Biomedical subjects
Publications and source records attributed to F Huidobro.
We report two diabetic patients who developed lactic acidosis following the use of Buformin. Treatment consisted of mechanical ventilation, massive bicarbonate administration, circulatory support with dopamine and peritoneal dialysis. Despite this, both patients died.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
1 Morphine, methadone, levorphanol, pethidine, etonitazene and related morphine-like alkaloids produced an increase in the electrically-evoked muscular contraction of the rat vas deferens. In contrast, the enkephalins and beta-endorphin caused inhibition of the twitching. 2 The concentration of beta-endorphin required to inhibit by 50% the muscular twitch was about 50 to 100 times less than that of the enkephalins. 3 Pretreatment of the vasa with morphine antagonized the inhibition of the neuromuscular transmission caused by either beta-endorphin or enkephalin. 4 Conversely, pretreatment with beta-endorphin sensitized the vasa to the increase in twitch tension caused by morphine. 5 Morphine did not alter the sensitivity to exogenously administered noradrenaline, dopamine or potassium.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Isamide, the N-chloroacetyl derivative of 5-methoxytryptamine, produced a dose-dependent competitive blockade of uterine contractions in vitro induced by 5-HT. The pA2 value for the 5-HT-isamide interaction was 4.42. The blockade was short-lasting and reversible; after recovery, a dose-dependent increase in the uterine sensitivity to 5-HT was found. The blockade proved to be selective to the 5-HT receptor. The simultaneous application of 5-HT plus isamide partially prevented the 5-HT-induced auto blockade phenomenon. In addition, isamide did not affect the contractile responses of the uterus to oxytocin or bradykinin or the contractile effects of the rat vas deferens to adrenaline.
N-Benzyl iodoacetamide, betsamide, at 10 mg kg-1 i.v. blocked the hypertensive and contractile responses of the nictitating membrane of the cat to adrenaline. The blockade had a lag period before full development. Pretreatment of cats with betsamide for 7 or 18 h showed a non-equilibrium type of alpha-adrenoceptor blockade. The responses of the nictitating membrane to adrenaline were markedly depressed and did not recover after high doses of adrenaline. In the same cats, adrenaline caused a profound hypotension. The effect of betsamide lasted for at least 72 h. In the rat isolated vas deferens, 3 X 10(-5) M betsamide non-competitively blocked the contractile responses to noradrenaline; the adrenoceptor blockade was less effective when betsamide was applied with noradrenaline. The blockade lasted for more than 24 h, and was not reversible after extensive washing. Betsamide antagonized the contractile effects of carbachol and 5-hydroxytryptamine on the rat vas deferens, but not the beta-responses of the guinea-pig trachea to adrenaline and isoproenaline. Results are discussed in relation to a probable mechanism of action.
The effect of morphine on urine and blood serum concentration of Na+, K+, Cl- and other chemicals was determined using Sprague Dawley rats, previously hydrated with 50 ml/kg of 0.5% NaCl to provoke an increased diuresis. Morphine caused about a 90% decrease in the urine concentration of Na+, K+ and Cl-. This reduction in the urine electrolyte excretion was associated with a small but significant increase in the concentration of the blood Na+ and Cl-. The antidiuresis and the decrease in urine electrolytes caused by morphine was paralleled by a 50% reduction of the endogenous creatinine clearance. An acute dose of 7.5 mg/kg morphine i.p. did not alter the concentration of 13 other clinical blood chemicals with the exception of urea. However, after 18 hr of morphine pellet implantation, a significant increase was found in the blood urea and in the activity of serum transaminases. Lactic dehydrogenases isoenzymes one and two were significantly increased in the blood of rats chronically administered with morphine.
1 Injection of rats with morphine or methadone, before they received a water load equivalent to 5% of their body weight, produced a dose-dependent antidiuretic effect. Following the antidiuresis, urine was eliminated with kinetics similar to control untreated rats. 2 The antidiuretic effect of morphine or methadone was blocked by naloxone administered before the opiate, or reversed when given after the opiate. 3 Rats implanted with morphine pellets developed a marked degree of tolerance to the antidiuretic effect of morphine. Tolerance was also obtained on injection of three daily doses of morphine or methadone over two days. 4 Withdrawal symptoms were precipitated by naloxone in rats implanted with pellets of morphine; under these conditions the animals showed a marked reduction in urine production as compared to naive rats.
The effects of acute administration of either water or 2% NaCl solution via a stomach tube and injections of diurecits, furosemide (5, 10 mg) and acetazoleamide (5, 20 mg per rat), in adult rats upon urinary kallikrein (Kal), Na and K, were studied. Hyperhydration with water (5% b.w.) produced in 121% increase and 2% NaCl overloading (5% b.w.) 275% increase in urinary Kal within 120 min after gavage, when compared with the excretion of non hyperhydrated rats. Furosemide 5 mg in hyperhydrated animals produced in the same period an excretion of 645 +/- 52 ng BR of Kal, which is 147% higher to that excreted by the hyperhydrated controls. The same dose of furosemide in 2% NaCl loaded rats, produced an excretion of Kal equivalent to 1333 +/- 72 ng BR which is 180% greater than in controls similarly loaded. Acetazoleamide 20 mg and furosemide 5 mg produced similar excretions of Kal even though natriuresis is greater tna kalliuresis is lesser in furosemide injected rats. Evaluation of total kidney Kal has shown that a single (10 mg) or a series of furosemide injections (8 days 5 mg + 1 day 10 mg), brings about a significant (p is less than 0.001) decrease in renal Kal, but the increase of Kal excreted in the urine (120 min) is 3.5 times more (under a single injection) and 42 times more (under 9 injections) than the amount which disappears from the kidneys. Apparently furosemide not only stimulates Kal excretion, but also Kal synthesis in the kidney. The results support the concept that the Kal system would be involved in excretory functions dealing both with sodium and water excretion.
Single-dose tolerance to the antinociceptive effect of morphine can be demonstrated using an adequate initial priming dose of morphine and allowing an interval of 48 to 72 hours for its development. The threshold dose necessary to produce tolerance was found to be about 3 to 4 times greater than that for producing analgesia but higher doses of morphine did not enhance further tolerance development. Evidence of tolerance was indicated by the fact that when the antinociceptive response to morphine was assessed by the hot-plate and the tail-flick procedures, a shift in the dose-response curve of morphine to the right occurred after an adequate single priming dose of morphine. Cross-tolerance was evidenced by a decrease in analgetic response to methadone 3 days after a single priming dose of morphine and a decrease in morphine response after a single dose of methadone. The development of single-dose tolerance was inhibited by cycloheximide. Single-dose tolerance was also blocked by 5,6-dihydroxytryptamine and perhaps enhanced by L-tryptophan. Cyclic 3',5'-adensine monophosphate did not affect single-dose tolerance development significantly although the direction was in favor of augmentation. Morphine uptake by the brain was not modified by the development of single-dose tolerance. Physical dependence, as measured by naloxone-precipitated withdrawal jumping, was not observed when single-dose analgetic tolerance was maximal. The results suggest that single-dose tolerance to morphine involves the synthesis of some macromolecule and support previous findings in this laboratroy involving an association with serotonin.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.