The Site of Cardiovascular Action of Angiotensin II in the Brain

1970 ◽  
Vol 39 (2) ◽  
pp. 327-336 ◽  
Author(s):  
M. D. Joy ◽  
R. D. Lowe
Keyword(s):  
Spinal Cord ◽  
Vertebral Artery ◽  
Basilar Artery ◽  
Cardiovascular Response ◽  
Cervical Cord ◽  
Central Effects ◽  
Small Arteries ◽  
Site Of Action ◽  
Cervical Segment ◽  
The Brain

1. The site of action of vertebral artery infusions of angiotensin was studied in the chloralose-anaesthetized greyhound. 2. The cardiovascular response to vertebral artery infusion of angiotensin (0·25–2·0 ng kg−1 min−1) was not reduced by clamping the basilar artery between the pons and the pyramidal decussation. There was no response to infusion of angiotensin through a catheter inserted in a rostral direction into the basilar artery above the clamp. The site of action must therefore lie caudal to the pons. 3. Transection of the spinal cord at the first cervical segment did not abolish the response to vertebral artery infusions, which was still mediated by the vagus nerve and abolished by subsequent vagotomy. The site of action must therefore lie rostral to the cervical cord. 4. Local infusions of angiotensin into the small arteries supplying the medulla produced a response similar to that obtained with vertebral artery infusion of angiotensin. 5. These results indicate that the site responsible for these central effects of angiotensin lies in the medulla.

Toxicology of ryegrass endophyte in livestock

1999 ◽  
Vol 7 ◽  
pp. 63-67
Author(s):  
S.C. Munday-Finch ◽  
I. Garthwaite
Keyword(s):  
Spinal Cord ◽  
Farm Animals ◽  
Response Analysis ◽  
Toxic Metabolites ◽  
Site Of Action ◽  
Specific Receptors ◽  
Lolitrem B ◽  
Dose Dependent ◽  
Brain And Spinal Cord ◽  
The Brain

The ryegrass endophyte/plant interaction produces a number of toxic metabolites responsible for a range of toxicoses including ryegrass staggers. Although lolitrem B has long been considered the toxin responsible for ryegrass staggers in farm animals, it is only recently that we have demonstrated that oral administration of the pure toxin causes tremors in mice consistent with the symptoms of ryegrass staggers. Various levels of the toxin were incorporated into the diet of mice and tremor response measured regularly. Mice were very susceptible to the tremorgenic action of lolitrem B with a dose of only 1.1 mg/kg per day being sufficient to induce a tremor response. Analysis of faeces from a dosed mouse showed that approximately 40% of the toxin ingested was excreted unchanged. The profile of tremor response shows that tremors build up over a 24-hour period and then reach a dose dependent plateau suggesting that toxin turnover reaches a steady state. In experiments designed to test the possibility that tremorgens bind to specific receptors in the brain, mice were injected with the 14C-labelled tremorgen, paxilline. Paxilline was chosen as it is similar in structure and possible action to lolitrem B and could be more easily prepared with an isotopic label. Following injection of 14C-paxilline to mice their brains and spinal cord were sectioned and analysed for 14C content. Localised binding was not detected but rather an even distribution of isotope was observed. This is probably due to the lipophilicity of the tremorgens, which distribute randomly throughout the fatty brain matrix, masking any binding to specific regions or receptors. This study showed, however, that only a minute proportion of the administered tremorgen reached the brain and spinal cord, indicating that, if this is the site of action, the receptors involved in the initiation of staggers are extremely sensitive to the tremorgens. Keywords: endophyte, lolitrem, Lolium perenne, mycotoxin, Neotyphodium lolii, neurotoxin, oral dosing, ryegrass staggers, tremor, tremorgen

Cardiovascular response to experimental spinal cord compression

1973 ◽  
Vol 38 (3) ◽  
pp. 326-331 ◽  
Author(s):  
Eduardo E. Eidelberg
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Compression ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Blocking Agent ◽  
Cord Compression ◽  
Left Ventricular ◽  
Cervical Cord ◽  
Content Type ◽  
Ectopic Beats

✓ Anesthetized, and unanesthetized decerebrate, cats were used to study the arterial pressor response to spinal cord compression. To produce a cervical compression it was necessary that the cervical cord be functionally connected to the thoracic cord, pressor response by the reverse was not true. A pressor response above 200 mm Hg systolic was associated with electrocardiographic (EKG) signs of left ventricular overload and ventricular ectopic beats. These changes were not prevented by atropine, hexamethonium, or propanolol. Both the pressor response and the EKG abnormalities were prevented by an alpha-adrenergic blocking agent. The authors conclude that alpha-adrenergically mediated arterial vasoconstriction is the effector mechanism in the pressor response to increased intracranial pressure or cord compression.

scholarly journals Differential Diagnostics of Vertebrogenic and Nonvertebrogenic Vascular Pathologies

Biomeditsina ◽  
2020 ◽  
pp. 47-59
Author(s):  
N. N. Karkischenko ◽  
A. A. Nikolaev ◽  
Yu. A. Chudina ◽  
D. B. Chaivanov ◽  
A. A. Vartanov
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Cervical Spine ◽  
Autonomic Nervous System ◽  
Vertebral Artery ◽  
Cardiovascular System ◽  
Blood Vessels ◽  
Vascular Diseases ◽  
Differential Diagnostics ◽  
The Brain

This article investigates consistency in the work of the heart and blood vessels in vascular diseases of a vertebrogenic and non-vertebrogenic nature, which are characterized by disorders of the cardiovascular system leading to an insuffi cient blood supply to the spinal cord and the brain. Vertebrogenic vascular pathologies were studied by the example of vertebral artery disorders in osteochondrosis of the cervical spine, while non-vertebrogenic pathologies were considered in the syndrome of somatoform dysfunction of the autonomic nervous system. It is shown that, compared to the norm, the degree of consistence in the work of the heart and blood vessels is lower in vertebrogenic and non-vertebrogenic vascular pathologies.

scholarly journals Multiple Sclerosis in the Emirati Population: Onset Disease Characterization by MR Imaging

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Manzoor Ahmed ◽  
Ruqqiya Mir ◽  
Mustafa Shakra ◽  
Safana Al Fardan
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Age Of Onset ◽  
Female Dominance ◽  
Cervical Cord ◽  
Gulf Region ◽  
Lesion Load ◽  
Disseminated Disease ◽  
Brain And Spinal Cord ◽  
The Brain

Background and Objectives. Multiple Sclerosis (MS) epidemiology is on the path of globalization mainly due to changing environmental factors. The prevalence of MS is on the rise in the Middle East and Persian Gulf region. Our observations has led us to hypothesize a heavy MRI lesion load at the onset of disease in a relatively younger native population. We aimed to estimate and characterize the onset disease on MRI using McDonald’s criteria while applying its terms of “Dissemination in Space (DIS) and Dissemination in Time (DIT)”. Materials and Methods. Retrospective review of onset MRI studies of 181 Emirati (native) individuals. Basic demographics were captured. Only 47 patients with Clinically Definite MS (CDMS) were included who had onset diagnostic MRI available. Lesion load was quantified using the specific zones of involvement designated for DIS: (1) Periventricular (PVZ) (I), (2) Juxta-cortical (II) (3) Infra-tentorial (III) and, (4) Spinal cord (IV). PVZ was sub-classified and lesions were quantified. A single enhancing lesion was required for DIT. Results. Average age of onset was about 26 years with female dominance of about 2 : 1. About 50% had all 4 zones and about 85% had at least 3 zones involved at the onset. Involvement of only 1 zone was rare. Dissemination in time (DIT) in brain and/or cord was present in approximately 50%. Each of the 4 zones were involved in at least 70% of cases. PVZ was not spared in any case with at least 3 lesions present in approx. 95% and ≥12 lesions in approx. half of the patients. Spinal cord specifically cervical cord was involved in up to 80% with typical patchy lesions. Conclusion. Onset disease characterization using MRI in a young Emirati cohort showed a heavy lesion load in the brain and spinal cord at the onset, signifying cumulative disease before presentation. Disseminated disease also facilitated early diagnosis of MS. The findings have significant potential ramifications for local environmental and cultural factors, as well as disease course and disability progression.

Spinal Cord Ischemia due to Vertebral Artery Dissection

2005 ◽  
Vol 18 (3) ◽  
pp. 390-394
Author(s):  
M. Bergui ◽  
G. Ventilii ◽  
F.M. Ferrio ◽  
D.R. Daniele ◽  
G.B. Bradač
Keyword(s):  
Spinal Cord ◽  
Differential Diagnosis ◽  
Vertebral Artery ◽  
Grey Matter ◽  
Spinal Cord Ischemia ◽  
Vertebral Artery Dissection ◽  
Cervical Cord ◽  
Artery Dissection ◽  
Spinal Cord Infarction ◽  
Central Regions

We reviewed clinical and neuroradiological findings in 37 consecutive patients with cervical cord infarction due to vertebral artery dissection diagnosed at our institution from 1996 to 2004. Four patients had clinical and neuroradiological findings consistent with spinal cord ischemia. Three patients had “pencil-like” infarction at C3-C5 level; one patient had an infarction of the anterior horns of the spinal grey matter at C3-C4 level. Symptoms were crural sensory deficit with mild tetraparesis and proximal strength deficit of the arms, respectively. Spinal cord infarction complicated vertebral artery dissection in about 10% of patients of our series. Infarctions involved the most central regions of the spinal cord, with relative sparing of the peripheral white matter tracts. Clinical and MRI pictures were almost typical, and consistent with a hemodynamic mechanism for the lesions. Vertebral artery dissection must be considered in the differential diagnosis in patients with cervical cord infarction.

Abstract 1122‐000032: Spinal Cord Infarction a Young Patient with a Hypoplastic Vertebral Artery

2021 ◽  
Vol 1 (S1) ◽  
Author(s):  
Ammar Jum'ah ◽  
Hassan Aboul Nour ◽  
Daniel Miller
Keyword(s):  
Risk Factors ◽  
Spinal Cord ◽  
Vertebral Artery ◽  
Cervical Spinal Cord ◽  
Vertebral Artery Dissection ◽  
Vascular Risk Factors ◽  
Cervical Cord ◽  
Artery Dissection ◽  
Spinal Cord Infarction ◽  
Vascular Risk

Introduction : Rare presentation of disease processes is absolutely intriguing to the human mind. Spinal cord infarction is abundantly reported to be secondary to cardiological procedures, patients carrying multiple vascular risk factors and vertebral artery dissections. But for it to happen in a patient who is young, relatively healthy and without vascular risk factors is quite interesting. Herein, we present the case of a patient presented with bilateral upper extremity weakness, who has a hypoplastic right vertebral artery that has coincided with him being a professional gamer with exerting compression from video‐gaming posturing of “forward leaning with neck hyperextension”, resulting in cervical spinal cord infarction. Methods : Case report Results : Vertebral artery dissection was excluded by CTA and MRA. our hypothesis was that the patient is a professional gamer and his posture of leaning forward and neck hyper‐extension had a role in inducing his spinal cord infarction given the fact of him having a hypoplastic right vertebral artery. Conclusions : Vertebral artery disease is a well‐recognized cause of ischemia in the posterior cerebral circulation. Recently, however, cervical cord infarction, albeit being extremely rare, has been increasingly reported as a complication of vertebral artery diseases such as dissection. Awareness must be raised that such condition can also happen in the young population due to compression of the vertebral arteries, especially when one is hypoplastic.

scholarly journals Cervical Spinal Cord Infarction Presenting as Chest Pain in Patients with Acute Cerebellar Infarction

2020 ◽  
Vol 38 (1) ◽  
pp. 42-45
Author(s):  
Yong-Won Kim ◽  
Yang-Ha Hwang
Keyword(s):  
Spinal Cord ◽  
Chest Pain ◽  
Vertebral Artery ◽  
Cervical Spinal Cord ◽  
Artery Occlusion ◽  
Cervical Cord ◽  
Spinal Cord Infarction ◽  
Cerebellar Infarction ◽  
Posterior Spinal Artery ◽  
Lumbar Level

Spinal cord infarction is rare, especially cervical cord infarction is lesser than thoracic and lumbar level. We describe two cases of cervical cord infarction following cerebellar infarction with vertebral artery occlusion, which initially presented with chest pain and dyspnea. Blood supply for the cervical cord comes from anterior and posterior spinal artery, which originated from the distal vertebral or posterior inferior cerebellar arteries. Therefore, occlusion of unilateral vertebral artery could cause a cervical cord infarction.

scholarly journals Pathological report on the histology of sleeping sickness and trypanosomiasis, with a comparison of the changes found in animals infected with T. Gambiense and other Trypanosomata

1906 ◽  
Vol 77 (516) ◽  
pp. 233-236 ◽  
Keyword(s):  
Spinal Cord ◽  
Plasma Cells ◽  
Sleeping Sickness ◽  
Glia Cells ◽  
Cervical Segment ◽  
The Central Nervous System ◽  
Thoracic Part ◽  
Pathological Report ◽  
Brain And Spinal Cord ◽  
The Brain

Three cases of Sleeping Sickness and one case of Trypanosomiasis dying in Liverpool have been histologically examined. The central nervous system of the sleeping sickness cases showed the changes described by different observers, Mott, Low, the Portuguese Commission and others. One case exhibited an intra-pial hæmorrhage of the spinal cord, extending from the sixth cervical segment to the third thoracic segment, about 7 mm. board. In another case there Occurred four larger hæmorrhages, besides numerous smaller ones, in the grey substance, chiefly affecting the posterior cornua and the thoracic part of the cord. Microscopically the brain and spinal cord showed small celled infiltration around the vessels, consisting for the most part of lymphocytes, Some plasma cells and phagocytes, between which were a Varying number of red cells in different stages of disintegration. The intima of the vessels showed a proliferation of the endothelial cells. Red and white blood corpuscles were often seen in the vessels walls. Here and there the blood vessels were filled with White blood corpuscles resembling a thrombosis. It is most striking that the small celled infiltration is much more marked in the grey substance of the nervous centres, especially in the large grey ganglia, than in the peripheral parts. Very numerous capillary hæmorrhages of different sizes were present in these situations. Infilteration around the vessels of the membranes and in the tissues of the pia and arachnoidea was observed. Around the infiltrated vessels degeneration of the fibres and an excess of glia cells were seen, sometimes exhibiting the picture of red softening. The ganglia cells showed an irregularly distributed degeneration, central and Peripheral chromatolysis and also partial pyknosis.

Central Nerve System Impairment, AMA Guides, Sixth Edition: An Overview

2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Neurological Impairment ◽  
Sixth Edition ◽  
Central Nerve System ◽  
The Central Nervous System ◽  
The One ◽  
Nerve System ◽  
The Brain

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.

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