HISTOPATHOLOGICAL CHANGES IN THE ADRENALS OF RABBITS AFTER DIRECT ACTION OF ULTRASOUND ON THE BRAIN

Medicine ◽  
1963 ◽  
Vol 42 ◽  
pp. 153-155
Keyword(s):  
Direct Action ◽  
Histopathological Changes ◽  
The Brain

Effect of Subarachnoid Bupivacaine Block on Anesthetic Requirements for Thiopental in Rats 

1998 ◽  
Vol 88 (4) ◽  
pp. 1036-1042 ◽  
Author(s):  
Sunil Eappen ◽  
Igor Kissin
Keyword(s):  
Local Anesthetic ◽  
Direct Action ◽  
Afferent Input ◽  
Crossover Design ◽  
Hemodynamic Parameters ◽  
Motor Responses ◽  
Withdrawal Reflex ◽  
Corneal Reflex ◽  
To Receive ◽  
The Brain

Background Subarachnoid bupivacaine blockade has been reported to reduce thiopental and midazolam hypnotic requirements in patients. The purpose of this study was to examine if local anesthetically induced lumbar intrathecal blockade would reduce thiopental requirements for blockade of motor responses to noxious and nonnoxious stimuli in rats. Methods After intrathecal and external jugular catheter placement, rats were assigned randomly to two groups in a crossover design study, with each rat to receive either 10 microl of 0.75% bupivacaine or 10 microl of normal saline intrathecally. The doses of intravenously administered thiopental required to ablate the eyelid reflex, to block the withdrawal reflex of a front limb digit, and to block the corneal reflex were compared. In two separate groups of animals, hemodynamic parameters and concentrations of thiopental in the brain were compared between intrathecally administered bupivacaine and saline. Results The thiopental dose required to block the described responses was decreased with intrathecally administered bupivacaine versus intrathecally administered saline from (mean +/- SD) 40 +/- 5 to 24 +/- 4 mg/kg (P < 0.001) for the eyelid reflex, from 51 +/- 6 to 29 +/- 6 mg/kg (P < 0.005) for front limb withdrawal, and from 67 +/- 8 to 46 +/- 8 mg/kg (P < 0.01) for the corneal reflex. The concentration of thiopental in the brain at the time of corneal reflex blockade for the group given bupivacaine was significantly lower than in the group given saline (24.1 vs. 35.8 microg/g, P = 0.02). Conclusion This study demonstrates that lumbar intrathecally administered local anesthetic blockade decreases anesthetic requirements for thiopental for a spectrum of end points tested. This effect is due neither to altered pharmacokinetics nor to a direct action of the local anesthetic on the brain; rather, it is most likely due to decreased afferent input.

Rapid correction of severe hyponatremia in the rat: histopathological changes in the brain

1985 ◽  
Vol 248 (5) ◽  
pp. F711-F719 ◽  
Author(s):  
J. C. Ayus ◽  
R. K. Krothapalli ◽  
D. L. Armstrong
Keyword(s):  
Serum Sodium ◽  
Brain Lesions ◽  
The Other ◽  
Histopathological Changes ◽  
Water Restriction ◽  
Severe Hyponatremia ◽  
Group Iii ◽  
Group I ◽  
The Brain ◽  
Rapid Correction

The purpose of the present studies was to examine the effects of rapid correction of severe hyponatremia (serum sodium less than 120 meq/liter) either to mildly hyponatremic levels (serum sodium = 130 meq/liter) or to normonatremic levels (serum sodium = 150 meq/liter) on the brain histology of rats. In group I, 13% of the rats revealed brain lesions following correction to mildly hyponatremic levels by the administration of 855 mM NaCl. All the rats (100%) in group II had brain lesions following correction to normonatremic levels by 24 h of water restriction. Similarly, all the rats in group III showed brain lesions following correction to normonatremic levels by the administration of 855 mM NaCl. Severe hyponatremia by itself did not cause any brain lesions in another group. We conclude that rapid correction of severe hyponatremia to mildly hyponatremic levels by the administration of 855 mM NaCl does not cause significant brain lesions. On the other hand, rapid correction to normonatremic levels either by water restriction or by the administration of 855 mM NaCl results in significant brain lesions.

Cardiovascular responses to insulin in the absence of hypoglycemia

1962 ◽  
Vol 202 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Santiago A. Pereda ◽  
John W. Eckstein ◽  
François M. Abboud
Keyword(s):  
Pressor Response ◽  
Direct Action ◽  
Cardiovascular Responses ◽  
Blocking Agent ◽  
Neuromuscular Blocking ◽  
Right Atrial ◽  
Systemic Vein ◽  
Anesthetized Dogs ◽  
Adrenergic Blocking ◽  
The Brain

Cardiovascular responses to intravenous administration of insulin were studied in lightly anesthetized dogs treated with a neuromuscular blocking agent. An early transient pressor response was observed. This abrupt increase in arterial pressure appeared 2–9 min after insulin was given. It was accompanied by increases in cardiac output and right atrial pressure. It occurred in the presence of hyperglycemia and in the absence of hypoglycemia. It was not altered by glucagon but it could be antagonized by ganglionic and adrenergic blocking drugs and by pentobarbital. The response could be produced when insulin was given in the carotid artery in doses that caused no effect when injected in a systemic vein. The experiments suggest that insulin may have a direct action on the brain.

scholarly journals Is mercury injected into the body for therapeutic purposes released into the spinal fluid?

1912 ◽  
Vol XIX (4) ◽  
pp. 803-813
Author(s):  
V. Lazarev
Keyword(s):  
Tuberculous Meningitis ◽  
Nervous Tissue ◽  
Direct Action ◽  
The Body ◽  
Spinal Fluid ◽  
Bile Pigment ◽  
Vascular Plexus ◽  
Points Of View ◽  
The Brain ◽  
Theoretical Side

Is mercury injected into the body excreted into the spinal fluid? This question occupied us with practical and theoretical points of view. On the practical side, we were interested in knowing how much we can count on the circulation of mercury in the spinal fluid and, therefore, on its direct action on the nervous tissue due to the communication of the perivascular (and pericellular) spaces with the sub-arachnoid. If mercury is released into the spinal fluid, it is necessary to search for the therapeutic effect (syphilis of the nervous system) of the drug that quickly and in large quantities passes into the spinal fluid. On the theoretical side, the issue of mercury release is of interest for solving the broader issue of the nature of spinal fluid in general. As is known, there is currently no agreement on this account. Is the spinal fluid transudate, the secretion of the vascular plexus epithelium or the sui generis lymph of the brain itself. In favor of the second1 views are inclined by Schultze, Imamura, Raubitschek, Molt, and others in favor of the last but Spina2 (also Lewandovsky and Blumenthal3. The first view is generally accepted. We thought that the saturation of blood with mercury, which happens with prolonged introduction of it into the body, should lead to the appearance of at least traces of it in the spinal fluid, if the latter is transudate. If the last secret, then apriori nothing can be predicted; extraction depends on the chemical and physical properties of the epithelium itself; the epithelium can secerne one substance and not pass another. The number of substances found so far in the spinal fluid when injected into the body is very limited. When the brain (and membranes) was normal, the substances introduced by the authors did not completely enter the spinal fluid. Widal, Monod4, Sicard was found in tuberculous meningitis iod when giving it during 2-3 days for 3-5 grams only in 3 cases. Guinon and Simon found only 1/2 cases of tuberculous meningitis; no iodine was found in cases of cerebrospinal meningitis. With uremia, Costaigne found iod and methylene blue. Sicard and Widal didnt find it. Gilbert and Castaigne found bile pigment in jaundice. Sicard denies. Archard Loeper5 did not find the lithium when it was injected into the blood. Regarding the fate of mercury introduced into the organism, there are no indications in the literature6.

scholarly journals Acute Toxicity of Leaf Extracts of Enydra fluctuans Lour in Zebrafish (Danio rerio Hamilton)

Scientifica ◽  
2020 ◽  
Vol 2020 ◽  
pp. 1-6 ◽  
Author(s):  
Jobi Xavier ◽  
Kshetrimayum Kripasana
Keyword(s):  
Acute Toxicity ◽  
Basal Membrane ◽  
Brain Parenchyma ◽  
Herbaceous Plant ◽  
Histopathological Changes ◽  
Oral Toxicity ◽  
Leaf Extracts ◽  
Toxicity Studies ◽  
The Brain ◽  
Oral Acute Toxicity

The present study was focused on the concentration-dependent changes in oral acute toxicity of leaf extracts of E. fluctuans in zebrafish. The study was also aimed at the details of histopathological changes in the gill, liver, brain, and intestine of zebrafish exposed to the leaf extracts of the plant E. fluctuans. Enydra fluctuans Lour is an edible semiaquatic herbaceous plant used widely for the alleviation of the different diseases. Since there were no toxicity studies conducted on this plant, the present study was an attempt to look into the elements of toxicity of the plants. Two types of experiments are conducted in the present study. First, the acute oral toxicity study was conducted as per the OECD guidelines 203. Second, histopathological changes were observed in the fishes exposed to the lethal concentrations of plant extract. The oral acute toxicity studies conducted on Zebrafish have revealed that the leave extracts of E. fluctuans were toxic to the tested fish at the concentration of 200 mg/kg body weight. The histopathological studies conducted on the intestine of treated fishes showed that treatment has induced rupturing of the villi structure and fusion of villi the membrane and detachment of the villi structure from the basal membrane of the intestine. The histology of the liver also showed severe vacuolization in the cells while it is not affected in control. The studies on gills showed the detachment of the basal epithelial membrane in the gills compared to control which might have led to death of the fish. The histopathological observations of brain tissues treated with test samples also revealed the marked impingement in the brain parenchyma while the control is normal without impingement of the brain.

Relevance of Otopathological Findings in the Treatment of Dizzy Patients

1984 ◽  
Vol 93 (4_suppl) ◽  
pp. 12-16 ◽  
Author(s):  
Pierre B. Montandon ◽  
Rudolf Häusler
Keyword(s):  
Retrospective Study ◽  
Endolymphatic Hydrops ◽  
Vestibular Neuritis ◽  
Common Symptom ◽  
Vestibular Disorders ◽  
Histopathological Changes ◽  
The Brain

Dizziness is a common symptom in disorders of the brain and the ear. In a retrospective study of 1,000 cases, dizziness is attributed to a peripheral disorder in 25%, to a CNS disorder in 46%, and to undetermined causes in 29% of the cases. Peripheral disorders can be defined in terms of histopathological changes; the most frequent is cupulolithiasis, followed by endolymphatic hydrops and vestibular neuritis. These vestibular disorders are reviewed and discussed in connection with accepted facts and current hypotheses.

The role of amylin in the control of energy homeostasis

2010 ◽  
Vol 298 (6) ◽  
pp. R1475-R1484 ◽  
Author(s):  
Thomas A. Lutz
Keyword(s):  
Energy Homeostasis ◽  
Area Postrema ◽  
Body Weight Gain ◽  
Direct Action ◽  
Central Administration ◽  
Experimental Conditions ◽  
Hypothalamic Area ◽  
Chronic Infusion ◽  
The Brain

Amylin is an important player in the control of nutrient fluxes. Amylin reduces eating via a meal size effect by promoting meal-ending satiation. This effect seems to depend on a direct action in the area postrema (AP), which is an area rich in amylin receptors. Subsequent to the activation of AP neurons, the neural signal is conveyed to the forebrain via relays involving the nucleus of the solitary tract (NTS) and the lateral parabrachial nucleus (lPBN) to the lateral hypothalamic area (LHA) and other hypothalamic nuclei. While the NTS and lPBN seem to be necessary for amylin's eating inhibitory effect, the role of the LHA has not yet been fully investigated. Amylin may also act as an adiposity signal. Plasma levels of amylin are higher in obese individuals, and chronic infusion of amylin into the brain reduces body weight gain and adiposity; chronic infusion of an amylin receptor antagonist into the brain increases body adiposity. Amylin increases energy expenditure in rats; this effect occurs under various experimental conditions after peripheral and central administration. Together, these animal data, but also clinical data in humans, indicate that amylin is a promising candidate for the treatment of obesity; effects are most pronounced when amylin is combined with leptin. Finally, recent findings indicate that amylin acts as a neurotrophic factor in specific brain stem areas. Whether this effect may be relevant under physiological conditions requires further studies.

scholarly journals Prion propagation in mice lacking central nervous system NF-κB signalling

2008 ◽  
Vol 89 (6) ◽  
pp. 1545-1550 ◽  
Author(s):  
C. Julius ◽  
M. Heikenwalder ◽  
P. Schwarz ◽  
A. Marcel ◽  
M. Karin ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Responses ◽  
Published Data ◽  
Histopathological Changes ◽  
Prion Infection ◽  
Prion Propagation ◽  
Proliferation Regulation ◽  
The Impact ◽  
The Brain

Prions induce highly typical histopathological changes including cell death, spongiosis and activation of glia, yet the molecular pathways leading to neurodegeneration remain elusive. Following prion infection, enhanced nuclear factor-κB (NF-κB) activity in the brain parallels the first pathological changes. The NF-κB pathway is essential for proliferation, regulation of apoptosis and immune responses involving induction of inflammation. The IκB kinase (IKK) signalosome is crucial for NF-κB signalling, consisting of the catalytic IKKα/IKKβ subunits and the regulatory IKKγ subunit. This study investigated the impact of NF-κB signalling on prion disease in mouse models with a central nervous system (CNS)-restricted elimination of IKKβ or IKKγ in nearly all neuroectodermal cells, including neurons, astrocytes and oligodendrocytes, and in mice containing a non-phosphorylatable IKKα subunit (IKKα AA/AA). In contrast to previously published data, the observed results showed no evidence supporting the hypothesis that impaired NF-κB signalling in the CNS impacts on prion pathogenesis.

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