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Biomedical subjects

K G Kagan

Publications and source records attributed to K G Kagan.

10 recordsLinked to original sources
PubMed1980

Thoracic trauma.

The physiologic equilibrium of chest injury patients is frequently precarious, and mild stress during examination and treatment may precipitate acute decompensation and death. This is particularly true with the respiratory system, where the normally large respiratory reserve capacity may be rapidly lost. Accurate assessment of the nature of the thoracic injury and the severity of that injury must be determined in order to formulate a therapeutic plan. Many thoracic injuries, such as pneumothorax, pulmonary contusions, or rib fractures, will be self-limiting. Other conditions must be recognized for their potentially lethal nature and dealt with aggressively, and these include cardiac tamponade, tension pneumothorax, and esophageal perforation. By performing a systematic evaluation of the patient and confirming or denying the presence of all possible types of thoracic injury, the veterinarian may avoid overtreatment of self-limiting lesions and recognize and aggressively treat those with potentially fatal outcomes.

Animals↗
PubMed1979

Variations in the canine thoracic duct system and the effects of surgical occlusion demonstrated by rapid aqueous lymphography, using an intestinal lymphatic trunk.

An alternative method for lymphography was developed in an attempt to improve the outlining of the thoracic duct system. Lymphograms obtained on 20 normal dogs demonstrated a large extent of anatomic variation. A complete obstruction of the thoracic duct was created in six dogs through transpleural resection and ligation. The lymphatic system responded by opening lymphaticovenous anastomoses proximal to the site of obstruction.

Animals↗
PubMed1978

Chemical cardioversion of electrically induced ventricular fibrillation in dogs.

An acetylcholine-potassium cocktail was used to defibrillate chemically the electrically induced ventricular fibrillating myocardium of thoracotomized dogs. This drug combination was highly effective (75%) in comparison with potassium alone (20%) and acetylcholine alone (zero %). Atropine prevented chemical defibrillation. On dogs which failed to defibrillate after the administration of the cocktail, high energies were required to defibrillate the ventricles electrically and not all could be electrically defibrillated. After the administration of the ionic-choline cocktail, increased ventilatory resistance, generalized skeletal muscle contraction, urination, and defecation were observed.

Acetylcholine↗
PubMed1978

Effects of ionic salts or acetylcholine, or both, on electrically induced ventricular fibrillation in dogs.

A dose-response curve was delineated for an acetylcholine-potassium chloride cocktail previously found to be highly effective in chemically defibrillating electrical induced ventricular fibrillation of thoracotomized dogs. The cocktail dosage responsible for the greatest percentage of chemical defibrillations was transthoracically given to nonthoracotomized dogs subjected to ventricular fibrillation; this resulted in 33% chemical defibrillation. Two clinical canine patients were transthoracically administered the acetylcholine-potassium chloride cocktail because they failed to respond to external electrical defibrillation; both were chemically defibrillated. Potassium citrate when substituted for potassium chloride, in the cocktail, or alone appeared to be more efficacious for chemical defibrillation. Magnesium chloride with acetylcholine failed to chemically defibrillate any dog administered this cocktail.

Acetylcholine↗