Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 7 de 7
Filter
Add more filters










Database
Language
Publication year range
1.
Stroke ; 17(6): 1272-6, 1986.
Article in English | MEDLINE | ID: mdl-3544349

ABSTRACT

In a canine model of global brain ischemia, six dogs received a selective thromboxane A2 synthetase inhibitor, UK 38,485 (dazmagrel) before the ischemic event; six received a saline placebo. Cerebral blood flow (CBF), systolic and diastolic arterial pressure, cardiac output, pH, PaCO2, PaO2, and arterial and jugular-vein thromboxane B2 (a stable metabolite of thromboxane A2) and 6-keto PGF1 alpha (a stable metabolite of prostacyclin) were measured at baseline, after release of aortic and venae caval occlusion and at intervals up to 120 min thereafter. Treated animals showed nearly complete post-ischemic inhibition of thromboxane B2 production; control animals showed increases in jugular venous thromboxane B2. Arterial and jugular venous levels of 6-keto PGF1 alpha were significantly higher in treated animals at most post-ischemic intervals. CBF in both groups was similar to baseline values at time 0, then declined similarly in both groups by 30 min to approximately equal to 35% of baseline values where it remained thereafter. There were no significant differences in other variables at any interval. We conclude that inhibition of thromboxane A2 production does not alter post-ischemic brain hypoperfusion.


Subject(s)
Brain Ischemia/drug therapy , Cerebrovascular Circulation , Imidazoles/therapeutic use , Thromboxane A2/antagonists & inhibitors , Thromboxane-A Synthase/antagonists & inhibitors , Animals , Brain Ischemia/physiopathology , Dogs , Epoprostenol/metabolism , Time Factors
2.
Ann Emerg Med ; 14(6): 594-6, 1985 Jun.
Article in English | MEDLINE | ID: mdl-3994087

ABSTRACT

Presented is a case of ethylene glycol poisoning in a 24-year-old man who subsequently developed adult respiratory distress syndrome. The noncardiogenic nature of the patient's pulmonary edema was documented with hemodynamic monitoring, and a successful outcome was achieved with hemodialysis, ethanol, and intermittent mechanical ventilation with positive end-expiratory pressure.


Subject(s)
Ethylene Glycols/poisoning , Respiratory Distress Syndrome/etiology , Adult , Blood Gas Analysis , Ethanol/therapeutic use , Ethylene Glycol , Humans , Male , Pulmonary Edema/diagnostic imaging , Pulmonary Edema/etiology , Pulmonary Edema/therapy , Radiography , Renal Dialysis , Respiration, Artificial , Respiratory Distress Syndrome/diagnostic imaging , Respiratory Distress Syndrome/therapy , Suicide, Attempted
4.
Crit Care Med ; 12(9): 734-7, 1984 Sep.
Article in English | MEDLINE | ID: mdl-6467954

ABSTRACT

Positive-pressure ventilation can increase dead space by trapping gas, especially at high frequencies. Under conditions of high airway resistance and high pulmonary compliance, gas trapping can increase alveolar pressure without affecting proximal airway pressure, due to impedance to expiratory gas flow. The difference between alveolar pressure and proximal airway pressure at end-expiration has been called auto-PEEP. Using a mechanical test lung, we altered compliance and resistance under a variety of high-frequency jet ventilator settings to evaluate the generation of auto-PEEP. High driving pressures and prolonged inspiratory times significantly increased gas trapping. This effect was most pronounced when both airway resistance and pulmonary compliance were elevated. These findings support the concept that high-frequency jet ventilation (HFJV) may have deleterious side-effects in patients with chronic obstructive pulmonary disease.


Subject(s)
Respiration, Artificial/adverse effects , Airway Resistance , Humans , Lung/physiopathology , Lung Compliance , Lung Diseases, Obstructive/physiopathology , Models, Biological , Monitoring, Physiologic , Pressure , Pulmonary Alveoli/physiopathology , Respiration , Respiratory Dead Space
7.
Ann Emerg Med ; 12(7): 449-51, 1983 Jul.
Article in English | MEDLINE | ID: mdl-6881636

ABSTRACT

A case of cyanide poisoning from laetrile ingestion is presented as an illustration of the recognition and treatment of cyanide intoxication. The pharmacology of laetrile, of cyanide, and of antidotes to cyanide intoxication are discussed as they relate to the acute management and successful treatment of this patient after this highly lethal ingestion.


Subject(s)
Amygdalin/adverse effects , Cyanides/poisoning , Acidosis/diagnosis , Acidosis/therapy , Adult , Amygdalin/metabolism , Antidotes/therapeutic use , Humans , Inactivation, Metabolic , Male
SELECTION OF CITATIONS
SEARCH DETAIL
...