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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to develop an experimental model of pulmonary hypertension, five mongrel dogs were treated with 1 mg/kg p. o. and five with 1.5 mg/kg p. o. of Aminorex base five days a week for two years. A control group was given empty capsules by months. The following effects of treatment with Aminorex were noted: 1. Anorexia and central stimulation, 2. Natriuresis, 3. an increase in respiration rate, heart rate and body temperature, 4. a tendency towards usually compensated metabolic acidosis, 5. an increase in pulmonary arterial pressure, total pulmonary resistance and right ventricular work, and, in the group given the higher dose, a slight increase in mean aortic pressure and peripheral resistance. 6. Only slight histopathological changes were detectable, e.g.: perivascular oedema; increase in the number of muscle arteries, occasionally with hypertrophy of the tunica media and slight, focal fibro-elastoid thickening of the intima in some elastic arteries. These changes were present in about 60% of the treated dogs. Only one dog that died after 91 weeks' treatment also showed moderate, focal phlebosclerosis of large pulmonary veins and focal, fibro-elastoid thickening in the coronary artery. Serious morphological changes in the pulmonary vessels such as are observed in the human pulmonary hypertension were not seen in our laboratory animals. Two dogs in each dosage group died in the course of the experiment. The results of this experiment show that it is, in general, possible to induce pulmonary hypertension by administering Aminorex orally. In two dogs, however, pressure in the pulmonary artery (measured under anaesthesia) was below 20 mm Hg (controls: 13.8 +/- 1.3 mm Hg). One possible pathogenetic mechanism underlying the pulmonary hypertension would appear to be precapillary vasoconstriction induced by Aminorex, which can lead to transient, persistent or, for some unknown reason, even permanent fixation of pulmonary resistance.
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PMID:[Two-year peroral administration of aminorex in the dog. 2]. 80 16

During neurophysiologic studies in the rat [Crl:COBS CD(SD)BR], chloral hydrate was given intraperitoneally to produce anesthesia for brain electrode implantation. The incidental occurrence of adynamic ileus in six of these rats, 5-16 days after surgery, prompted further investigation. Pathological evaluations and transmission experiments using ingesta and viscera from affected rats failed to reveal an infectious agent. Subsequently chloral hydrate-induced adynamic ileus leading to morbidity or death was experimentally produced in 14 of 27 rats, 3--36 days after intraperitoneal administration of the anesthetic at a dose of 400 mg/kg body weight and concentrations of 125--275 mg/ml. The experimentally produced condition was characterized by lethargy, anorexia, abdominal distension, ruffled hair coat, inactivity, drowsy expression, constipation, and death. Gross pathologic findings included gaseous distension and atony of the cecum and segments of the small intestine. Small intestine contents varied from liquid to solid. The colon and rectum contained only a few dry hard fecal pellets. A few animals showed excess abdominal fluid. Microscopic findings were limited to focal chronic serositis and serosal fibrosis affecting the visceral peritoneum. On the basis of the experimental studies, it was concluded that the condition described was not an infectious disease but was an abnormal physiologic condition produced by the irritating or pharmacologic action of chloral hydrate given at high concentrations in the abdominal cavity.
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PMID:Adynamic ileus in the rat induced by chloral hydrate. 85 88

Two adult Hampshire rams, unrelated and from separate farms, were examined for the cause of intermittent bloat and, or anorexia which lasted for three to six weeks and caused depression and cachexia. The rumen of each ram was hypermotile and ballottement of the ventral abdomen of each animal revealed an enlarged doughy viscus. Mild prerenal azotaemia, hypokalaemia with metabolic alkalosis, and high rumen chloride concentrations were evident. One ram died during the induction of anaesthesia for an abomasotomy and the other was euthanased after unsuccessful medical therapy. The abomasum of each ram was four to six times larger than that of a normal adult ram and filled with coarse, semi-moist, impacted ingesta. This abnormality was clinically identical to the abomasal emptying syndrome which has been described only in the Suffolk breed.
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PMID:Abomasal dilatation and impaction in two Hampshire rams. 162 57

Administration of furazolidone as a bolus dose (8-500 mg/kg), produced a decrease in plasma corticosterone in chickens. In contrast, addition of furazolidone or furaltadone to the diet (0.04% or above, 10 days), increased plasma corticosterone. Pre-treatment with a 200-mg/kg bolus of furazolidone or furaltadone did not affect pentobarbitone anaesthesia time in the birds. In chickens pre-treated with a nitrofuran in the diet, however, pentobarbitone anaesthesia time was significantly less than that in controls. Furaltadone in the diet, produced significant increases in the amount of cytochrome P-450 and the activity of aniline hydroxylase in the liver microsomes. It is suggested that nitrofurans given in the diet stimulated corticosterone biosynthesis in the adrenal glands and induced mixed-function oxidase activity in the liver. Nitrofurans given as a bolus did not produce these effects. Furazolidone (200 mg/kg) produced severe anorexia, which lasted 2 days in T-line birds. The anorexia seemed to be associated with tissue damage in the birds rather than the ensuing adrenal cortical insufficiency.
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PMID:Contrasting effects of nitrofurans on plasma corticosterone in chickens following administration as a bolus or diet additive. 223 66

Halothane hepatitis is now a well-recognized distinct entity in adults, but there prevails an often-taught "axiom" that halothane hepatitis "does not occur" in children. We describe 2 children who developed cholestatic hepatitis following halothane anesthesia. The first patient had no antecedent liver disease, and presented with anorexia, abdominal pain and delayed onset of jaundice after multiple halothane exposures. Halothane-specific antibodies were positive, and liver tests resolved completely. The second patient had antecedent liver disease and presented with delayed onset of unexplained high fevers for 10 days following a single halothane exposure. Gradually increasing cholestasis ensued in the absence of other causes of liver disease. Halothane antibodies were negative. These cases illustrate different clinical presentations of halothane hepatitis, such as delayed onset of jaundice or fever following halothane exposure. The difficulties in making a definitive diagnosis and the need to exclude other causes of liver disease are detailed. Risk factors and other presentations are discussed. While halothane hepatitis appears to be an uncommon entity in children, it does occur, and may present with manifestations less than fulminant hepatic failure. A high index of suspicion and a detailed history of the time sequence of events are necessary as the diagnosis is primarily clinical. Halothane-specific antibodies are helpful if positive. In any child developing unexplained jaundice or high fevers following halothane anesthesia, further exposures should be avoided and halothane-specific antibodies obtained.
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PMID:Halothane hepatitis in children. 178 63

Intracisternal (IC) injection of the GABA-transaminase inhibitor, ethanolamine-O-sulfate (EOS), has been previously shown to induce dose-dependent anorexia in normal rats as well as to reverse overeating in several rodent models of acute and chronic hyperphagia. To determine if such anorexia might be mediated by cells within or fibers of passage which traverse the lateral hypothalamus (LH), adult female rats received bilateral radiofrequency heat lesions of the LH vs. anesthesia control injections and were allowed to recover normal feeding and drinking responses. Using a longitudinal design, all animals then received 100, 0, and 200 micrograms EOS in 20 microliters deionized water IC with 1 week separating each injection. In addition to daily measures of feeding, drinking and body weight, all animals were screened 24 hr after injections for sensorimotor competence and general health by testing open-field activity, catalepsy, paw-lick responses on a hot-plate and rectal temperature. As reported previously, IC EOS induced dose-dependent hypophagia and weight loss. However, the magnitude and duration of these effects were equivalent in lesioned and control rats. In addition, open-field activity and body temperature were reliably lowered as a function of dosage while catalepsy was increased. Again, this effect was equivalent in lesioned and control rats. Subsequent tests of drinking and feeding in response to hyperosmotic and hypoglycemic challenges, respectively, confirmed that lesioned rats were deficient compared to controls. These findings suggest that an intact LH axis is not required for the anorexigenic effects of IC EOS.
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PMID:Effects of lateral hypothalamic lesions on the anorexia induced by ethanolamine-O-sulfate. 273 38

A retrospective study of 22 calves afflicted with intestinal atresia was performed to determine typical signs of disease, treatment, and survival rate. All 22 calves, except 2 heifers with atresia ani and rectovaginal fistula, were examined when they were between 1 and 10 days old because of depression, anorexia, abdominal distention, and lack of feces. All calves had been observed to stand and suckle shortly after birth. Survival rate was influenced by the atretic segment affected: 0% (0/2 surgically treated) for atresia jejunal; 42% (5/12 examined) or 71% (5/7 recovering from general anesthesia) for atresia coli; and 63% (5/8 examined) or 71% (5/7 surgically treated) for atresia ani. Survival appeared to depend principally on early recognition, anatomic site affected, and successful surgical establishment of a patent intestinal tract.
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PMID:Intestinal atresia in calves: 22 cases (1978-1988). 277 96

A novel model of nutritionally induced hypertension in the rat is described. Dietary obesity was produced by providing sweet milk in addition to regular chow, which elicited a 52% increase in caloric intake. Despite 54% greater body weight gain and 139% heavier retroperitoneal fat pads, 120 days of overfeeding failed to increase systolic pressure in the conscious state (125 +/- 8 vs. 121 +/- 4 mmHg in chow-fed controls) or mean arterial pressure under urethan anesthesia (71 +/- 4 vs. 63 +/- 3 mmHg). In contrast, mild hypertension developed in intermittantly fasted obese animals (a 21-mmHg increase in systolic blood pressure measured in the conscious state and a 16-mmHg increase in mean arterial pressure under anesthesia relative to chow-fed controls). The first 4-day supplemented fast was initiated 4 wk after the introduction of sweet milk, when the animals were 47 g overweight relative to chow-fed controls. Thereafter, 4 days of starvation were alternated with 2 wk of refeeding for a total of 4 cycles. A rapid fall in systolic blood pressure (12 +/- 2 mmHg at 2 days) accompanied the onset of supplemented fasting and was maintained thereafter (2.7 +/- 2.6 mmHg further decrease during the latter half of the fast). With refeeding, blood pressure rose precipitously (13 +/- 3 mmHg in the 1st 2 days), despite poststarvation anorexia. Blood pressure tended to rise slightly over the remainder of the realimentation period (5.2 +/- 2.8 mmHg). After the 4th supplemented fast, hypertension was sustained during 30 days of refeeding. Cumulative caloric intake in starved-refed rats fell within 2% of that in chow-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Refeeding hypertension in dietary obesity. 333 69

This report describes five cases of hepatocellular injury following halothane anesthesia. Four patients had multiple exposures to the anesthetic. Three of the five died from submassive to massive liver cell necrosis. The two survivors developed jaundice and/or dark urine following each exposure to halothane; liver biopsy in one showed centrilobular and linear areas of necrosis. Fever, anorexia, nausea, vomiting, abdominal pain and jaundice were present in all cases. In the two survivors the prothrombin time was less than 20 seconds throughout the course of the disease, whereas in the three who died the prothrombin time was more than 20 seconds from the onset. The English literature to the end of 1971 is reviewed. Approximately 600 cases of halothane-related hepatitis have been reported
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PMID:Halothane hepatitis. 468 24

The morphine withdrawal syndrome was studied in rats which had been made dependent on morphine administered by the intermittent infusion technique. Rats made rapidly dependent on morphine by an hourly infusion of 0.12-4 mg/kg/h showed a withdrawal syndrome when they were abruptly withdrawn, after infusion for 7 days, or when they were challenged by naloxone after infusion for 4 days. Abruptly withdrawn rats showed a marked weight loss and other mild symptoms. The weight loss seems to mainly due to anorexia, partly because it was attenuated by IV feeding throughout the withdrawal and partly because the fasted rats showed a weight loss comparable to the withdrawn rats. The naloxone-precipitated withdrawal syndrome showed characteristics, which, from their time course of incidence and their three groups; motor excitation, cholinergic signs, and others. These groups and their interrelationships were discussed. All characteristics were suppressed by deep anesthesia with ether or pentobarbital. A sudden fall in blood pressure was indicated in the anesthetized morphine-dependent rats immediately after the naloxone challenge. This suggests that the intrinsic withdrawal syndrome was progressing even under anesthesia.
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PMID:Characterization of withdrawal syndrome of morphine-dependent rats prepared by intermittent infusion technique. 678 42


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