Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 1 to 10 of 11

Publication Record

Connections

Intraarterial administration of norcantharidin attenuates ischemic stroke damage in rodents when given at the time of reperfusion: novel uses of endovascular capabilities.
Khan IS, Odom M, Ehtesham M, Colvin D, Quarles CC, McLaughlin B, Singer RJ
(2016) J Neurosurg 125: 152-9
MeSH Terms: Animals, Brain Ischemia, Bridged Bicyclo Compounds, Heterocyclic, Disease Models, Animal, Injections, Intra-Arterial, Male, Matrix Metalloproteinase 9, Matrix Metalloproteinase Inhibitors, Rats, Stroke
Show Abstract · Added April 25, 2016
OBJECT Matrix metalloprotease-9 (MMP-9) plays a critical role in infarct progression, blood-brain barrier (BBB) disruption, and vasogenic edema. While systemic administration of MMP-9 inhibitors has shown neuroprotective promise in ischemic stroke, there has been little effort to incorporate these drugs into endovascular modalities. By modifying the rodent middle cerebral artery occlusion (MCAO) model to allow local intraarterial delivery of drugs, one has the ability to mimic endovascular delivery of therapeutics. Using this model, the authors sought to maximize the protective potential of MMP-9 inhibition by intraarterial administration of an MMP-9 inhibitor, norcantharidin (NCTD). METHODS Spontaneously hypertensive rats were subjected to 90-minute MCAO followed immediately by local intraarterial administration of NCTD. The rats' neurobehavioral performances were scored according to the ladder rung walking test results and the Garcia neurological test for as long as 7 days after stroke. MRI was also conducted 24 hours after the stroke to assess infarct volume and BBB disruption. At the end of the experimental protocol, rat brains were used for active MMP-9 immunohistochemical analysis to assess the degree of MMP-9 inhibition. RESULTS NCTD-treated rats showed significantly better neurobehavioral scores for all days tested. MR images also depicted significantly decreased infarct volumes and BBB disruption 24 hours after stroke. Inhibition of MMP-9 expression in the ischemic region was depicted on immunohistochemical analysis, wherein treated rats showed decreased active MMP-9 staining compared with controls. CONCLUSIONS Intraarterial NCTD significantly improved outcome when administered at the time of reperfusion in a spontaneously hypertensive rat stroke model. This study suggests that supplementing endovascular revascularization with local neuroprotective drug therapy may be a viable therapeutic strategy.
1 Communities
1 Members
0 Resources
10 MeSH Terms
Quality improvement guidelines for transhepatic arterial chemoembolization, embolization, and chemotherapeutic infusion for hepatic malignancy.
Brown DB, Nikolic B, Covey AM, Nutting CW, Saad WE, Salem R, Sofocleous CT, Sze DY, Society of Interventional Radiology Standards of Practice Committee
(2012) J Vasc Interv Radiol 23: 287-94
MeSH Terms: Antineoplastic Agents, Chemoembolization, Therapeutic, Embolization, Therapeutic, Evidence-Based Medicine, Hepatic Artery, Humans, Infusions, Intra-Arterial, Injections, Intra-Arterial, Liver Neoplasms, Patient Selection, Quality Improvement, Risk Assessment
Added March 5, 2014
0 Communities
1 Members
0 Resources
12 MeSH Terms
Outcomes of neoadjuvant transarterial chemoembolization to downstage hepatocellular carcinoma before liver transplantation.
Chapman WC, Majella Doyle MB, Stuart JE, Vachharajani N, Crippin JS, Anderson CD, Lowell JA, Shenoy S, Darcy MD, Brown DB
(2008) Ann Surg 248: 617-25
MeSH Terms: Adult, Antineoplastic Agents, Carcinoma, Hepatocellular, Chemoembolization, Therapeutic, Dose-Response Relationship, Drug, Follow-Up Studies, Humans, Injections, Intra-Arterial, Liver Neoplasms, Liver Transplantation, Neoadjuvant Therapy, Neoplasm Staging, Preoperative Care, Retrospective Studies, Treatment Outcome
Show Abstract · Added March 5, 2014
PURPOSE - To evaluate outcomes of downstaging patients with advanced (American liver tumor study group stage III/IV) hepatocellular carcinoma (HCC) with transarterial chemoembolization (TACE) to allow eligibility for orthotopic liver transplant (OLT).
METHODS - From 1999 to 2006, 202 patients with HCC were referred for transplant evaluation. Seventy-six (37.6%) patients with stage III/IV HCC were potential transplant candidates if downstaging was achieved by TACE. OLT was considered based on follow-up imaging findings. The number of patients who were successfully downstaged within the Milan criteria, tumor response using Response Evaluation Criteria in Solid Tumors criteria, findings at explant, and outcomes after transplant were tracked.
RESULTS - Eighteen of 76 (23.7%) patients had adequate downstaging to qualify for OLT under the Milan criteria. By Response Evaluation Criteria in Solid Tumors, 27/76 (35.5%) patients had a partial response, 22/76 (29%) had stable disease, and 27/76 (35.5%) had progressive disease. Seventeen of 76 (22.4%) patients who met other qualifications underwent OLT after successful downstaging (13/38 stage III;4/38 stage IV). Explant review demonstrated 28 identifiable tumors in which post-TACE necrosis was greater than 90% in 21 (75%). At a median of 19.6 months (range 3.6-104.7), 16/17 (94.1%) patients who underwent OLT are alive. One patient expired 11 months after OLT secondary to medical comorbidities. One of 17 (6%) OLT patients had recurrent HCC. This patient underwent resection of a pulmonary metastasis and is alive, 63.6 months from OLT.
CONCLUSION - Selected patients with stage III/IV HCC can be downstaged to Milan criteria with TACE. Importantly, patients who are successfully downstaged and transplanted have excellent midterm disease-free and overall survival, similar to stage II HCC.
0 Communities
1 Members
0 Resources
15 MeSH Terms
Bradykinin type 2 receptor BE1 genotype influences bradykinin-dependent vasodilation during angiotensin-converting enzyme inhibition.
Van Guilder GP, Pretorius M, Luther JM, Byrd JB, Hill K, Gainer JV, Brown NJ
(2008) Hypertension 51: 454-9
MeSH Terms: Adult, Angiotensin-Converting Enzyme Inhibitors, Blood Pressure, Bradykinin, Drug Synergism, Enalaprilat, Endothelium, Vascular, Female, Forearm, Genotype, Humans, Injections, Intra-Arterial, Male, Methacholine Chloride, Nitroprusside, Polymorphism, Genetic, Receptor, Bradykinin B2, Regional Blood Flow, Sex Factors, Tissue Plasminogen Activator, Vascular Resistance, Vasodilation, Vasodilator Agents
Show Abstract · Added December 10, 2013
To test the hypothesis that the bradykinin receptor 2 (BDKRB2) BE1+9/-9 polymorphism affects vascular responses to bradykinin, we measured the effect of intra-arterial bradykinin on forearm blood flow and tissue-type plasminogen activator (t-PA) release in 89 normotensive, nonsmoking, white American subjects in whom degradation of bradykinin was blocked by enalaprilat. BE1 genotype frequencies were +9/+9:+9/-9:-9/-9=19:42:28. BE1 genotype was associated with systolic blood pressure (121.4+/-2.8, 113.8+/-1.8, and 110.6+/-1.8 mm Hg in +9/+9, +9/-9, and -9/-9 groups, respectively; P=0.007). In the absence of enalaprilat, bradykinin-stimulated forearm blood flow, forearm vascular resistance, and net t-PA release were similar among genotype groups. Enalaprilat increased basal forearm blood flow (P=0.002) and decreased basal forearm vascular resistance (P=0.01) without affecting blood pressure. Enalaprilat enhanced the effect of bradykinin on forearm blood flow, forearm vascular resistance, and t-PA release (all P<0.001). During enalaprilat, forearm blood flow was significantly lower and forearm vascular resistance was higher in response to bradykinin in the +9/+9 compared with +9/-9 and -9/-9 genotype groups (P=0.04 for both). t-PA release tended to be decreased in response to bradykinin in the +9/+9 group (P=0.08). When analyzed separately by gender, BE1 genotype was associated with bradykinin-stimulated t-PA release in angiotensin-converting enzyme inhibitor-treated men but not women (P=0.02 and P=0.77, respectively), after controlling for body mass index. There was no effect of BE1 genotype on responses to the bradykinin type 2 receptor-independent vasodilator methacholine during enalaprilat. In conclusion, the BDKRB2 BE1 polymorphism influences bradykinin type 2 receptor-mediated vasodilation during angiotensin-converting enzyme inhibition.
0 Communities
2 Members
0 Resources
23 MeSH Terms
Gastrointestinal complications associated with hepatic arterial Yttrium-90 microsphere therapy.
Murthy R, Brown DB, Salem R, Meranze SG, Coldwell DM, Krishnan S, Nunez R, Habbu A, Liu D, Ross W, Cohen AM, Censullo M
(2007) J Vasc Interv Radiol 18: 553-61; quiz 562
MeSH Terms: Adenocarcinoma, Adult, Aged, Brachytherapy, Embolization, Therapeutic, Gastrointestinal Tract, Hepatic Artery, Humans, Injections, Intra-Arterial, Liver Neoplasms, Male, Microspheres, Peptic Ulcer, Peptic Ulcer Hemorrhage, Radionuclide Imaging, Radiopharmaceuticals, Retrospective Studies, Technetium Tc 99m Aggregated Albumin, Yttrium Radioisotopes
Show Abstract · Added March 5, 2014
Hepatic arterial therapy with yttrium-90 microspheres exploits the avenue provided by the neoplastic microvasculature to deliver high-energy, low-penetrating therapeutic doses of radiation. Variant hepatic arterial anatomy, collateral vessels, and changes in flow dynamics during treatment can affect particle dispersion and lead to nontarget particle distribution and subsequent gastrointestinal morbidity. Awareness of these variances and techniques to prevent gastrointestinal tract microsphere delivery is essential in mitigating this serious complication. Our aim is to increase the understanding of the role of various imaging and preventative techniques in minimizing this undesired effect.
0 Communities
1 Members
0 Resources
19 MeSH Terms
Adenosine, a metabolic trigger of the exercise pressor reflex in humans.
Costa F, Diedrich A, Johnson B, Sulur P, Farley G, Biaggioni I
(2001) Hypertension 37: 917-22
MeSH Terms: Adenosine, Adult, Afferent Pathways, Axillary Artery, Brachial Artery, Exercise, Forearm, Hand Strength, Humans, Injections, Intra-Arterial, Injections, Intravenous, Microdialysis, Muscle, Skeletal, Peroneal Nerve, Sympathetic Nervous System
Show Abstract · Added December 10, 2013
There is substantial evidence that adenosine activates muscle afferent nerve fibers leading to sympathetic stimulation, but the issue remains controversial. To further test this hypothesis, we used local injections of adenosine into the brachial artery while monitoring systemic muscle sympathetic nerve activity (MSNA) with peroneal microneurography. The increase in MSNA induced by 3 mg intrabrachial adenosine (106+/-32%) was abolished if forearm afferent traffic was interrupted by axillary ganglionic blockade (21+/-19%, n=5, P:<0.05). Furthermore, the increase in MSNA induced by intravenous adenosine was 3.7-fold lower and later (onset latency 20.9+/-4.8 seconds versus 8.5+/-1 seconds) than intrabrachial adenosine. Finally, we used forearm exercise (dynamic handgrip at 50% and 15% maximal voluntary contraction, MVC), with or without superimposed ischemia, to modulate interstitial levels of adenosine (estimated with microdialysis) while monitoring MSNA. Fifteen minutes of intense (50% MVC) and moderate (15% MVC) exercise increased adenosine dialysate concentrations from 0.31+/-0.1 to 1.24+/-0.4 micromol/L (528+/-292%) and from 0.1+/-0.02 to 0.419+/-0.16 micromol/L (303+/-99%), respectively (n=7, P:<0.01). MSNA increased 88+/-25% and 38+/-28%, respectively. Five minutes of moderate exercise increased adenosine from 0.095+/-0.02 to 0.25+/-0.12 micromol/L, and from 0.095+/-0.02 to 0.48+/-0.19 micromol/L when ischemia was superimposed on exercise (n=7, P:=0.01). The percent increase in MSNA induced by the various interventions correlated with the percent increase in dialysate adenosine levels (r=0.96). We conclude that adenosine activates muscle afferent nerves, triggering reflex sympathetic activation.
0 Communities
1 Members
0 Resources
15 MeSH Terms
Norepinephrine release in the human forearm: effects of epinephrine.
Stein CM, Nelson R, He HB, Wood M, Wood AJ
(1997) Hypertension 30: 1078-84
MeSH Terms: Adult, Blood Vessels, Brachial Artery, Epinephrine, Forearm, Humans, Hypertension, Injections, Intra-Arterial, Male, Norepinephrine, Reference Values, Time Factors
Show Abstract · Added December 10, 2013
It has been postulated that delayed facilitation of norepinephrine release by epinephrine is causally related to the development of hypertension. It has been proposed that a brief increase in epinephrine concentrations results in the uptake of epinephrine into the sympathetic nerve terminal. Subsequent rerelease of epinephrine stimulates presynaptic beta-adrenergic receptors, resulting in a prolonged increase in plasma norepinephrine (NE) concentrations, with amplified sympathetic responses and vasoconstriction. To determine whether such epinephrine-induced, delayed facilitation of NE release occurs in a vascular bed draining resistance vessels and, if it occurs, whether that facilitation differs in hypertension, we used a radioisotope dilution method to measure unstimulated and isoproterenol-stimulated forearm NE spillover before, during, and after a 50 ng/min infusion of epinephrine for 30 minutes directly into the brachial artery. No delayed facilitatory effects of epinephrine on forearm NE spillover were observed in either 6 normotensive (NT) or 8 borderline hypertensive (BHT) subjects (NT unstimulated forearm NE spillover preepinephrine 1.79+/-0.41 ng/min versus postepinephrine 2.36+/-0.65 ng/min, P=.38; BHT preepinephrine 2.24+/-0.70 ng/min versus postepinephrine 1.93+/-0.46 ng/min, P=.51; NT isoproterenol-stimulated forearm NE spillover preepinephrine 4.61+/-1.01 ng/min versus postepinephrine 4.4+/-0.98 ng/min, P=.9; BHT preepinephrine 4.04+/-1.36 ng/min versus postepinephrine 4.69+/-1.49 ng/min P=.5). We conclude that the short-term local infusion of epinephrine does not have a delayed facilitatory effect on forearm NE spillover in NT or BHT subjects. Therefore, the prolonged increase in NE concentrations after epinephrine infusion previously shown systemically, and not seen locally in the forearm, suggests that the delayed facilitatory response to epinephrine may occur in other organs.
0 Communities
1 Members
0 Resources
12 MeSH Terms
Adenosine activates afferent fibers in the forearm, producing sympathetic stimulation in humans.
Costa F, Biaggioni I
(1993) J Pharmacol Exp Ther 267: 1369-74
MeSH Terms: Adenosine, Adult, Dose-Response Relationship, Drug, Exercise, Forearm, Humans, Injections, Intra-Arterial, Injections, Intravenous, Ischemia, Male, Middle Aged, Neurons, Afferent, Regional Blood Flow, Stimulation, Chemical
Show Abstract · Added December 10, 2013
Whereas adenosine is generally considered an inhibitory neuromodulator, there is evidence that adenosine may excite a variety of afferent fibers thereby evoking sympathetic activation. To determine whether adenosine also excites afferent fibers located in the forearm, adenosine was administered into the left branchial artery at doses without systemic effects while sympathetic nerve activity was monitored through a recording electrode placed in the right peroneal nerve in the lower limb. The i.a. adenosine produced a dose-dependent increase in forearm blood flow (647 +/- 209% above base line at a dose of 1.5 mg i.a.) and in muscle sympathetic nerve activity (97 +/- 30% above base line). No significant effect was observed on heart rate or systemic blood pressure. The effects of i.a. adenosine were not caused by spill over into the systemic circulation because these doses had no effect when given i.v. The increase in sympathetic nerve activity was not secondary to the local vasodilatory effects of adenosine because nitroprusside, given i.a. at doses that evoked the same degree of vasodilation, had no effect on muscle sympathetic nerve activity. The authors interpreted these results as indicative of activation of forearm afferent fibers by adenosine. The precise nature of these afferent fibers cannot be determined from these studies and may include sensory afferents and chemosensitive afferents involved in the exercise pressor reflex. By contrast with the known neuroinhibitory actions of adenosine in the central nervous system and in efferent nerves, these observations are in agreement with the concept that adenosine-induced activation of sympathetic afferent fibers is a widespread phenomenon.
0 Communities
1 Members
0 Resources
14 MeSH Terms
Hemodynamic effects of adenosine in conscious hypertensive and normotensive rats.
Ohnishi A, Biaggioni I, Deray G, Branch RA, Jackson EK
(1986) Hypertension 8: 391-8
MeSH Terms: Adenosine, Animals, Blood Pressure, Heart Rate, Hemodynamics, Hypertension, Injections, Intra-Arterial, Injections, Intravenous, Male, Nerve Block, Norepinephrine, Rats, Rats, Inbred SHR, Rats, Inbred WKY
Show Abstract · Added December 10, 2013
Mean arterial pressure and heart rate were measured during intra-aortic arch (i.a.a.), intravenous, and suprarenal artery (s.r.a.) infusions of adenosine in conscious, unrestrained normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) in the absence and presence of ganglionic blockade. In both groups, i.a.a. and i.v. infusions of adenosine induced comparatively larger dose-dependent reductions in mean arterial pressure than did s.r.a. infusions. In WKY, i.a.a. and i.v. infusions of adenosine were equipotent in reducing mean arterial pressure. In contrast, i.a.a. infusion of adenosine was approximately twice as potent as i.v. infusion in SHR. Also, SHR were approximately 6.5 and 2.6 times more sensitive to i.a.a. and i.v. infusions of adenosine, respectively, than were WKY. Further, i.a.a. and s.r.a. infusions of adenosine caused tachycardia in WKY, while i.v. infusions did not alter heart rate. In SHR, neither i.a.a. nor s.r.a. infusion of adenosine altered heart rate, but i.v. infusion induced a profound bradycardia. In ganglionic-blocked WKY that received a norepinephrine infusion to restore blood pressure and heart rate to pre-ganglionic blockade levels, depressor responses to i.a.a. infusion of adenosine were unchanged while the increase in heart rate was abolished. In SHR, ganglionic blockade markedly decreased the depressor response to i.a.a. and i.v. infusions of adenosine and abolished the bradycardic response to i.v. infusion. These results suggest that adenosine is an effective hypotensive agent in both WKY and SHR; however, marked between-strain differences exist in the cardiovascular response to adenosine. These differences most likely are due to changes in adenosine-pulmonary interactions and increases in the importance of adenosine-autonomic interactions in SHR.
0 Communities
1 Members
0 Resources
14 MeSH Terms
In vivo measurements of ethanol concentration in rabbit brain by 1H magnetic resonance spectroscopy.
Petroff OA, Novotny EJ, Ogino T, Avison M, Prichard JW
(1990) J Neurochem 54: 1188-95
MeSH Terms: Animals, Brain, Catheterization, Ethanol, Hydrogen, Injections, Intra-Arterial, Kinetics, Magnetic Resonance Spectroscopy, Models, Neurological, Osmolar Concentration, Rabbits, Stomach
Show Abstract · Added February 12, 2015
In vivo 1H magnetic resonance spectroscopy was used to measure the cerebral ethanol concentration in the rabbit after both intraarterial and intragastric administration. There was good agreement between cerebral and blood ethanol concentrations at all times after administration by either route. Cerebral ethanol levels, measured using in vivo 1H spectroscopy, agreed well with those measured in perchloric acid extracts of brain, analyzed by both high-resolution 1H spectroscopy and gas chromatography. Ethanol may be useful as an indicator to measure cerebral blood flow by 1H spectroscopy and chemical shift-selective magnetic resonance imaging.
0 Communities
1 Members
0 Resources
12 MeSH Terms