An analysis of electrophysiological events in cerebral structures during ether anesthesia

1958 ◽  
Vol 10 (2) ◽  
pp. 305-324 ◽  
Author(s):  
J. Schlag ◽  
H. Brand
Author(s):  
M. Ashraf ◽  
F. Thompson ◽  
S. Miki ◽  
P. Srivastava

Iron is believed to play an important role in the pathogenesis of ischemic injury. However, the sources of intracellular iron in myocytes are not yet defined. In this study we have attempted to localize iron at various cellular sites of the cardiac tissue with the ferrocyanide technique.Rat hearts were excised under ether anesthesia. They were fixed with coronary perfusion with 3% buffered glutaraldehyde made in 0.1 M cacodylate buffer pH 7.3. Sections, 60 μm in thickness, were cut on a vibratome and were incubated in the medium containing 500 mg of potassium ferrocyanide in 49.5 ml H2O and 0.5 ml concentrated HC1 for 30 minutes at room temperature. Following rinses in the buffer, tissues were dehydrated in ethanol and embedded in Spurr medium.The examination of thin sections revealed intense staining or reaction product in peroxisomes (Fig. 1).


Author(s):  
Richard L. Klein ◽  
Åsa K. Thureson-Klein ◽  
Harihara M. Mehendale

KeponeR (decachlorooctahydro-1,3,4-metheno-2H-cyclobuta[cd]pentalen-2-one) is an insecticide effective against ants and roaches. It can cause severe toxicity in fishes, birds, rodents and man. Prominent effects include hepatic lipid deposition and hypertrophy, impairment of reproductive capacity and neurological disorders. Mitochondrial oligomycin-sensitive Mg2+-ATPase is also inhibited. The present study is a preliminary investigation of tissue ultrastructural changes accompanying physiological signs of acute toxicity, which after two days treatment include: pronounced hypersensitivity and tremor, various degrees of anorexia and adipsia, and decreased weight gain.Three different series of adult male Sprague-Dawley rats (Charles River or CD-I) were treated by intubation with Kepone in corn oil at a dose of 50 mg per kg for 3 successive days or at 200 ppm in food for 8 days. After ether anesthesia, rats were immediately perfused via a cannula in the left ventricle with 4% p-formaldehyde and 0.5% glutaraldehyde in Millonig's phosphate buffer at pH 7.2 for 20-30 min at 22°C.


1971 ◽  
Vol 50 (6) ◽  
pp. 1635-1641 ◽  
Author(s):  
William K. Elwood

β-Streptococcal infection and its sequelae did not play a significant role in the development of hypoplastic enamel defects. Hypoplastic enamel faults occurred that could not be related to any of the experimental procedures. A genetic or other component may influence the susceptibility of guinea pigs to hypoplastic enamel lesions.


1946 ◽  
Vol 84 (4) ◽  
pp. 277-292 ◽  
Author(s):  
S. Edward Sulkin ◽  
Christine Zarafonetis ◽  
Andres Goth

Anesthesia with diethyl ether significantly alters the course and outcome of experimental infections with the equine encephalomyelitis virus (Eastern or Western type) or with the St. Louis encephalitis virus. No comparable effect is observed in experimental infections produced with rabies or poliomyelitis (Lansing) viruses. The neurotropic virus infections altered by ether anesthesia are those caused by viruses which are destroyed in vitro by this anesthetic, and those infections not affected by ether anesthesia are caused by viruses which apparently are not destroyed by ether in vitro. Another striking difference between these two groups of viruses is their pathogenesis in the animal host; those which are inhibited in vivo by ether anesthesia tend to infect cells of the cortex, basal ganglia, and only occasionally the cervical region of the cord. On the other hand, those which are not inhibited in vivo by ether anesthesia tend to involve cells of the lower central nervous system and in the case of rabies, peripheral nerves. This difference is of considerable importance in view of the fact that anesthetics affect cells of the lower central nervous system only in very high concentrations. It is obvious from the complexity of the problem that no clear-cut statement can be made at this point as to the mechanism of the observed effect of ether anesthesia in reducing the mortality rate in certain of the experimental neurotropic virus infections. Important possibilities include a direct specific effect of diethyl ether upon the virus and a less direct effect of the anesthetic upon the virus through its alteration of the metabolism of the host cell.


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