ICP and Systemic Blood Pressure Changes After Administration of Prostaglandin E1 in Acute Stage of SAH

1993 ◽  
pp. 638-640
Author(s):  
K. Kamiya ◽  
N. Yamashita ◽  
N. Sugiyama ◽  
M. Ohno ◽  
H. Nagai
2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e121
Author(s):  
Fernando Garcia ◽  
Beatriz Fidale ◽  
Sebastião Ferreira-Filho

1975 ◽  
Vol 43 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Robert M. Clark ◽  
Norman F. Capra ◽  
James H. Halsey

✓ The authors report a method for measuring total local brain tissue pressure (BTP) using a miniature catheter transducer stereotaxically introduced into the white matter of the cat's cerebrum. Quantitative rapid phasic pressure changes were satisfactorily demonstrated. Due to some drift of baseline of the transducers and inability to perform in vivo calibration, reliable long-term quantitative pressure measurements sometimes could not be studied. The BTP from each cerebral hemisphere and the cisternal pressure (CP) were monitored during alterations of pCO2 and systemic blood pressure, and distilled H2O injection prior to and after right middle cerebral artery (MCA) ligation. The catheter transducers functioned well on chronic implantation for up to 6 weeks. Compared to the chronically implanted catheters, acutely implanted catheters responded identically except for drift. The response of intracranial pressure and CP to MCA occlusion, alterations in pCO2, and systemic blood pressure were similar. No BTP gradients appeared in response to MCA ligation, hypercapnia, hypertension, or progressive swelling of the resulting infarction.


1998 ◽  
Vol 26 (1) ◽  
pp. 126-131 ◽  
Author(s):  
Yuichi Ishibe ◽  
Yasuhiro Shiokawa ◽  
Takashi Umeda ◽  
Hiroshi Uno ◽  
Masato Nakamura ◽  
...  

2018 ◽  
Vol 24 (3) ◽  
pp. 297-302 ◽  
Author(s):  
Denise Brunozzi ◽  
Sophia F Shakur ◽  
Fady T Charbel ◽  
Ali Alaraj

Objective Pipeline embolization devices (PED) are commonly used for endovascular treatment of cerebral aneurysms but changes in intracranial hemodynamics after PED deployment are poorly understood. Here, we assess middle cerebral artery (MCA) and systemic blood pressure before and after PED treatment. Methods Records of patients with cerebral aneurysms proximal to the internal carotid artery terminus treated with PED at our institution between 2015 and 2017 were retrospectively reviewed. Patients were included if ipsilateral MCA pressure measurements were available. Ipsilateral MCA pressure was transduced via the microcatheter before and after PED deployment. Systemic arterial blood pressure was also simultaneously recorded. MCA, systemic blood pressure, and ratios of MCA to systemic blood pressure values were compared before and after treatment among the study cohort using the two-sample paired Student t test. Results Fourteen patients were included. Mean age was 54 years. Among the entire cohort, the ratio of MCA to systemic systolic and mean blood pressure were significantly higher after treatment (respectively 0.76 vs. 0.69, p = 0.01, and 0.94 vs. 0.89, p = 0.03), and the ratio of MCA to systemic diastolic pressures showed an increasing trend (1.08 vs. 1.03, p = 0.09). The percentage of ratio increase was independent of aneurysm size ( r = –0.24, p = 0.42 for systolic ratio; r = –0.09, p = 0.74 for diastolic ratio; r = –0.09; p = 0.76 for mean ratio, respectively). Conclusions Following PED deployment, the ratio of ipsilateral MCA to systemic systolic and mean blood pressure increased. These pressure changes should be further evaluated in a larger sample size.


1986 ◽  
Vol 61 (1) ◽  
pp. 185-191 ◽  
Author(s):  
C. A. Hales ◽  
R. D. Brandstetter ◽  
C. F. Neely ◽  
M. B. Peterson ◽  
D. Kong ◽  
...  

Acute pulmonary and systemic vasomotor changes induced by endotoxin in dogs have been related, at least in part, to the production of eicosanoids such as the vasoconstrictor thromboxane and the vasodilator prostacyclin. Steroids in high doses, in vitro, inhibit activation of phospholipase A2 and prevent fatty acid release from cell membranes to enter the arachidonic acid cascade. We, therefore, administered methylprednisolone (40 mg/kg) to dogs to see if eicosanoid production and the ensuing vasomotor changes could be prevented after administration of 150 micrograms/kg of endotoxin. The stable metabolites of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay. Methylprednisolone by itself did not alter circulating eicosanoids but when given 2.5 h before endotoxin not only failed to inhibit endotoxin-induced eicosanoid production but actually resulted in higher circulating levels of 6-keto-PGF1 alpha (P less than 0.05) compared with animals receiving endotoxin alone. Indomethacin prevented the steroid-enhanced concentrations of 6-keto-PGF1 alpha after endotoxin and prevented the greater fall (P less than 0.05) in systemic blood pressure and systemic vascular resistance with steroid plus endotoxin than occurred with endotoxin alone. Administration of methylprednisolone immediately before endotoxin resulted in enhanced levels (P less than 0.05) of both TxB2 and 6-keto-PGF1 alpha but with a fall in systemic blood pressure and vascular resistance similar to the animals pretreated by 2.5 h. In contrast to the early steroid group in which all of the hypotensive effect was due to eicosanoids, in the latter group steroids had an additional nonspecific effect. Thus, in vivo, high-dose steroids did not prevent endotoxin-induced increases in eicosanoids but actually increased circulating levels of TxB2 and 6-keto-PGF1 alpha with a physiological effect favoring vasodilation.


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