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Biomedical subjects

L E Pinegin

Publications and source records attributed to L E Pinegin.

7 recordsLinked to original sources
PubMed1984

[Mechanism of the decrease in intracranial pressure as affected by furosemide].

The correlation was established between the increase in diuresis and natriuresis and fall of CSF pressure after intravenous injection of 10 mg/kg furosemide into dogs. Osmolarity and ion concentration in the serum and CSF did not change in these experiments. In nephrectomized dogs, furosemide did not changes CSF pressure. Furosemide dehydrated brain with traumatic edema, reduced brain Fe content probably due to diminishing brain blood content. The mechanism of intracranial pressure fall after furosemide injection can be explained by acute excretion of a large volume of fluid by the kidneys, leading to a decrease in the blood content of the skull cavity.

Animals↗
PubMed1983

[Effect of furosemide on intracranial pressure in patients with intracranial hypertension].

Furosemid administration to patients with intracranial hypertension of tumour genesis was associated with temporal regression of general cerebral symptoms, coinciding in time with the period marked by a decrease in cerebrospinal fluid pressure. A correlation between the magnitude of this decrease and the furosemid-induced elevated secretion of urine containing chlorine and sodium was established. Restoration of the liquid lost from the body following drug administration was not accompanied by either a fall in the cerebrospinal fluid pressure or a change in the intensity of general cerebral symptoms. The action of furosemid on intracranial pressure is explained by a reduction in the central venous pressure, by an increased outflow of the venous blood from the cranial cavity as well as by its diminished volume. Concomitant administration of large quantities of water lowers or completely precludes the hypotensive action of the agent on intracranial pressure and, thus, is considered unadvisable.

Brain Diseases↗
PubMed1980

[Dynamics of central venous, arterial, and cerebrospinal fluid pressures following polyethyleneglycol administration].

The polyethylenglycol -- 400 (PEG) in dose 6 ml/kg at the rate of 0.2 ml/kg/min was i. v. administered to 12 anesthetized cats. The increase of osmolarity in the blood serum caused the hypervolemia, increase of arterial (by 20-30 mm Hg) and systemic venous (by 80-100 mm H2O) pressures, but in 30 min after the end of PEG infusion the hemodynamics returned to the initial levels due to increased diuresis, whereas the cistern CSF pressure decreased as a result of dehydration of the brain. This decrease was counteracted by the high venous and arterial pressures, but, after normalizing of hemodynamics the CSF pressure was decreased by 90-100 mm H2O as against initial level.

Animals↗
PubMed1980

[Redistribution of fluid phases of the brain during an increase in blood osmolarity].

Intravenous injection of polyethylene glycol 400 to rats (1.5 mmole/100 g body weight) increases blood osmolarity, the total water content in the brain hemispheres exhibiting insignificant changes. Cellular dehydration is accompanied by an augmentation of the volume of extracellular fluid in the intact skull cavity. The increased blood content of the brain is pointed to be a 24% increase in the iron level in its tissues. Skull trepanation enhances the dehydrating effect of polyethylene glycol 400 but does not affect the blood content of the brain.

Animals↗
PubMed1979

[Cerebral water and electrolytes during changes in the osmolarity and volume of the extracellular fluid].

The increase of osmolarity in the blood serum after administration of polyethylenglycol-400 (PEG) as well as the sharp increase of the renal loss of fluid under the influence of furosemide insignificantly affected the water contents in the white and grey brain substance. A slight dehydration of the grey substance occured on combination of osmotic gradient effect and the renal loss of fluid. Preservation of initial hydration of the brain within the skull on administration of PEG and furosemide is due to redistribution of the fluid phases: dehydration of cells is followed by an increase in the volume of sodium-containing tissue fluid where upon the amount of sodium and calcium in the tissue practically does not change.

Animals↗
PubMed1978

[Ion excretion by the rat kidney in depressed reabsorption in proximal tubule and ascending protion of the loop of Henle].

Simultaneous suppression of reabsorption in the proximal tubule with the aid of polyethylenglucole 400 (PEG) and in ascending part of Henle's loop with furosemide increased diuresis by 121 times and natri-uresis by 242 times on the average. The increase was based on changes in the tubule reabsorption and secretion. The changes of sodium and calcium excretion as well as excretion of potassium and magnesium were parallel. Excretion of sodium and calcium was lesser than the diuresis while that of magnesium and potassium exceeded it. Furosemide reduced the reabsorption of osmotically free water.

Absorption↗