scholarly journals ULTRASTRUCTURAL IDENTIFICATION OF CATECHOLAMINE-CONTAINING CENTRAL SYNAPTIC TERMINALS

1973 ◽  
Vol 21 (4) ◽  
pp. 333-348 ◽  
Author(s):  
FLOYD E. BLOOM
Keyword(s):  
Nervous System ◽  
Nerve Terminals ◽  
Synaptic Terminals ◽  
Direct Localization ◽  
Sympathetic Nervous ◽  
Neurotransmitter Substances ◽  
6 Hydroxydopamine ◽  
The Brain ◽  
Selective Accumulation ◽  
Peripheral Sympathetic Nervous System

Cytochemical methods for the localization of central catecholamine-containing synaptic terminals have been developed from an extensive foundation of biochemical work and from extrapolation of results on the peripheral sympathetic nervous system. Direct localization of catecholamines in central nerve terminals in some parts of the brain can now be obtained by fixation with permanganates. More broadly applicable, but less direct localizing methods depend upon selective accumulation of tritiated catecholamines for autoradiography or the accumulation of reactive catecholamine congeners which act as markers with conventional fixation. The pattern of acute degenerative changes which result after treatment with 6-hydroxydopamine can also be used to provide an indirect localization of the terminals which had stored catecholamines. When the results of each of the methods are combined, the present techniques indicate that catecholamine-containing terminals in the brain can be identified more confidently than any other system of neurotransmitter substances. Nevertheless, there is considerable need for future cytochemical innovation.

Attenuation of Haemodynamic Response to Placement of Mayfield Skull Pin Head Holder - Comparison of Dexmedetomidine Versus Propofol Infusion - A Randomized Interventional Trial Done in a Tertiary Centre in Central Kerala

2021 ◽  
Vol 8 (29) ◽  
pp. 2639-2643
Author(s):  
Sruthy Unni ◽  
Ranju Sebastian ◽  
Elizabeth Joseph ◽  
Remani Kelan Kamalakshi ◽  
Jamsheena Muthira Parambath
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Stress Response ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurosurgical Procedures ◽  
Sympathetic Nervous ◽  
The Brain ◽  
Group 1

BACKGROUND Anaesthesia for neurosurgery requires special considerations. The brain is enclosed in a rigid cranium, so the rise in intracranial pressure (ICP) which impairs cerebral perfusion pressure (CPP), results in irrepairable damage to various vital areas in the brain. Stable head position is required in long neurosurgical procedures. This is obtained with the use of clamps which fix the head rigidly. This is done usually under general anaesthesia because it produces intense painful stimuli leading to stimulation of sympathetic nervous system which in turn causes release of vasoconstrictive agents. This can impair perfusion in all organ systems. The increase in blood pressure due to sympathetic nervous system causes increase in blood flow. This causes increases in intracranial pressure which result in reduction in cerebral perfusion pressure once the auto regulatory limits are exceeded. We compared the effects of dexmedetomidine 1 µgm/kg and propofol 100 µgm/kg given as infusion over a period of 10 minutes before the induction of anaesthesia and continued till 5 minutes after pinning to attenuate the stress response while cranial pinning. In this study, we wanted to compare the effects of dexmedetomidine and propofol as infusion to attenuate the stress response while cranial pinning in patients undergoing neurosurgical procedures. METHODS This is a randomized interventional trial. Patients were divided into 2 groups of 20 each. Group 1 receiving dexmedetomidine and group 2 receiving propofol, both drugs given as infusion. Haemodynamic variables were monitored before and after cranial pinning. Data was analysed using IBM statistical package for social sciences (SPSS) statistics. The parameters recorded were analysed with the help of a statistician. RESULTS The two groups were comparable in demographic data. Incidence of tachycardia between group 1 and 2 showed that tachycardia to pinning was better controlled with propofol than dexmedetomidine (P < 0.05) which is statistically significant. There is no statistically significant difference in blood pressure values between group 1 and 2 after pinning. CONCLUSIONS From our study, we came to a conclusion that propofol was superior to dexmedetomidine in attenuating the heart rate response to cranial pinning. The effect of propofol and dexmedetomidine was comparable in attenuating the blood pressure response to cranial pinning. KEYWORDS Cranial Pinning, Dexmedetomidine, Propofol

Central and peripheral mechanisms of arterial pressure lability following baroreceptor denervation

1987 ◽  
Vol 65 (8) ◽  
pp. 1615-1618 ◽  
Author(s):  
R. H. Alper ◽  
H. J. Jacob ◽  
M. J. Brody
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Humoral Factors ◽  
Neural Transmission ◽  
Sympathetic Transmission ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine ◽  
Alpha Adrenergic Agonist ◽  
Arterial Pressure Lability

Deafferentation of sinoaortic baroreceptors produces a marked increase in the lability of arterial pressure that is sustained chronically. Studies reviewed in this paper were designed to determine the mechanisms responsible for generating arterial pressure lability. Pharmacological interruption of the humoral vasopressin and angiotensin systems failed to alter arterial pressure lability. In contrast, blockade of sympathetic nervous system transmission at both ganglionic and alpha-adrenergic receptor levels significantly attenuated lability. A similar effect was observed with the peripheral neurotoxin, 6-hydroxydopamine. After blockade of sympathetic transmission, a further reduction in lability was produced by blocking the renin–angiotensin or vasopressin systems. The dissociation of the level of arterial pressure from lability was achieved with parachloroamphetamine which raised arterial pressure but reduced lability. A substantial peripheral contribution to lability was obtained in experiments in which the alpha-adrenergic agonist, phenylephrine, produced a marked increase in lability in both normal and baroreceptor-denervated animals in which humoral and neural transmission were blocked. These data demonstrate that following baroreceptor deafferentation, arterial pressure lability is produced primarily by the sympathetic nervous system and secondarily by circulating humoral factors that appear to act on vascular smooth muscle to induce fluctuations in the level of arterial pressure.

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