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Biomedical subjects

E E Johnson

Publications and source records attributed to E E Johnson.

At least 91 records · Page 5Linked to original sources

Morphine: a dual effect at the canine choledochoduodenal junction.

The effects of i.v. bolus injections of morphine sulfate on resistance to flow through the choledochoduodenal junction were studied in acutely prepared dogs anesthetized with pentobarbital. Dose-response studies indicate that the spasmogenic effect of 0.1 mg/kg of morphine is greater than that of 1.0 mg/kg of morphine. These and other data indicate a combination of stimulatory and inhibitory activity with the relaxing activity occurring at higher doses. Inhibitory activity was potentiated by neostigmine, given 1 hr before morphine. Prior administration of atropine or vagotomy enhanced the stimulatory effect, possibly by blockade of the inhibitory effect. Vagotomy did not block the inhibitory effect of morphine in dogs pretreated with neostigmine. After three serial injections of 1.0 mg/kg, of morphine, naloxone challenge elicited strong choledochoduodenal contractions in reserpine-treated dogs, neostigmine-treated dogs and dogs given 0.1 mg/kg of morphine 1 hr before 1.0 mg/kg of morphine. In dogs pretreated with neostigmine, contractions upon naloxone challenge were always completely blocked by atropine. Acetylcholine release may be involved in the inhibitory effect of morphine at the canine choledochoduodenal junction.

Animals↗

Effect of nicotine upon uterine blood flow in the pregnant rhesus monkey.

Acute effects of nicotine upon the uterine blood flow, blood pressure, maternal and fetal acid-base state, and oxygenation were determined in eight pregnant rhesus monkeys near term. Nicotine was infused intravenously to the mother in a dose of 100 microgram/kg per body weight/minute over 20 minutes. The flow rate was measured with the use of the electromagnetic flowmeter. Significant decrease in the uterine arterial blood flow rate, as much as 38% of the control value, was observed during the first 15 minutes of the infusion while aortic pressure increased by 14%. Acidosis and hypoxia resulted in the fetus. Considered together with our previously reported data, the present investigation appears to indicate that the adverse effects of nicotine to the fetus are due to the combined effects of the reduced uterine blood flow and the transmitted nicotine to the fetus.

Acid-Base Equilibrium↗

Radiologic consultation to a remote Canadian hospital using Hermes spacecraft.

Access to medical services in north Canada is limited by geography, climate, communication and transportation. A geostationary spacecraft, Hermes, was used to provide dependable, high-quality communication between a remote nursing station, a base hospital and a health science centre. Teleradiology formed an important component of the telemedicine services. Remote supervision of radiography and fluoroscopy was made possible; consultation services were shown to be 90% effective.

Adult↗

End-respiratory pressure ventilation and sulfobromophthalein sodium excretion in dogs.

Sulfobromophthalein sodium (BSP) 25 mg/kg body wt was given as a single iv injection to 32 fasted dogs. Serum samples at 3, 5, 10, 20, 30, 45, 60, 80, and 120 min postinjection were analyzed for total concentration of BSP and from 30 to 120 min for percent conjugated BSP. Four groups were compared: spontaneous ventilation; intermittent positive-pressure ventilation (IPPV) and continuous positive-pressure ventilation (CPPV) (2 groups). During CPPV, one group of dogs was given a continuous infusion of cholecystokinin octapeptide (CCK-8, 1 ng/kg per min). Central venous pressure averaged 11.3 +/- 0.7 (SE) cmH2O in dogs with CPPV + CCK-8 and 11.8 +/- 0.8 (SE) cmH2O in dogs with CPPV alone. At 3, 5, and 10 min postinjection serum BSP levels were similar in all groups. From 30 to 120 min postinjection serum levels of both free and conjugated BSP were higher in dogs ventilated with CPPV alone than in any other group (P less than 0.01). Dogs given CCK-8 during CPPV had serum BSP levels that were statistically similar to dogs breathing spontaneously or ventilated with IPPV. We conclude that CPPV impairs BSP excretion. This effect is counteracted by CCK-8.

Airway Resistance↗

Splanchnic hemodynamic response to passive hyperventilation.

Two groups of anesthetized, splenectomized, and paralyzed dogs were hyperventilated (Vt 40 ml/kg). Normocapnia was maintained in one group (mean Paco2 37.6 mm"h'g, mean p"h '7.41) and respiratory alkalosis (mean Paco2 8 mmHg, mean pH 7.75) in the other. Splanchnic hemodynamic responses were similar in both groups. Average hepatic venous pressure increased from 3.2 to 6.4 mmHg in the normocapnic group and from 3.8 to 7.7 mmHg in the hypocapnic group. Average portal venous pressure increased from 10.7 to 12.0 mmHg and 10.8 to 12.7 mmHg in the normocapnic and hypocapnic groups, respectively. Mesenteric vascular resistance increased in 93 per cent of dogs. A decrease in functional intestinal capillary surface area during hyperventilation was indicated by a significant reduction in mesenteric Vo2 (from 15 to 11 ml/min, average 30 per cent), and a concomitant reduction in mesenteric O2 extraction ratio. Changes in mesenteric Vo2 were reflected in calculated splanchinic Vo2. Hepatic O2 uptake was essentially unchanged by tidal hyperventilation with or without hypocapnia.

Alkalosis, Respiratory↗

Continuous positive-pressure ventilation and choledochoduodenal flow resistance.

Resistance to flow through the choledochoduodenal junction was measured during constant perfusion (0.8 ml saline/min). In eight dogs, intermittent positive-pressure ventilation (IPPV) and continuous positive-pressure ventilation (CPPV) were compared. Pressure in the common bile duct was always higher during JPPV than IPPV. With the first application of CPPV the rate of intravenous fluid was adjusted to maintain constant Hct. Mean hepatic venous pressure (Phv) increased from 6.6 to 11.5 cmH2O (P less than 0.001). Mean pressure in the common bile duct increased (P less than 0.001) from 11.6 to 14.1 cmH2O. The average increase in resistance was 21%. Changes reversed with return to IPPV. During the second application of CPPV, intravenous fluid was increased to maintain constant arterial pressure. Phv increased to 12.8 cmH2O and pressure in the common bile duct increased to 15.0 cmH2O (30% increase). In four additional dogs, choledochoduodenal resistance during continuous CPPV was reduced by intravenous vasopressin, intravenous norepinephrine and intraducta phenylephrine. CPPV increases resistance to flow through the choledochoduodenal junction, probably by vascular engorgement.

Animals↗