Trigeminal Control of Cranio-Facial Vasomotor Response: I. Histamine Test in Patients with Unilateral Gasserian Ganglion Lesions

Cephalalgia ◽  
1984 ◽  
Vol 4 (4) ◽  
pp. 243-251 ◽  
Author(s):  
Milena De Marinis ◽  
Nicola Martucci ◽  
Franco Maria Gagliardi ◽  
Massimo Feliciani ◽  
Alessandro Agnoli
Keyword(s):  
Intravenous Injection ◽  
Cerebral Arteries ◽  
Trigeminal System ◽  
Gasserian Ganglion ◽  
Vasomotor Response ◽  
Unilateral Headache ◽  
Sensory Pathway

It has been hypothesized that the trigeminal system may control vasomotor changes and pain in vascular headaches. In this study, headache was induced by an intravenous injection of histamine in 37 patients with trigeminal rhizotomy and in 12 controls. The vasomotor response to histamine was studied with facial telethermography. The headache in patients with trigeminal lesions differed, in a prevalence of unilateral localization contralaterally to the operated side (21 patients), from that in controls. No relationship was found between the hypoesthesia caused by the operation and the prevalence of unilateral headache. A statistically significant correlation ( p < 0.001) was found between unilateral absence of headache and decreased vasomotor response on the operated side. These reactions occurred more in patients who underwent thermocoagulation than in patients who underwent retro-gasserian rhizotomy. Thus the gasserian ganglion seems to control the cranio-facial vasomotor response and the headache through a vascular pathway, acting on cerebral arteries, which differs from the sensory pathway.

scholarly journals KIR channels tune electrical communication in cerebral arteries

2016 ◽  
Vol 37 (6) ◽  
pp. 2171-2184 ◽  
Author(s):  
Maria Sancho ◽  
Nina C Samson ◽  
Bjorn O Hald ◽  
Ahmed M Hashad ◽  
Sean P Marrelli ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Pcr Analysis ◽  
Vasomotor Response ◽  
Rightward Shift ◽  
Voltage Dependent

The conducted vasomotor response reflects electrical communication in the arterial wall and the distance signals spread is regulated by three factors including resident ion channels. This study defined the role of inward-rectifying K+ channels (KIR) in governing electrical communication along hamster cerebral arteries. Focal KCl application induced a vasoconstriction that conducted robustly, indicative of electrical communication among cells. Inhibiting dominant K+ conductances had no attenuating effect, the exception being Ba2+ blockade of KIR. Electrophysiology and Q-PCR analysis of smooth muscle cells revealed a Ba2+-sensitive KIR current comprised of KIR2.1/2.2 subunits. This current was surprisingly small and when incorporated into a model, failed to account for the observed changes in conduction. We theorized a second population of KIR channels exist and consistent with this idea, a robust Ba2+-sensitive KIR2.1/2.2 current was observed in endothelial cells. When both KIR currents were incorporated into, and then inhibited in our model, conduction decay was substantive, aligning with experiments. Enhanced decay was ascribed to the rightward shift in membrane potential and the increased feedback arising from voltage-dependent-K+ channels. In summary, this study shows that two KIR populations work collaboratively to govern electrical communication and the spread of vasomotor responses along cerebral arteries.

Gene expression in human cerebral arteries

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S520-S520
Author(s):  
Petter Vikman ◽  
Lars Edvinsson
Keyword(s):  
Gene Expression ◽  
Cerebral Arteries

Loss of distensibility in cerebral arteries with chronic hypertension and vasospasm after subarachnoid hemorrhage

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S557-S557
Author(s):  
Takeshi Kondoh ◽  
Seiji Nakajima ◽  
Akitsugu Morishita ◽  
Haruo Yamashita ◽  
Eiji Kohmura ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Chronic Hypertension

Multiple infarctions in a woman with carcinomatous meningitis infiltrating basal cerebral arteries

2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
E Leinisch ◽  
F Schlachetzki ◽  
C Müller ◽  
U Bogdahn ◽  
W Jakob ◽  
...  
Keyword(s):  
Cerebral Arteries ◽  
Carcinomatous Meningitis

The Local Sanarelli-Shwartzman Phenomenon in Rats Induced by Human Leukaemic Cells

1973 ◽  
Vol 29 (02) ◽  
pp. 353-362
Author(s):  
J Lisiewicz ◽  
A Pituch ◽  
J. A Litwin
Keyword(s):  
Chronic Lymphocytic Leukaemia ◽  
Intravenous Injection ◽  
Peripheral Blood ◽  
Lymphocytic Leukaemia ◽  
Acute Myeloblastic Leukaemia ◽  
Demarcation Line ◽  
E Coli ◽  
Leukaemic Cells ◽  
Shwartzman Phenomenon

SummaryThe local Sanarelli-Shwartzman phenomenon (SSP-L) in the skin of 30 rats was induced by an intr a cutaneous sensitizing injection of leukaemic leucocytes isolated from the peripheral blood of patients with chronic lymphocytic leukaemia (CLL), acute myeloblastic leukaemia (AL) and chronic granulocytic leukaemia (CGL) and challenged by an intravenous injection of 100(μ of E. coli endotoxin. SSP-L was observed in 7 rats after injection of CLL lymphocytes and in 6 and 2 rats after AL myeloblasts and the CGL granulocytes, respectively. The lesions in the skin after AL myeloblasts appeared in a shorter time and were of longer duration compared with those observed after CLL lymphocytes and CGL granulocytes. Histologically, the lesions consisted of areas of destruction in the superficial layers of the skin ; the demarcation line showed the presence of neutrophils, macrophages and erythrocytes. Haemorrhages and fibrin deposits near the demarcation line were larger after injection of CLL lymphocytes and AL myeloblasts than after CGL granulocytes. The possible role of leucocyte procoagulative substances in the differences observed have been discussed.

Ultrastructural Changes of the Tissue Thromboplastin after Intravenous Injection in Rabbits

1978 ◽  
Vol 39 (01) ◽  
pp. 201-209 ◽  
Author(s):  
Hiroshi Hasegawa ◽  
Hiroshi Nagata ◽  
Makoto Murao
Keyword(s):  
Intravenous Injection ◽  
Vascular Endothelium ◽  
Model Experiment ◽  
Venous Return ◽  
Ultrastructural Changes ◽  
Membrane Structures ◽  
Tissue Thromboplastin ◽  
Short Time ◽  
Sheet Membrane

SummaryAttempts were made to demonstrate ultrastructural changes of the tissue thromboplastin after intravenous injection, as a model experiment on the pulmonary microthrombi formation induced by the tissue thromboplastin circulating from venous return.Concentrically arranged membrane structures of the injected thromboplastin disappeared in extremely short time after the injection of the thromboplastin in rabbits. The long sheet membrane of the injected thromboplastin was frequently seen as adhered to the vascular endothelium or to the surface of blood corpuscles. Furthermore, fibrin fibres were formed in contact with the long sheet membrane of the thromboplastin. Membrane structures were not found anywhere in the control rabbits.

Turnover of Human Extrinsic (Tissue-Type) Plasminogen Activator in Rabbits

1981 ◽  
Vol 46 (03) ◽  
pp. 658-661 ◽  
Author(s):  
C Korninger ◽  
J M Stassen ◽  
D Collen
Keyword(s):  
Plasminogen Activator ◽  
Intravenous Injection ◽  
Active Site ◽  
Half Life ◽  
Degradation Products ◽  
Gel Filtration ◽  
Tissue Type ◽  
Organ Distribution ◽  
Small Rise

SummaryThe turnover of highly purified human extrinsic plasminogen activator (EPA) (one- and two-chain form) was studied in rabbits. Following intravenous injection, EPA-activity declined rapidly. The disappearance rate of EPA from the plasma could adequately be described by a single exponential term with a t ½ of approximately 2 min for both the one-chain and two-chain forms of EPA.The clearance and organ distribution of EPA was studied by using 125I-labeled preparations. Following intravenous injection of 125I-1abeled EPA the radioactivity disappeared rapidly from the plasma also with a t ½ of approximately 2 min down to a level of 15 to 20 percent, followed by a small rise of blood radioactivity. Gel filtration of serial samples revealed that the secondary increase of the radioactivity was due to the reappearance of radioactive breakdown products in the blood. Measurement of the organ distribution of 125I at different time intervals revealed that EPA was rapidly accumulated in the liver, followed by a release of degradation products in the blood.Experimental hepatectomy markedly prolonged the half-life of EPA in the blood. Blocking the active site histidine of EPA had no effect on the half-life of EPA in blood nor on the gel filtration patterns of 125I in serial plasma samples.It is concluded that human EPA is rapidly removed from the blood of rabbits by clearance and degradation in the liver. Recognition by the liver does not require a functional active site in the enzyme. Neutralization in plasma by protease inhibitors does not represent a significant pathway of EPA inactivation in vivo.

Inhibition of Fibrinoid Deposition by Heparin

1961 ◽  
Vol 06 (01) ◽  
pp. 157-159 ◽  
Author(s):  
Saul B. Gilson
Keyword(s):  
Intravenous Injection ◽  
Gamma Globulin ◽  
Physiological Significance

ConclusionExperimental glomerulitis in rabbits following intravenous injection of gamma globulin was inhibited by heparinization. The physiological and patho-physiological significance of this observation is considered.

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