Method for measuring brain tissue pressure

1975 ◽  
Vol 43 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Robert M. Clark ◽  
Norman F. Capra ◽  
James H. Halsey
Keyword(s):  
Blood Pressure ◽  
Brain Tissue ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Tissue Pressure ◽  
Content Type ◽  
Pressure Changes ◽  
Local Brain

✓ 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.

Methylprednisolone on circulating eicosanoids and vasomotor tone after endotoxin

1986 ◽  
Vol 61 (1) ◽  
pp. 185-191 ◽  
Author(s):  
C. A. Hales ◽  
R. D. Brandstetter ◽  
C. F. Neely ◽  
M. B. Peterson ◽  
D. Kong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Physiological Effect ◽  
High Dose ◽  
Systemic Blood ◽  
Eicosanoid Production ◽  
Circulating Levels

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.

PS 02-65 ASSOCIATION BETWEEN POSTPRANDIAL AND SLEEPING SYSTEMIC BLOOD PRESSURE CHANGES IN THE NON-DIABETIC ELDERLY

2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e121
Author(s):  
Fernando Garcia ◽  
Beatriz Fidale ◽  
Sebastião Ferreira-Filho
Keyword(s):  
Blood Pressure ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Pressure Changes

The histopathology of experimental spinal cord trauma

1978 ◽  
Vol 48 (6) ◽  
pp. 1002-1007 ◽  
Author(s):  
Stephen E. Rawe ◽  
William A. Lee ◽  
Phanor L. Perot
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Systemic Blood Pressure ◽  
Post Injury ◽  
Systemic Blood ◽  
Edema Formation ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Thoracic Spinal ◽  
Marked Enhancement

✓ The early sequential histopathological alterations following a concussive paraplegic injury to the posterior thoracic spinal cord in cats were studied. The lack of significant progression of hemorrhages over a 4-hour period after injury indicates that most hemorrhages probably occur within the first hour. The marked enhancement or retardation of hemorrhages in the post-injury period, when the blood pressure was increased or decreased, respectively, demonstrates the loss of autoregulation of spinal cord vasculature at the trauma site after a concussive paraplegic injury. Progressive edema formation was evident over a 4-hour period following injury, and it could be enhanced or retarded by elevation or reduction of the systemic blood pressure.

Abstract 066: The Undescribed Protein Caskin2 Is a Novel Regulator of eNOS Phosphorylation and Systemic Blood Pressure

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Sarah B Mueller ◽  
Susan B Gurley ◽  
Christopher D Kontos
Keyword(s):  
Blood Pressure ◽  
Molecular Mechanisms ◽  
Systemic Blood Pressure ◽  
Regulatory Subunit ◽  
Systemic Blood ◽  
Homologous Expression ◽  
Ongoing Work ◽  
Inducing Factors

Disruptions in the function of the quiescent endothelial cells (ECs) that line mature vessels can both result in and contribute to the progression of numerous cardiovascular diseases including hypertension, atherosclerosis, and disorders of vascular permeability. Despite recent attention, the signaling pathways that are active in quiescent ECs remain poorly characterized relative to those that regulate EC activation. In an effort to provide mechanistic insight into these pathways, we have characterized the previously undescribed protein Caskin2, which we hypothesize is a novel regulator of EC quiescence. Caskin2 is expressed in ECs throughout the vasculature, including the aorta, coronary arteries, and renal glomeruli. In vitro, Caskin2 promotes a quiescent EC phenotype characterized by decreased proliferation and increased resistance to apoptosis-inducing factors. Caskin2 knockout mice are viable and fertile. However, preliminary radiotelemetry measurements indicate that Caskin2 knockout (KO) mice have mildly elevated systemic blood pressure (BP). Compared to wild type (WT) littermates (n=8), Caskin2 KO mice (n=7) had increased mean arterial pressure (119+/-1 vs. 113+/-1, p=0.012), systolic BP (138+/-2 vs. 132+/-2, p=0.023), and diastolic BP (99+/-1 vs. 93+/-1, p=0.014) at baseline. To explore the molecular mechanisms of Caskin2’s effects, we used mass spectrometry to identify interacting proteins. Among the 67 proteins identified were the Ser/Thr phosphatase protein phosphatase 1 (PP1) and eNOS. Using standard in vitro biochemical techniques, we demonstrated that Caskin2 acts as a PP1 regulatory subunit. Interestingly, homologous expression of Caskin2 in vitro resulted in a marked increase in phosphorylation of eNOS on S1177, which is known to promote eNOS activity, and a decrease in phosphorylation on T495, which is associated with eNOS inhibition. Finally, PP1 has been shown to dephosphorylate eNOS T495 in vitro, suggesting a molecular mechanism for our in vivo findings. Ongoing work aims to determine if the interaction of Caskin2 and PP1 is required for the Caskin2-induced increase in activating phosphorylation of eNOS and to characterize the physiological mechanisms responsible for Caskin2’s effects on BP in more detail.

Neural mechanism underlying basilar arterial constriction by intracisternal L-NNA in anesthetized dogs

1993 ◽  
Vol 265 (1) ◽  
pp. H103-H107 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
T. Okamura
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cerebral Arteries ◽  
Neural Mechanism ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Anesthetized Dogs ◽  
Arterial Constriction ◽  
Synthase Inhibitor

Basilar arterial diameters were angiographically measured in anesthetized dogs in which systemic blood pressure and heart rate were also monitored. Injections of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, into the cisterna magna produced a significant, persistent decrease in arterial diameter, the effect being reversed by intracisternal injections of L-arginine. The vasoconstrictor effect of L-NNA was diminished in dogs treated with hexamethonium. On the other hand, treatment with phentolamine in a dose sufficient to lower blood pressure to a level similar to that attained with hexamethonium did not inhibit, but rather potentiated, the effect of intracisternal L-NNA. Nicotine injected into the vertebral artery significantly dilated the basilar artery. The effect was abolished by treatment with L-NNA applied intracisternally, the inhibition being reversed by the addition of L-arginine. Systemic blood pressure and heart rate were not altered by intracisternally applied L-NNA and L-arginine. These findings support the hypothesis that basilar arterial constriction caused by intracisternal L-NNA is associated with a suppression of NO synthesis in nitroxidergic nerves innervating the cerebroarterial wall rather than an elimination of basal release of NO from the endothelium. Functional importance of nitroxidergic vasodilator innervation in cerebral arteries in vivo is thus clarified.

Long-term prognosis in surgically treated intracranial aneurysms

1981 ◽  
Vol 54 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Lydia Artiola i Fortuny ◽  
Luis Prieto-Valiente
Keyword(s):  
Outcome Measure ◽  
Systemic Blood Pressure ◽  
Neurological Status ◽  
Long Term Results ◽  
Control Group ◽  
Aneurysm Surgery ◽  
Systemic Blood ◽  
Content Type ◽  
Long Term Prognosis

✓ An evaluation of long-term results following aneurysm surgery is presented. Five different outcome measures are used in a population of 204 survivors followed for a minimum of 18 months and a maximum of 5½ years. The findings show that 1) results vary depending on the outcome measure used, and 2) outcome can be predicted with a considerable degree of accuracy using preoperative and early postoperative variables. The most important predictive factors were postoperative vasospasm, age, systemic blood pressure on admission, and preoperative neurological status. The results are compared with a control group.

scholarly journals HIGH SYSTEMIC BLOOD PRESSURE IN PRETERM INFANTS WITH BRONCHOPULMONARY DYSPLASIA AND LONG-TERM OUTCOMES

2018 ◽  
Vol 23 (suppl_1) ◽  
pp. e20-e20
Author(s):  
Florence Cayouette ◽  
Sarah Spénard ◽  
Anie Lapointe ◽  
Véronique Dorval ◽  
Julie Sommer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Preterm Infants ◽  
Bronchopulmonary Dysplasia ◽  
Neurodevelopmental Outcome ◽  
Systemic Blood Pressure ◽  
Control Group ◽  
Neurodevelopmental Outcomes ◽  
Systemic Blood ◽  
Neurodevelopmental Impairment

Abstract BACKGROUND Bronchopulmonary dysplasia (BPD) is a known risk factor for neurodevelopmental impairment in preterm infants. BPD is also associated with an increased incidence of high systemic blood pressure (HBP). However, it is not known if a diagnosis of HBP in BPD patients relates to later neurodevelopmental outcomes. OBJECTIVES We aimed to determine the incidence of neonatal HBP diagnosis in a cohort of preterm infants born <29 weeks of gestational age (GA) with BPD. The secondary objective was to assess if a concomitant diagnosis of BPD and HBP influences neurodevelopmental outcomes at 18 months. DESIGN/METHODS We performed a single center retrospective study using data from medical charts. All infants born <29 weeks GA admitted to our level-IV neonatal intensive care unit between January 2010 and December 2012 diagnosed with BPD at 36 weeks of corrected GA were included. Patients transferred before 36 weeks of corrected GA, that died before 18 months or had congenital anomalies were excluded. Patients were classified in the HBP group if HBP was a documented diagnosis in the chart. The control group was the remaining patients with BPD at 36 weeks corrected GA but without HBP. Severe neurodevelopmental impairment at 18 months was defined as either any Bailey-III score <70, cerebral palsy or severe hearing or visual impairment. Descriptive statistics for prenatal and postnatal patients’ characteristics were analyzed. Logistic regression was performed for factors associated with long-term disability. Level of significance was determined as a p value <0.05. RESULTS During the study period, 337 preterm infants <29 weeks of GA were identified and after exclusions, 98 newborns met the criteria of BPD at 36 weeks corrected GA. Mean GA and mean birth weight were 26.7 ± 1.7 weeks and 882 ± 199 g respectively. The majority were males (57%) and received antenatal steroids (87.8%). We identified twenty-five newborns (25.5%) with a diagnosis of HBP. Demographic data was similar between the 2 groups. 56% of the HBP group received a post-natal course of steroids, compared to 36% for the control group (p 0.07). The neurodevelopmental outcome at 18 months was similar between the two groups (p 0.54) and was not influenced by the presence of a HBP diagnosis after regression analysis (p 0.8). CONCLUSION The diagnosis of HBP was frequent in our cohort of preterm infants born <29 weeks GA with BPD but did not seem to be related to long-term neurodevelopmental outcomes.

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