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Biomedical subjects

E S Flamm

Publications and source records attributed to E S Flamm.

At least 91 records · Page 5Linked to original sources
PubMed1981

Loss of essential membrane lipids and ascorbic acid from rat brain following cryogenic injury and protection by methylprednisolone.

Previous work has shown that unsaturated fatty acid components of model membrane phospholipids in vitro, damaged via a free radical mechanism, are protected by the presence of cholesterol in these membranes. The participation of these membrane lipids in the pathogenesis of traumatic injury to brain was studied in vivo using the Klatzo method of cryogenic injury in rats. Increased edema 4 hr after cryogenic injury was noted on the lesioned side. Total cerebral cholesterol was decreased significantly in the lesioned hemispheres 10 hr following injury. In lesioned animals pretreated and post-treated with methylprednisolone, there were no significant differences in the cholesterol levels. Arachidonic acid isolated from total membrane phospholipids was significantly reduced on the injured side 24 hr after injury, but not before. Other fatty acids were not significantly affected. Methylprednisolone treatment prevented the decrease in arachidonic acid. Animals that had received a cold injury had significant decreases in ascorbic acid levels after 4 hr on the lesioned side of the brain. This decrease was significantly ameliorated by corticosteroid administration. These results support the hypothesis that the protective effect of corticosteroids in cryogenic cerebral trauma may be due to antioxidant protection of major cell membrane lipid components such as cholesterol and phospholipids.

Animals↗
PubMed1981

Suction decompression of aneurysms. Technical note.

A technique utilizing suction decompression of large aneurysms to allow safer application of a clip is described. Large aneurysms are punctured with a No. 21 scalp vein needle attached to the operating room suction device. This procedure causes relaxation of the aneurysm itself and allows safer application of the clip. The technique has been used in six cases of giant aneurysms.

Humans↗
PubMed1981

Effect of naloxone on posttraumatic ischemia in experimental spinal contusion.

The effect of naloxone on blood flow and somatosensory evoked potentials was studied in cats subjected to 400 gm-cm contusion injuries of the thoracic spinal cord. Eight cats were treated with 10 mg/kg naloxone 45 to 60 minutes after injury, 11 cats were given 10 ml of saline instead of naloxone, and six cats were neither injured nor treated. Hydrogen clearance was used to measure blood flow in the lateral white columns at the contusion site. Naloxone, given intravenously, significantly inproved the blood flow rates in the lateral column white matter. At 2 hours after injury, the mean blood flow in the saline-treated cats fell to 50% (p greater than 0.01) of preinjury flow rates, whereas it increased 6% (p greater than 0.50) in naloxone-treated cats, and 12% (p greater than 0.50) in uninjured cats. At the 3rd hour after injury, the respective flows fell 47% (p less than 0.01), and 6% (p greater than 0.50), and increased 15% (p greater than 0.50) of the preinjury flow rates. The naloxone-treated cats had striking preservation of sensory function and somatosensory evoked potentials at 24 hours after injury. At 24 hours, responses had returned in all the naloxone-treated cats and in only 11% of the saline-treated cats. The probability of this combination of events occurring by chance is 0.0030. The authors conclude that naloxone may be useful for the treatment of spinal cord injury. The mechanism of the effect is unknown.

Animals↗
PubMed1980

Vestibulospinal monitoring in experimental spinal trauma.

Vestibulospinal tract function was monitored in experimental contusion of the spinal cord in cats, and compared with somatosensory cortical evoked potentials. Both white and gray matter portions of the vestibular and somatosensory pathways were evaluated in cord injuries at T-7 and L-4. Severe contusions of 20 gm-20 cm force impact resulted in a rapid (less than 1 second) abolition of thoracic white matter conductivity, but a somewhat slower (4 to 5 minutes) loss of lumbar gray matter responses. A paradoxical transient recovery of white matter conductivity occurred 1 to 2 hours after injury, despite eventual progression to central hemorrhagic necrosis at the contusion site. In contrast, mild contusions (20 gm-10 cm force impact) produced only a temporary loss of neuronal activity: white matter for 1 to 2 hours, and gray matter for 30 to 40 minutes. In general, vestibular and somatosensory potentials showed similar sensitivity to contusion, although the former tended to recover earlier. We conclude that contusion injury causes two types of neuronal dysfunction in spinal cord: 1) a low-threshold concussion-related loss of activity lasting 30 to 120 minutes; and 2) a higher threshold necrotic process, requiring 1 to 2 hours to develop, which apparently spreads from gray to white matter.

Animals↗
PubMed1980

Intracranial pressure during nitroglycerin-induced hypotension.

Nitroglycerin was given intravenously to five anesthetized, hyperventilated (PaCO2 25 to 30 torr) patients during craniotomy, to facilitate surgery by creating a relatively bloodless field, and to decrease the potential need to blood transfusion. A subarachnoid screw and an indwelling radial artery catheter were inserted to monitor intracranial pressure (ICP) and mean arterial pressure (MAP). As MAP decreased from 10.4 +/- 4.0 (SE) to 69.0 +/- 1.8 torr, ICP increased from 14.2 +/- 0.7 (SEM) to 30.8 +/- 1.1 torr. Cerebral perfusion pressure decreased from 90.2 +/- 3.6 (SEM) to 38.2 +/- 2.3 torr (p < 0.0005). We attribute this nitroglycerin-induced ICP increase to capacitance vessel dilation within the relatively noncompliant cranial cavity, with subsequent cerebral blood volume increase.

Adult↗
PubMed1980

Effect of aminophylline and isoproterenol on spinal cord blood flow after impact injury.

A study of the effects of spinal cord injury upon spinal cord blood flow was carried out in cats. A 400 mg-cm impact produced an overall reduction in spinal cord blood flow of 24% in the white matter and 30% in the gray matter, as determined by 14C-antipyrine autoradiography. At the level of the injury, white-matter flow was 8.1 ml/100 gm/min, a reduction of 49%, and in the gray matter, 12.5 ml/100 gm/min, a reduction of 76%. Treatment with aminophylline and isoproterenol improved the overall blood flow in the spinal cord. At the level of the injury, white-matter flow after this treatment was no longer significantly different from control values. The gray-matter flow remained decreased to 26.2 ml/100 gm/min, a reduction of only 47%. It is proposed that aminophylline and isoproterenol may increase cyclic adenosine monophosphate (AMP) and prevent platelet aggregation along the endothelial surfaces of the microcirculation, and may thereby help to maintain improved perfusion of the injured spinal cord.

Aminophylline↗
PubMed1977

Ruptured intracranial aneurysms. Case morbidity and mortality.

The authors review 100 consecutive cases of ruptured intracranial aneurysms to assess the overall morbidity and mortality. Patients were placed on a regimen of bed rest, sedation, control of blood pressure, anticonvulsants, and antifibrinolytic therapy. Surgery was performed on 86 patients with hypotensive anesthesia and microsurgical techniques. The incidence of early rebleeding while on epsilon aminocaproic acid and control of blood pressure was 11.8%. The overall surgical mortality was 8.1%, and the surgical mortality of patients in Grades 1, 2, and 3 was 6.3%. Of the 100 patients, 60 were able to return to their prior activities, and 25 had moderate neurological deficits that required limitation of their activities. The total case mortality was 15%. The evidence presented indicates that the regimen of active medical treatment before microsurgical intervention has improved the overall case morbidity and mortality, as well as the chance for long-term survival.

Adult↗
PubMed1977

Ethanol potentiation of central nervous system trauma.

Two models have been used to study the effects of ethanol on injuries of the central nervous system. The spinal cords of cats were injured by delivering a 200 gm-cm impact to the exposed dura mater. A second group of animals received a similar injury to the exposed dura mater overlying the cerebral hemispheres. The animals were divided into two groups, those that received an infusion of ethanol before injury, and control animals that received no ethanol. The parameters of injury used in this model produced small and insignificant lesions in those animals that received no ethanol; however, when the animals were pretreated with ethanol, a considerable increase in the extent of the injury was noted. These include alterations in membranes-bound enzymes and clotting mechanisms, and alteration of cell membranes through abnormal free radical reactions.

Animals↗