Effect of furosemide (lasix) on acute severe experimental cerebral edema.
The effect of furosemide (Lasix) therapy on a standardized experimental cerebral edema, induced in rats by applying a cooling stamp to the right side of the skull over the right coronal suture by means of a stereotactic instrument, was examined. The hemispherically separated water and electrolyte contents of the brain were analyzed after 24 h. Following furosemide therapy, the behavior of these edema parameters was compared statistically with dexamethasone, glycerol and albumin. An increase of the water and sodium content, and a decrease of potassium was observed 24 h after the trauma, especially in the right hemisphere. Furosemide did not improve either the water content or the electrolyte balance. By contrast, the administration of dexamethasone, glycerol and albumin was followed by a significant improvement of the edema. In experiments with cats, the course of the edema and the effect of furosemide on the cold brain injury of the right hemisphere were observed by measuring the intracranial pressure (ICP) values, and by continuous monitoring of the EEG. The ventricular CSF pressure and epidural pressures were also recorded. The electrical brain activity was continuously compared with the course of the ICP by means of computer analysis. In addition, the blood osmolality and diuresis were monitored. The ICP increased rapidly after the trauma, establishing considerable pressure gradients, and the EEG power intensities decreased markedly on the right side. Histologically, there was an extended edema of the white matter of both hemispheres. The ICP was not lowered by single injections or high dose infusions of furosemide, and the EEG power intensities also did not improve. Infusions of large volumes of furosemide even resulted in an increase of ICP, but infusion of 40% sorbitol effected a rapid decrease of ICP and EEG recovery over the left hemisphere. Sorbitol infusion also caused a marked rise in the blood osmolality, whereas furosemide had no such effect. The results raise considerable doubts as to the propriety of the exclusive use of furosemide for cases of acute cerebral edema with raised ICP. The diuretic effect is insufficient to establish an osmotic gradient, and its general dehydrating effect does not acutely influence the ICP. The absence of effect on the experimental tissue edema would not appear to commend furosemide as basic therapy for cases of traumatic cerebral edema.
D000418:Albumins / Q000627:therapeutic use; D000818:Animals; D001923:Brain Chemistry; D001929:Brain Edema / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism; D002415:Cats; D003907:Dexamethasone / Q000627:therapeutic use; D004569:Electroencephalography; D005665:Furosemide / Q000008:administration & dosage / Q000627:therapeutic use*; D005990:Glycerol / Q000627:therapeutic use; D006982:Hypertonic Solutions / Q000627:therapeutic use; D007427:Intracranial Pressure; D008297:Male; D011188:Potassium / Q000032:analysis; D051381:Rats; D012964:Sodium / Q000032:analysis; D013012:Sorbitol / Q000627:therapeutic use; D013997:Time Factors; D014867:Water / Q000032:analysis
D000418:Albumins; D006982:Hypertonic Solutions; D014867:Water; D013012:Sorbitol; D005665:Furosemide; D003907:Dexamethasone; D012964:Sodium; D005990:Glycerol; D011188:Potassium