6-ketoprostaglandin-f1-alpha and Craniocerebral-Trauma

Head injury was induced in the left hemisphere of rats. The rats were killed at various time intervals after trauma (immediately, 15 min, 1 and 18 h, and 4 and 10 days), and the rates of synthesis and release of prostaglandin PGE2, 6-keto-PGF1 alpha, and thromboxane TXB2 from cortical slices of both hemispheres were studied. The rate of synthesis of PGE2 after 18 h was six and four times higher than control in the contused and contralateral hemispheres, respectively. By 10 days post-trauma, both hemispheres had normal rate of PGE2 release. TXB2 and 6-keto-PGF1 alpha synthetases were affected already 15 min after the injury, and a similarly elevated rate of synthesis was found in both hemispheres. The maximal effect was detected after 1 or 18 h with return to normal after 4 or 10 days for TXB2 and 6-keto-PGF1 alpha, respectively. Tissue specific gravity was determined for both hemispheres using linear gradient columns. The results of these determinations indicate that development of edema occurs in the contused hemisphere as early as 15 min post trauma; it reaches its maximal level at 18 h and returns to normal at 10 days. Arterial pressure was monitored, and a transient increase was found at 10 min post trauma. We suggest that the production of edema after brain injury may be related to the increased rate of PGE2 and PGI2 synthesis, which occurs at similar time intervals after injury.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blood Pressure; Brain; Brain Edema; Craniocerebral Trauma; Dinoprostone; Male; Prostaglandins; Prostaglandins E; Rats; Thromboxane B2

Plasma levels of thromboxane A2 and prostacyclin have been elevated during experimental acute respiratory failure (ARDS). The present study evaluates the relationship of plasma levels of thromboxane A2 and prostacyclin, measured by radioimmunoassay as the stable metabolites thromboxane B2 (TxB) and prostaglandin 6-K-F1 alpha (PGI) to the incidence of clinical ARDS. Sixty-seven consecutive patients at risk for ARDS were studied prospectively. TxB, PGI, platelet, and leukocyte counts were measured daily for up to 5 days. Of 55 patients without cerebral injury, 25 (45%) developed ARDS, and 30 did not. Of 12 patients with cerebral injury, none developed ARDS. This difference was highly significant (P less than 0.01). TxB was increased and age lower with head injury (P less than 0.05). PGI was significantly lower in ARDS (110 +/- 32 vs 227 +/- 211 pg/ml, P less than 0.05), and mean TxB was unchanged. TxB was increased in age greater than 60 and decreased with prostaglandin inhibitors. ARDS was significantly associated with TxB greater than 70 pg/ml, PGI below the detectable level of 103 pg/ml, TxB/PGI ratio greater than 0.7, and age greater than 60 years. Peak TxB occurred before or simultaneously with onset of ARDS in 68%. Leukocytes were decreased in ARDS (8.6 +/- 4 vs 11.1 +/- 4.4 X 10(3)/mm3) and platelets were unchanged. ARDS was decreased with steroid therapy. Elevated TxB is related to a high incidence of ARDS. Elevated PGI may protect against ARDS. Cerebral injury patients in this study were resistant to ARDS in spite of increased TxB.

Topics: 6-Ketoprostaglandin F1 alpha; Adrenal Cortex Hormones; Age Factors; Craniocerebral Trauma; Epoprostenol; Female; Humans; Male; Platelet Count; Prostaglandin Antagonists; Respiratory Insufficiency; Thromboxane B2; Thromboxanes

The purpose of this study was to determine the levels of prostaglandins in ventricular cerebrospinal fluid (CSF) from severely head injured humans on successive days following injury. Sixteen samples from three patients were purified using XAD-2 and high pressure liquid chromatography and PGE2, PGF2alpha, and 6-keto-PGF1alpha were quantitated utilizing deuterated internal standards and gas chromatography-mass spectrometry. Generally, the levels of PGs in ventricular CSF were found to be higher than has previously been reported for PGs in CSF from spinal taps. PG levels ranged from reported for PGs in CSF from spinal taps. PG levels ranged from nondetectable to 11.8, 3.3 and 27.3 ng per ml for PGE2, PGF2alpha, and 6-keto-PGF2alpha, respectively. However, in one sample, PG levels were much higher than this range and approached the levels found in human cortical tissue. Analysis of red and white blood cell numbers in the CSF showed no relationship between cell numbers and prostaglandin levels. This study confirms a previous report that 6-keto-PGF2alpha is the major prostaglandin in CSF and demonstrates that PG levels in ventricular CSF from head traumatized humans can be greatly elevated.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Cerebral Ventricles; Craniocerebral Trauma; Dinoprost; Dinoprostone; Humans; Male; Middle Aged; Prostaglandins; Prostaglandins E; Prostaglandins F; Time Factors