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Biomedical subjects

S Cotev

Publications and source records attributed to S Cotev.

At least 19 recordsLinked to original sources
PubMed1992

Brain edema and neurologic status following head trauma in the rat. No effect from large volumes of isotonic or hypertonic intravenous fluids, with or without glucose.

Disagreement exists regarding the need to restrict the administration of fluid and glucose following head injury to prevent cerebral edema and neurologic deterioration. We examined whether blood osmolality and glucose, neurologic outcome, and the development of brain edema following head trauma were altered by intravenous infusion of large volumes of isotonic or hypertonic fluids that contained or did not contain glucose. Fifty-five rats that survived ether anesthesia and closed head trauma (delivered using a weight drop device) were assigned to one of five groups. In the first group no fluid was infused. In the second group minimal volumes of saline were infused during placement of a jugular vein catheter. In the three remaining groups 10 ml.kg-1.h-1 of either total parenteral nutrition (TPN) (glucose 25%, amino acids 4.25%, 40 mEq/l sodium and 40 mEq/l potassium, 1935 mOsm/kg), dextrose 5% in 0.45% saline (495 mOsm/kg), or Haemaccel (isotonic plasma expander, 298 mOsm/kg) was infused via the jugular vein. Following head trauma and cannula placement, ether was discontinued. Neurologic severity score at 1 and 18 h after head trauma was used to assess neurologic outcome. A score between 0 and 6 was assigned by an observer who was blinded as to the experimental groups, with 0 representing no neurologic damage and 6 representing severe damage. Specific gravity of brain tissue samples containing gray matter and subcortical white matter from the traumatized and contralateral hemispheres was measured at 18 h after head trauma to determine the development of brain edema. There were no statistically significant differences in neurologic outcome and brain edema between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

[Combined spinal-epidural anesthesia].

Combined spinal and epidural anesthesia is a new regional anesthetic modality which combines the benefits of both the spinal and epidural approaches. 24 patients (11 after cesarean section and 13 after orthopedic operations on the lower limbs) were studied. Muscle relaxation and anesthesia were excellent, and regional anesthesia can be prolonged after the original spinal anesthesia wears off. No other anesthetics were needed. Methadone or morphine were given through the epidural catheter in the recovery room for postoperative analgesia. All patients were followed for 24 hours postoperatively.

Analgesia↗
PubMed1990

Protective effect of MK801 in experimental brain injury.

The effect of a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, MK801, was studied in a model of closed head injury in rats. Head trauma (HT) was induced over the left cerebral hemisphere by a calibrated weight-drop device. One or 3 h later, MK801 in saline was given i.p. in a single bolus of either 1, 3, or 10 mg/kg. The rats were killed at 4, 24, or 48 h after HT. Cortical tissue samples were taken from the injured zone and from the corresponding region of the contralateral hemisphere and analyzed for specific gravity (SG) by linear gradient columns. The neurological status of the traumatized rats was evaluated by a neurological severity score (NSS) 1 h after trauma and just before death. Pathological evaluation, based on size and severity of the lesion, was performed 24 and 48 h after HT on control and MK801-treated rats. A dose of 3 mg/kg MK801 given 1 h after trauma effectively prevented the reduction in tissue SG only at 24 h. The NSS could not be evaluated at 24 h after trauma because of the sedating effect of the drug. At 48 h posttrauma, however, the drug significantly improved the neurological state of the rats. No significant difference was found in the pathological score between treated and untreated rats. The results demonstrate neuroprotective properties of MK801, as expressed in two different variables--reduced edema formation and improved neurological recovery after HT. These findings support existing evidence that pharmacological intervention with NMDA receptor antagonist after head injury may be of clinical value in the management of head-injured patients.

Animals↗
PubMed1990

Military medicine: trauma anesthesia and critical care on the battlefield.

This article presents a few of the basic guidelines that must be considered once a decision is made to provide anesthesia and advanced surgical care in the battlefield--or in civilian catastrophes (for example, terrorist incidents, and man-made or natural disasters) that resemble the battlefield. However, it must be stressed that the most central consideration in battlefield anesthesia is the selection, training, and experience of the battlefield anesthesiologist. There are strict guidelines for providing safe anesthesia under the dire circumstances of war or similar civilian circumstances; the properly trained and experienced TA/CCS, however, will be best able to deliver battlefield anesthesia and to improvise equipment and agents for its safest delivery in those circumstances.

Anesthesia↗
PubMed1989

OKY-046 inhibits thromboxane synthesis with no effect on brain edema and neurological status in head traumatized rats.

Head trauma (HT) was induced in the left hemisphere of rats by a weight drop device. Edema was maximal 24 h after HT in the injured zone, and PGE2, TXB2 and 6-keto-PGF1 alpha were elevated in both the injured and remote areas. The effect of a specific thromboxane synthetase inhibitor, OKY-046, on the outcome of HT was studied. OKY-046, 100 mg/kg, was given to rats immediately and 8 h after HT. The neurological severity score (NSS) was evaluated at 1 h after HT, and at 24 h, just prior to sacrifice. Specific gravity (SG) of both hemispheres was measured after decapitation. Prostaglandins (PGs) were extracted from the site of injury and from the frontal lobes, remote from the injury, and assayed by RIA. Basal levels of PGE2 and 6-keto-PGF1 alpha were not reduced by the drug while basal TXB2 levels were lowered. However, the increased production due to HT of all PGs, was inhibited by OKY-046, especially that of TXB2. The ratio of TXB2/6-keto-PGF1 alpha, known to affect vascular tone, was reduced by OKY-046 treatment as a result of TXA2 synthesis inhibition. Still, no effect was found on the neurological outcome (as evaluated by the NSS), or on edema formation (expressed by reduced SG). Thus, based on the present findings increased TXA2 synthesis cannot be implicated in the pathophysiology of cerebral edema or dysfunction following HT.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Accumulation of calcium in the brain following head trauma.

Previous studies have reported accumulation of calcium (Ca) in brain tissue of injured or ischaemic experimental animals. In the present study, head trauma (HT) was induced in the left hemisphere of rats which were subsequently sacrificed 15 min, 1, 2, 4, 24 or 48 h later. Their brains were analysed for oedema formation by the determination of specific gravity (SG), using linear gradient columns, and water content, by dry to wet weight ratio. Total tissue Ca content was measured by atomic absorption spectroscopy. These values, in both the injured and contralateral hemispheres were compared with values obtained from sham-operated rats. Specific gravity of the contused hemisphere was lower than that of the contralateral hemisphere or sham and its water content was higher, at all time points studied. Calcium content was significantly higher in the contused grey matter at 1 h, and in the grey and white matter of both hemispheres at 24 and 48 h after HT. Statistical analysis revealed excellent correlation (cc = 0.65, p less than 0.001) between Ca levels and water content in the grey matter, whenever Ca concentrations were elevated (1, 24 and 48 h). These findings suggest that in the late phase of the post-HT period, Ca accumulation might play a role, along with other mediators, in the development of brain oedema after HT.

Animals↗
PubMed1988

Pulmonary barotrauma including orbital emphysema following inhalation of toxic gas.

Severe pulmonary barotrauma occurred following smoke and toxic gas inhalation in a 20-year-old male. He developed pneumothorax, pneumomediastinum, and extensive facial subcutaneous emphysema which intensified during treatment with positive pressure ventilation. Following the appearance of diplopia and exotropia, orbital emphysema was demonstrated radiologically. The diplopia and exotropia were manifestations of mechanical interference in extra-ocular muscle function by the intra-orbital air, an unusual expression of pulmonary barotrauma.

Adult↗
PubMed1988

Dexamethasone and indomethacin do not affect brain edema following head injury in rats.

Head trauma was induced in rats by a weight-drop device, falling over the exposed skull over the left hemisphere. The neurological state of the rats was evaluated by a neurological severity score at 1 h and 18 h post head trauma. At 18 h post head trauma, rats were decapitated and tissue from the vicinity of the injury and from a corresponding area in the contralateral hemisphere was taken for specific gravity (SG) determination using linear gradient columns. Slices were taken from the same sites for incubation in Krebs-Ringer solution, and the concentrations of prostaglandin (PG)E2, 6-keto-PGF1 alpha, and thromboxane B2 accumulated in the medium during 1 h were measured by radioimmunoassay. In one experimental group, rats were pretreated with intraperitoneal dexamethasone sodium phosphate (4 mg/kg) 18 and 2 h before head trauma, and a third dose was given 8 h post head trauma. Another group was treated with intraperitoneal indomethacin (10 mg/kg) 1 h before and 7 h after head trauma. Other groups were treated immediately and 8 h after head trauma with 4, 8, 15, or 30 mg/kg of dexamethasone sodium phosphate. Another group of rats was treated with free dexamethasone (10 mg/kg) right after head trauma and 8 h later. Head trauma induced edema, as expressed by decreased SG, in the left hemisphere of all traumatized rats. Neither treatment protocol affected the neurological severity score of the injured rats or the SG of the contused hemisphere. PG synthesis, on the other hand, was significantly reduced following indomethacin or free dexamethasone, both in sham and traumatized rats, but not in dexamethasone sodium phosphate-treated rats. We conclude that pretreatment with indomethacin, dexamethasone sodium phosphate, or dexamethasone, used in the present protocols, does not affect posttraumatic cerebral edema. Thus, the role of PGs as mediators of edema formation remains unclear.

Animals↗
PubMed1988

Experimental closed head injury in rats: mechanical, pathophysiologic, and neurologic properties.

A model of closed head injury in rats was developed using a calibrated weight-drop device. The development of edema was studied in various brain regions (cerebral hemispheres, brain stem, cerebellum) using a linear specific gravity gradient column. Regional brain tissue density was measured within 1 min, at 15 and 60 min, 18 h, 4 and 10 days after injury to the left cerebral hemisphere, and was compared with values in sham-operated and control rats. Significant edema (i.e., reduced specific gravity) occurred only in the traumatized hemisphere and was maximal at 18 h. A neurologic severity score (NSS) was developed to evaluate the status of the rat after injury. Specific gravity was significantly correlated with NSS at 18 h after injury. The affected hemisphere displayed hemorrhagic lesions as early as one hour post head trauma (HT), which evolved into hemorrhagic necrosis at 18 h. A pathologic score, evaluated 18 h post HT based on size and severity of the lesion, was correlated with the NSS and evaluated for each rat at one hour and 18 h postimpact. This correlation was found to be highly significant. This model of brain injury may be useful in future studies on the effects of therapeutic agents.

Animals↗
PubMed1988

Life-threatening torsade de pointes arrhythmia associated with head injury.

Torsade de pointes (atypical ventricular tachycardia) occurred in a 75-year-old man 1 day after blunt head injury, in association with a focal intracerebral hematoma in the left thalamic area. The causal relationship between the traumatic stimulation of the left sympathetic pathway and the development of this life-threatening arrhythmia is discussed.

Aged↗
PubMed1988

Intracranial pressure monitoring after elective intracranial surgery. A retrospective study of 514 consecutive patients.

A retrospective study of 514 consecutive patients whose intracranial pressure (ICP) was monitored after elective supratentorial or infratentorial surgery is reported. Of the 412 patients operated on in the supratentorial region, 76 (18.4%) had a postoperative sustained ICP elevation exceeding 20 torr. Abnormally high ICP occurred after 13 (12.7%) of the 102 infratentorial operations. Risk factors for postoperative ICP elevation were: resection of glioblastoma in 27.2% of cases, repeat surgery in 42.9% of cases, and protracted surgery (greater than 6 hours) in 41.7% of cases. Of the 89 patients with elevated ICP, 47 (52.8%) had an associated clinical deterioration. In 19 of these, the rise in ICP occurred before this deterioration was noticed, leading as a rule to quick diagnostic and management response. In eight patients clinical deterioration was noticed before the rise in ICP, and in 20 it happened simultaneously. The higher the level of ICP elevation, the greater were the chances of associated deterioration. The most common findings on computerized tomography scanning in 35 of 89 patients with elevated ICP were brain edema (19 cases) and bleeding in the tumor bed (15 cases). Mannitol, thiopental, additional hyperventilation, and reintubation (in patients who were previously extubated) were used to reduce ICP, in addition to surgical decompression whenever indicated. Thirteen patients with raised ICP and clinical deterioration underwent reoperation. The postoperative infection rate was 1.2% (six cases). In only one patient could infection be attributed to ICP monitoring. It was concluded that ICP monitoring is advantageous in the immediate postoperative management after elective intracranial surgery and is almost risk-free. It should therefore be used liberally, especially when risk factors for ICP elevation can be identified prior to the end of surgery.

Brain Neoplasms↗
PubMed1988

Experimental closed head injury in rats: prostaglandin production in a noninjured zone.

In a model of closed head injury in rats, a calibrated weight drop device was allowed to fall onto the skull's convexity over the left hemisphere 1 to 2 mm lateral from the midline. Prostaglandin (PG) levels were determined in the frontal cortex region remote from the site of injury where no macroscopic damage could be seen. Differential patterns of temporal changes were evident for PGE2, PGD2, thromboxane (TX) B2, and 6-keto-PGF1 alpha in the contused hemisphere, but no changes were found in the contralateral hemisphere. The major changes in PG levels were increased levels of PGD2 and 6-keto-PGF1 alpha that persisted from 18 hours until 10 days after injury. The ratio between TXB2 and 6-keto-PGF1 alpha, which reflects the vascular tone, increased during the early postinjury period (15 minutes and 1 hour) and decreased later, up to 10 days. Thus, a sustained imbalance in favor of the vasodilator is apparent; this may suggest an improved blood supply to the region. Both PGD2 and PGI2 have protective effects in the brain. We suggest that their endogenous increase may be part of a repair mechanism at the periphery of the injured zone.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Head injury induces increased prostaglandin synthesis in rat brain.

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.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Systolic blood pressure variation is a sensitive indicator of hypovolemia in ventilated dogs subjected to graded hemorrhage.

Systolic pressure variation (SPV) is defined as the difference between the maximum and minimum values of systolic blood pressure following a single positive pressure breath. An increase in the SPV is known to occur clinically during hypovolemia. This study aims to quantify SPV during graded hemorrhage in ventilated dogs, and to compare its reliability relative to other hemodynamic indicators of hypovolemia. Ten anesthetized dogs were mechanically ventilated with a fixed tidal volume. A continuously inflated vest was applied around the chest to maintain the ratio of lung to chest wall compliance similar to that of humans (0.83 +/- 0.12). SPV was further divided into delta up and delta down components relative to apneic (5 s) systolic blood pressure. Dogs were bled 5, 10, 20, and 30% of their estimated blood volume. The measured parameters best correlated to the amount of bleeding were SPV (rs = 0.993), delta down (rs = 0.981), and cardiac output (rs = 0.976). The SPV and its delta down component correlated to the degree of hemorrhage as well as the CO and the pulmonary capillary wedge pressure, and significantly better than the central venous pressure and the mean systemic blood pressure. Thus, SPV and its delta down component are accurate indicators of hypovolemia in ventilated dogs subjected to hemorrhage.

Animals↗