"Pulsatile Vs Non-Pulsatile Intracranial Blood Flow: Animal Model of Blood Flow Restoration in Brain Tamponade"

Intracoronary thrombus resulting in acute myocardial ischemia can be lysed by thrombolytic agents, such as, streptokinase or t-PA. We examined the potential of a recombitant tissue-plasminogen activator (rt-PA)and a fibrin (ogen)-degradation productpentapeptide 6A, Ala-Arg-Pro-Ala-Lys, corresponding to aminoacids 43-47 in the BB-chain of fibrinogen, which causes marked increase in coronary blood flow and stimulates prostacyclin release, in restoring coronary blood flow in dqgs with experimentally-induced thrombus. An occlusive thrombus was created in the circumflex (Cx) coronary artery in 8 dcgs by electricalstimulation of the endothelial surface. The electrically-induced Cx thrombus consisted primarily of platelets and fibrin. After the occlusive thrcmbus was stable without electrical currant, rt-PA (10ug/kg/minute for 30 minutes intravenously)or peptide 6A (5 unoles/minute for 20 minutes intracorcnary) were randomly administered. Infusion of t-PA restored coronar blood flow (peak 22 ±12 ml/minute, mean ±SD) in five of seven animlas. The time to flow restoration was 12.3 ± 9.1 minutes and the reflow persistedfor20.0 ± 10.9 minutes. Peptide 6A administration also restored coronary blood flow (peak 20 ± 4 ml/ minute) in seven of eight animals with occlusive coronary thrombus. Mean time to blood flow restoration (4.3 ±2.9 minutes) wasshorter(P>0.05) than with rt-PA, but thereflow persisted only for the duration of tine infusion (16.3 ± 10.2 minutes).Peptide 6A adninistration was associatedwith a significant (P±0.05) increase in plasma 6-keto-PGF1α indicating stimulation of prostacyclin release. In addition, plasma t-PA concentrations also increased (F>0.01) at the peak effect of peptide 6A indicating releaseof endogenous t-PA as another potentialmechanism of the thrombolytic effects of peptide 6A. This study demonstrates that peptide 6A exerts coronary thrombolytic effectsccmpa rable to those of t-PA in a canine model of coronary thrombosis.

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A Conscious Animal Model for Studies of Coronary Collateral Blood Flow Dynamics

Coronary Circulation ◽

10.1007/978-4-431-68087-1_21 ◽

1990 ◽

pp. 267-278 ◽

Cited By ~ 2

Author(s):

Dean Franklin ◽

Atsushi Mikuniya ◽

Masatoshi Fujita ◽

Masaaki Takahashi ◽

Michael McKown ◽

...

Keyword(s):

Animal Model ◽

Blood Flow ◽

Flow Dynamics ◽

Collateral Blood Flow ◽

Coronary Collateral ◽

Conscious Animal ◽

Blood Flow Dynamics ◽

Coronary Collateral Blood Flow

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Measurement of Blood Flow Before and After Embolization with Use of Fluorescent Microspheres in an Animal Model

Journal of Vascular and Interventional Radiology ◽

10.1097/01.rvi.0000195398.70290.be ◽

2006 ◽

Vol 17 (1) ◽

pp. 103-111 ◽

Cited By ~ 6

Author(s):

Tirath Y. Patel ◽

David M. Hovsepian ◽

James R. Duncan

Keyword(s):

Animal Model ◽

Blood Flow ◽

Fluorescent Microspheres ◽

Before And After

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An animal model for the analysis of cochlear blood flow disturbance and hearing threshold in vivo

European Archives of Oto-Rhino-Laryngology ◽

10.1007/s00405-009-1095-4 ◽

2009 ◽

Vol 267 (2) ◽

pp. 205-205

Author(s):

Martin Canis ◽

Warangkana Arpornchayanon ◽

Catalina Messmer ◽

Markus Suckfuell ◽

Bernhard Olzowy ◽

...

Keyword(s):

Animal Model ◽

Blood Flow ◽

Hearing Threshold ◽

Flow Disturbance ◽

Cochlear Blood Flow

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Effect of Low-Frequency Therapeutic Ultrasound on Induction of Nitric Oxide in CKD: Potential to Prevent Acute Kidney Injury

Kidney Diseases ◽

10.1159/000509819 ◽

2020 ◽

Vol 6 (6) ◽

pp. 453-460

Author(s):

Michael W. Dae ◽

Kathleen D. Liu ◽

Richard J. Solomon ◽

Dong W. Gao ◽

Carol A. Stillson

Keyword(s):

Nitric Oxide ◽

Acute Kidney Injury ◽

Animal Model ◽

Blood Flow ◽

Radionuclide Imaging ◽

Therapeutic Ultrasound ◽

Low Frequency ◽

Kidney Injury ◽

Large Animal Model ◽

Large Animal

Introduction: Post-contrast acute kidney injury (PC-AKI) develops in a significant proportion of patients with CKD after invasive cardiology procedures and is strongly associated with adverse outcomes. Objective: We sought to determine whether increased intrarenal nitric oxide (NO) would prevent PC-AKI. Methods: To create a large animal model of CKD, we infused 250 micron particles into the renal arteries in 56 ± 8 kg pigs. We used a low-frequency therapeutic ultrasound device (LOTUS – 29 kHz, 0.4 W/cm2) to induce NO release. NO and laser Doppler probes were used to assess changes in NO content and blood flow. Glomerular filtration rate (GFR) was measured by technetium-diethylene-triamine-pentaacetic acid (Tc-99m-DTPA) radionuclide imaging. PC-AKI was induced by intravenous infusion of 7 cm3/kg diatrizoate. In patients with CKD, we measured GFR at baseline and during LOTUS using Tc-99m--DTPA radionuclide imaging. Results: In the pig model, CKD developed over 4 weeks (serum creatinine [Cr], mg/dL, 1.0 ± 0.2–2.6 ± 0.9, p < 0.01, n = 12). NO and renal blood flow (RBF) increased in cortex and medulla during LOTUS. GFR increased 75 ± 24% (p = 0.016, n = 3). PC-AKI developed following diatrizoate i.v. infusion (Cr 2.6 ± 0.7 baseline to 3.4 ± 0.6 at 24 h, p < 0.01, n = 3). LOTUS (starting 15 min prior to contrast and lasting for 90 min) prevented PC-AKI in the same animals 1 week later (Cr 2.5 ± 0.4 baseline to 2.6 ± 0.7 at 24 h, p = ns, n = 3). In patients with CKD (n = 10), there was an overall 25% increase in GFR in response to LOTUS (p < 0.01). Conclusions: LOTUS increased intrarenal NO, RBF, and GFR and prevented PC-AKI in a large animal model of CKD, and significantly increased GFR in patients with CKD. This novel approach may provide a noninvasive nonpharmacological means to prevent PC-AKI in high-risk patients.

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