Thomas W. Pollock

Computed tomography in the diagnosis and localization of intraabdominal abscesses

Computed tomographic scanning of the abdomen in 50 patients evaluated for suspected intraabdominal abscess resulted in an overall accuracy of 92 percent. It proved the most accurate diagnostic tool in determining the presence of intraabdominal abscess. Computed tomography of the abdomen is a useful diagnostic adjunct to clinical judgment and may assist in localizing intraabdominal abscesses and planning early surgical intervention.

Verapamil attenuates stress-induced gastric ulceration

Since many of the proposed etiologic factors leading to gastric stress ulceration involve stimulation of calcium influx, the effect of verapamil, a potent calcium channel blocker, on the gastric mucosa in cold-restrained inbred rats was assessed. Twenty-nine rats received intraperitoneal normal saline (2 ml) while the experimental group (N = 29) received 1 mg/kg verapamil in an equal volume of normal saline intraperitoneally. All animals were then stressed at 4 degrees C for 4 hr and sacrificed. Gastrin and fatty acid levels were measured and blinded ulcer scoring of the gastric mucosa was carried out. Verapamil-treated animals had decreased frequency and severity of gastric stress ulceration as assessed by ulcer index, ulcer grade, and number of ulcers/animal. In addition, the plasma gastrin levels tended to be lower in the verapamil group. Fatty acid levels were similarly depressed following cold restraint in both groups. Pretreatment with verapamil significantly decreased gastric ulcerative response to cold-restraint stress in the rat. This effect of verapamil pretreatment may be secondary to cytoprotection of the gastric mucosa, preservation of gastric mucosal blood flow, or blockade of calcium-mediated ulcerogenic stimuli.

Effects of chronic hypoxia on canine gastric secretion

Interdigestive gastirc acid output and acid secretory response to histamine, insulin and pentagastrin were studied in five dogs before and after creation of a right to left extracardiac vascular shunt. The arterial PO2 decreased from 81.5 +/- 5.5 mm Hg to 39.8 +/- 6.0 mm Hg postoperatively with no change in arterial pH or PaCO2. Basal (interdigestive) acid output increased from 1.19 +/- 0.26 mEq/hr to 4.97 +/- 0.81 mEq/hr postoperatively. Acid secretory response to insulin was increased after the induction of chronic hypoxia. Increased sensitivity to pentagastric was also observed although parietal cell mass (maximum histamine-stimulated output) was unchanged postoperatively. Changes in acid secretory response and PaO2 were present at one week and were sustained through twelve weeks after shunting. Chronic hypoxia resulted in gastric acid hypersecretion secondary to enhanced sensitivity of the parietal cell to a combination of neural and humoral stimuli.

Changes in Extravascular Lung Water and Fatty Acids in a Hyperdynamic Canine Model of Sepsis

: Several mediators, including fatty acids, have been postulated to induce the increase in permeability of the pulmonary endothelium and subsequent accumulation of extravascular lung water (EVLW) which are generally considered to be among the first events in the development of adult respiratory distress syndrome. In a canine model of hyperdynamic sepsis (hemodynamically similar to human sepsis) changes in EVLW and in concentrations of different fatty acids in the aortic and pulmonary arterial blood were measured. Two days after induction of sepsis, EVLW increased from 6.6 +/- 0.6 to 9.2 +/- 1.0 ml/kg, and the pulmonary arterial concentration of oleic acid increased from 52 +/- 4 to 73 +/- 5 mg/dl. Three days after induction of sepsis, EVLW increased further to 14.4 +/- 3.8 ml/kg and the mean concentration of oleic acid increased to 74 +/- 7 mg/dl. Twenty-four hours later, both EVLW and the mean pulmonary arterial concentration of oleic acid were not different from basal. We postulate that oleic acid, a known inducer of experimental ARDS, is one of the mediators of endothelial damage of the lung during sepsis.

CHANGES IN EXTRAVASCULAR LUNG WATER AND FATTY ACIDS IN A HYPERDYNAMIC CANINE MODEL OF SEPSIS

Several mediators, including fatty acids, have been postulated to induce the increase in permeability of the pulmonary endothelium and subsequent accumulation of extravascular lung water (EVLW) which are generally considered to be among the first events in the development of adult respiratory distress syndrome. In a canine model of hyperdynamic sepsis (hemodynamically similar to human sepsis) changes in EVLW and in concentrations of different fatty acids in the aortic and pulmonary arterial blood were measured. Two days after induction of sepsis, EVLW increased from 6.6 +/- 0.6 to 9.2 +/- 1.0 ml/kg, and the pulmonary arterial concentration of oleic acid increased from 52 +/- 4 to 73 +/- 5 mg/dl. Three days after induction of sepsis, EVLW increased further to 14.4 +/- 3.8 ml/kg and the mean concentration of oleic acid increased to 74 +/- 7 mg/dl. Twenty-four hours later, both EVLW and the mean pulmonary arterial concentration of oleic acid were not different from basal. We postulate that oleic acid, a known inducer of experimental ARDS, is one of the mediators of endothelial damage of the lung during sepsis.