traumatic-shock lung: postmortem microangiographic and pathologic correlation.

In post-traumatic-shock lung, increased pulmonary vascular resistance and pulmonary hypertension are prominent features. The explanation for them was sought by postmortem microangiography of the lungs of 17 patients dying of respiratory failure after trauma. The 10 patients with thoracic injury died earlier (1-8 days). Extravasation of contrast material due to alveolar capillary rupture was present in all but one specimen and occupied 20% of the sampled area. Pulmonary artery thrombi lay proximal to these extravasations. Hypovascular areas due to infection and hemorrhagic alveolitis were found in all patients and involved 40% of the surface area. The small pulmonary arteries were poorly filled and contained many microthrombi. Some patients had hematomas, cavities, and areas of interstitial edema occupying about 5% of the lung area and associated with compressed or occluded vessels. Several mechanisms including pulmonary trauma may be responsible for the antemortem rupture and obstruction of small blood vessels. In the post-traumatic-shock lung, small artery occlusion and compression are associated with pulmonary hemorrhage, infarction, and infection and are important contributors to perfusion abnormalities and respiratory failure.

Adolescent↗
PubMed1989

[Therapeutic effect of nalorphine and naloxone in experimental traumatic shock].

In their acute experiments on 86 rabbits the authors have established that the intravenous administration of nalorphine and naloxone produces a marked therapeutic effect only during the early period of experimental traumatic shock. In most of the animals there was a reliable extension of the lifetime (nalorphine) and an increase in the survival rate (naloxone). In a lesser part of the animals the administration of nalorphine had no considerable influence on the outcomes. During the late period the therapeutic effect of these drugs has not yet been manifested. A conclusion has been made that the contradictory data in the literature concerning the effect of nalorphine and naloxone on the course of experimental traumatic shock seem to depend on the fact that they were administered at various stages of this pathologic process. It is pointed out that it is advisable to administer these drugs (especially naloxone) at the pre-hospital stage in the patients with traumatic shock.

Animals↗