Plasmin-induced endothelium-dependent vasodilatation versus fibrinolysis — Two pathways of blood flow restoration in the thrombotically occluded vessels?

1994 ◽  
Vol 8 ◽  
pp. 113-115 ◽  
Author(s):  
S.Y. Mashina ◽  
G.V. Bashkov
Keyword(s):  
Blood Flow ◽  
Flow Restoration

THROMBOLYSIS BY TISSUE-PLASMNOCEN ACTIVATOR AND A FIBRIN (OCEN) -DEGRADATION PRODUCT, PEPTIDE 6A, IN A CANINE MDDEL OF ELECTRICALLY-INDUCED CORONARY THROMBOSIS

1987 ◽  
Author(s):  
T Saldeen ◽  
J Mehta ◽  
W Nichols ◽  
D Lew
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Thrombosis ◽  
Canine Model ◽  
Peak Effect ◽  
Endothelial Surface ◽  
Tissue Plasminogen ◽  
Flow Restoration ◽  
Mean Time ◽  
Stimulation Of

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.

Role of Delayed Neuroglial Activation in Impaired Cerebral Blood Flow Restoration Following Comorbid Injury

2019 ◽  
Vol 40 (3) ◽  
pp. 369-380 ◽  
Author(s):  
Zareen Amtul ◽  
Jasmine Randhawa ◽  
Abdullah N. Najdat ◽  
David J. Hill ◽  
Edith J. Arany
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Restoration

Microvascular remodeling and accelerated hyperemia blood flow restoration in arterially occluded skeletal muscle exposed to ultrasonic microbubble destruction

2004 ◽  
Vol 287 (6) ◽  
pp. H2754-H2761 ◽  
Author(s):  
Ji Song ◽  
Patrick S. Cottler ◽  
Alexander L. Klibanov ◽  
Sanjiv Kaul ◽  
Richard J. Price
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Occlusion ◽  
Pulsed Ultrasound ◽  
Medial Region ◽  
Lateral Region ◽  
Microvascular Remodeling ◽  
Flow Restoration ◽  
Normal Rat ◽  
Ultrasound Microbubbles

We showed previously that microbubble destruction with pulsed 1-MHz ultrasound creates a bioeffect that stimulates arteriogenesis and a chronic increase in hyperemia blood flow in normal rat muscle. Here we tested whether ultrasonic microbubble destruction can be used to create a microvascular remodeling response that restores hyperemia blood flow to rat skeletal muscle affected by arterial occlusion. Pulsed ultrasound (1 MHz) was applied to gracilis muscles in which the lateral feed artery was occluded but the medial feed artery was left intact. Control muscles were similarly occluded but did not receive ultrasound, microbubbles, or both. Hyperemia blood flow and number of smooth muscle (SM) α-actin-positive vessels, >30-μm arterioles, and capillaries per fiber were determined 7, 14, and 28 days after treatment. In ultrasound-microbubble-treated muscles, lateral region hyperemia blood flow was increased at all time points and restored to normal at day 28. The number of SM α-actin vessels per fiber was increased over control in this region at days 7 and 14 but decreased by day 28, when larger-diameter arterioles became more prevalent in the medial region. The number of capillaries per fiber was increased over control only at day 7 in the lateral region and only at days 7 and 14 in the medial region, indicating that the angiogenesis response was transient and likely did not contribute significantly to flow restoration at day 28. We conclude that ultrasonic microbubble destruction can be tailored to stimulate an arteriogenesis response that restores hyperemia blood flow to skeletal muscle in a rat model of arterial occlusion.

Organ dysfunction after blood flow restoration in patients with acute lower limb ischemia

2019 ◽  
Vol 12 (5) ◽  
pp. 477
Author(s):  
Yu. V. Belov ◽  
G. V. Sinyavin ◽  
I. A. Vinokurov ◽  
G. V. Mnatsakanyan
Keyword(s):  
Blood Flow ◽  
Organ Dysfunction ◽  
Lower Limb ◽  
Limb Ischemia ◽  
Lower Limb Ischemia ◽  
Flow Restoration

scholarly journals Cerebral Blood Flow Restoration and Reperfusion Injury After Ultraviolet Laser–Facilitated Middle Cerebral Artery Recanalization in Rat Thrombotic Stroke

Stroke ◽  
2002 ◽  
Vol 33 (2) ◽  
pp. 428-434 ◽  
Author(s):  
Brant D. Watson ◽  
Ricardo Prado ◽  
Alexander Veloso ◽  
J-P. Brunschwig ◽  
W. Dalton Dietrich
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Reperfusion Injury ◽  
Cerebral Artery ◽  
Ultraviolet Laser ◽  
Flow Restoration

Effect of hypothermia and HTK on the microcirculation in the rat cremaster muscle after ischaemia

2005 ◽  
Vol 109 (1) ◽  
pp. 117-123 ◽  
Author(s):  
Jacqueline BASTIAANSE ◽  
Dick W. SLAAF ◽  
Mirjam G. A. oude EGBRINK ◽  
Gary L. ANDERSON ◽  
Hans VINK ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vessel Wall ◽  
Tissue Perfusion ◽  
Cremaster Muscle ◽  
Capillary Perfusion ◽  
Combined Application ◽  
Warm Ischaemia ◽  
Preservation Method ◽  
Flow Restoration ◽  
Wall Interactions

Hypothermia is an important preservation method for tissues and solid organs. The aim of the present study was to assess in rat cremaster muscle the effect of hypothermia, without or with pre-ischaemic HTK (histidine-tryptophan-ketoglutarate–Bretschneider solution) perfusion, on microvascular consequences of 4 or 6 h ischaemia and 2 h of reperfusion. Intravital microscopy was applied to examine capillary perfusion and leucocyte–endothelium interactions. The cremaster muscle was subjected to 4 or 6 h of cold (4 °C) or warm (33–34 °C) ischaemia and 2 h of reperfusion. Measurements were performed at baseline, prior to HTK perfusion and ischaemia, and at 0, 1 and 2 h after blood flow restoration. Hypothermia completely prevented the 50% reduction in capillary perfusion that was observed previously at start of reperfusion after 4 h warm ischaemia. After 6 h of warm ischaemia, perfusion resumed in only 45% of capillaries and remained at this low level during reperfusion. In contrast, only a slight decrease (<10%) in capillary perfusion was observed after 6 h of cold ischaemia. Pre-ischaemic HTK perfusion had no beneficial effect on tissue perfusion. Both hypothermia and HTK attenuated the significant increase in venular leucocyte–vessel wall interactions, which was observed after 4 h of warm ischaemia in a previous study. Combined application of both interventions had no additional effects. After 6 h of warm ischaemia, no increase in leucocyte–vessel wall interactions was observed, possibly due to venular flow reduction. In conclusion, hypothermia preserves capillary perfusion and prevents an increase in leucocyte–vessel wall interactions during reperfusion after muscle tissue ischaemia. Preischaemic perfusion of the vasculature with HTK does not improve the effects of cold storage on tissue perfusion, but attenuates the inflammatory response independently of temperature effect.

scholarly journals The chemokine (C-X-C motif) receptor 4 inhibitor AMD3100 accelerates blood flow restoration in diabetic mice

Diabetologia ◽  
2006 ◽  
Vol 49 (11) ◽  
pp. 2786-2789 ◽  
Author(s):  
C. Jiao ◽  
S. Fricker ◽  
G. C. Schatteman
Keyword(s):  
Blood Flow ◽  
Diabetic Mice ◽  
Flow Restoration
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