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Biomedical subjects

F Schiebel

Publications and source records attributed to F Schiebel.

8 recordsLinked to original sources
PubMed1988

Beneficial effect of norepinephrine in the treatment of circulatory shock caused by tricyclic antidepressant overdose.

The beneficial effect of dopamine in circulatory shock induced by tricyclic antidepressants (TCA) overdose may be decreased due to compromise of the endogenous stores of norepinephrine caused by TCA. The successful outcome of two cases of TCA overdose complicated by hypotension, unresponsive to an initial treatment with physostigmine fluid challenge and dopamine (greater than 15 micrograms/kg/min) but subsequently responsive to an infusion of norepinephrine is reported.

Antidepressive Agents, Tricyclic↗
PubMed1988

Cardiac arrest after acute hyperphosphatemia.

Symptoms of hyperphosphatemia usually relate to the associated hypocalcemia. In a 33-year-old patient accidental infusion of a bolus of potassium phosphate (5 ml intravenously) was immediately followed by cardiac arrest. During CPR, clinically important hypocalcemia or hyperkalemia was not detected, but serum phosphorus was significantly increased. Because acute phosphate load can precipitate life-threatening cardiac arrhythmias, familiarity with doses and rate of infusion of phosphate is extremely important.

Acute Disease↗
PubMed1987

Beneficial effect of thyrotropin-releasing hormone in canine hemorrhagic shock.

The effects of thyrotropin-releasing hormone (TRH) on hemodynamic variables, oxygen delivery (DO2), and oxygen consumption (VO2) variables in canine hemorrhagic shock were studied. Anesthetized adult dogs were bled over 30 min to a mean arterial pressure (MAP) of 50 mm Hg. Shock was maintained at this level for half an hour. The animals were divided alternatively into two groups. In the first group (n = 5) a bolus of TRH (2 mg/kg) was given intravenously. The second group (n = 5) served as control and received equal amounts of D5W. Blood samples were obtained regularly up to 120 minutes after TRH or placebo. Differences in the two groups were statistically tested. After TRH, MAP pressure, cardiac output, and systemic vascular resistance increased significantly. DO2 improved after TRH but VO2 remained unchanged. In all dogs, sequential beta endorphin level were measured and were shown to rise after induction of shock. This data indicates that TRH may be of therapeutic benefit in the treatment of hemorrhagic shock and that beta endorphin may be an important pathophysiologic factor.

Animals↗