scholarly journals Depression of Collateral Blood Flow Following Arterial Thrombosis

1977 ◽  
Author(s):  
R.G. Schaub ◽  
K.M. Meyers
Keyword(s):  
Blood Flow ◽  
Arterial Thrombosis ◽  
Collateral Circulation ◽  
Therapeutic Interventions ◽  
Collateral Blood Flow ◽  
Flow Measurements ◽  
Clinical Consequences ◽  
Blood Flow Measurements ◽  
Collateral Vessels ◽  
Iliac Bifurcation

Permanent ligation of the feline aorta at the iliac bifurcation is followed by rapid opening of pre-existing collateral blood vessels. However, if ligation is combined with formation of a clot these protective collateral vessels do not function. This study was undertaken to determine if drugs which alter serotonin (5-HT) function can improve collateral blood flow after arterial thrombosis. Permanent ligations were placed at the iliac bifurcation, circumflex iliac and sixth lumbar arteries in all cats. Control cats (8) were acutely ligated. In all other cats a clot was produced in the aorta by injection of 0.1 ml of thromboplastin. Clotted cats were untreated (8); had blood 5-HT depleted using a single dose of reserpine (0.1 mg/kg i.m.) followed by para-chlorophenylalanine (p-CPA) (100 mg/kg orally) every 3 days (9); or were treated prior to surgery with a 5-HT antagonist cinanserin HCl (4 mg/kg i.v.) (8). Collateral circulation was determined by blood flow measurements and aortograms 3 days after occlusion of the aorta. The hindlimb blood flow of untreated clotted animals was 20% of the acutely ligated control animals 3 days following aortic occlusion. However, hindlimb blood flow was 90% of control in reserpine and p-CPA treated cats and 60% of control in cinanserin HCl treated cats. Blood flow measurements correlated with aortograms. These results suggest: (1) The clinical consequences of arterial thrombosis cannot be entirely attributed to mechanical occlusion of an artery, but may be due to depression of protective collateral blood flow induced by thrombosis, (2) Serotonin is an important factor in this depression of collateral blood flow, and (3) Isolation of the factors responsible for collateral inhibition could permit the development of therapeutic interventions.

Depression of Collateral Blood Flow Following Arterial Thrombosis

1977 ◽  
Vol 38 (04) ◽  
pp. 0850-0862 ◽  
Author(s):  
Robert G. Schaub ◽  
Ronald Sande ◽  
Kenneth M. Meyers
Keyword(s):  
Blood Flow ◽  
Arterial Thrombosis ◽  
Hind Limb ◽  
Therapeutic Interventions ◽  
Collateral Blood Flow ◽  
Serotonin Antagonist ◽  
Limb Perfusion ◽  
Clinical Consequences ◽  
Collateral Vessels ◽  
Iliac Bifurcation

SummaryPermanent ligation of the feline aorta at the iliac bifurcation is followed by rapid opening of pre-existing collateral blood vessels. However, if ligation is combined with formation of a clot, these protective collateral vessels do not function. This study was undertaken to determine if drugs which alter serotonin function can improve collateral blood flow after arterial thrombosis. Permanent ligations were placed at the iliac bifurcation, circumflex iliac and sixth lumbar arteries in all cats. A clot was produced in the aorta of 27 cats by injection of 0.1 ml of thromboplastin. Ligated clot-occluded cats were untreated (10); had blood serotonin depleted using a single dose of reserpine (0.1 mg/kg i. m.) followed by para-chlorophenylanine (p-CPA) (100 mg/kg orally) every 3 days (9) ; or were treated prior to surgery with a serotonin antagonist cinanserin HC1 (4 mg/kg i. v.) (8). Control cats (18) were acutely ligated. 9 of these cats were untreated, 5 were cinanserin HC1-treated, and 4 were reserpine/p-CPA-treated. Extent of collateral development was assessed by aortograms 3 days after occlusion and by neurologic rating. Aortograms of acutely ligated cats indicated a significant collateral blood flow around the segment of ligated aorta, while ligated clot-occluded cats had a severely depressed hind-limb perfusion. Reserpine/p-CPA-treated ligation clot-occluded cats had aortograms similar to acutely ligated cats. The cinanserin HC1-treated ligation clot-occluded cats had aortograms which indicated hind-limb perfusion was not as adequate as the acutely ligated cats. However, the perfusion of these animals was improved over untreated ligation clot-occluded cats. Neurologic rating correlated with aortograms. These results suggest: 1) the clinical consequences of arterial thrombosis cannot be entirely attributed to mechanical occlusion of an artery, but may be due to depression of protective collateral blood flow induced by thrombosis, 2) serotonin is an important factor in this depression of collateral blood flow, and 3) isolation of the factors responsible for collateral inhibition could permit the development of therapeutic interventions.

Improvement of Collateral Circulation after Arterial Thrombosis with Indomethacin Therapy

1980 ◽  
Vol 44 (02) ◽  
pp. 069-071 ◽  
Author(s):  
Cecelia Helenski ◽  
Robert G Schaub ◽  
Royce Roberts
Keyword(s):  
Blood Flow ◽  
Platelet Activation ◽  
Arterial Thrombosis ◽  
Collateral Circulation ◽  
Thromboxane A2 ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Vasoactive Substance ◽  
Aortic Thrombosis ◽  
Platelet Counts

SummaryWe compared development of feline hindlimb collateral circulation and coagulation changes 3 hours following aortic thrombosis in five non-treated and five indomethacin treated (20 mg/kg) cats. Coagulation changes were monitored with the one stage prothrombin time (OSPT), partial thromboplastin time (PTT), protamine sulfate dilution test for fibrin monomer (PSD), and platelet counts. Collateral circulation was assessed with aortograms. Significant changes in coagulation parameters with the exception of platelet counts were not observed in either group. Platelet counts of non-treated cats were reduced to 63 ± 5% of control while platelet counts of treated cats were 96 ± 3% of control. Aortograms of non-treated cats indicated poor hindlimb perfusion around the thrombus, while aortograms of indomethacin treated animals indicated significant blood flow to the hindlimbs through collateral channels. These results support a role for the platelet in post thrombosis vasospasms and suggest that anti-platelet therapy could have positive effects in reducing the extent of ischemic damage which follows arterial thrombosis.Several studies, using cat and dog models, have demonstrated a significant reduction of collateral blood flow can occur following formation of an occlusive arterial thrombus (1–5). The collateral flow which developed after thrombosis was significantly less than when occlusion was accomplished with mechanical methods such as ligation (1, 3, 4). This suggested the presence of a thrombus produced effects on blood vessels more complex than simple mechanical obstruction. Imhoff originally suggested that the inhibition of collateral flow which followed thrombosis was related to the release or formation of a vasoactive substance which would induce constriction of collateral source or re-entry vessels (1). Butler, in later studies, suggested that it was serotonin which was responsible for the post thrombosis inhibition of collateral blood flow (2). The involvement of serotonin would seem logical, since the majority of blood serotonin is found in the platelet (6), is released upon platelet activation (7-9), and is a potent vasoconstrictor (10). A mechanism for serotonin involvement has proposed that the platelets in the flowing blood come into contact with the thrombus, are activated and release serotonin (2–4). Consideration of the biochemistry of platelet activation makes it apparent that serotonin is neither the only nor the most powerful vasoactive substance released by the platelet. Thromboxane A2 (TxA) is a critical substance in the activation, release, and aggregation of platelets (11, 12, 13). Thromboxane A2 is a particularly powerful vasoconstrictor which would be a more likely candidate to produce the type of long lasting vasospasm necessary to reduce collateral flow in the post thrombosis state (11, 12, 13). The relationship between thromboxane A2 and serotonin is suggested by recent studies which demonstrate that serotonin can initiate thromboxane A2 release from canine and feline platelets (14). Therefore, serotonin could be an intermediate mechanism in the process of collateral inhibition.If this hypothesis is correct, then inhibition of TxA synthesis should prove as beneficial in improving collateral flow after thrombosis as serotonin antagonists. To test this hypothesis we examined the effect of indomethacin treatment on development of collateral circulation following aortic thrombosis. Indomethacin is a non-steroidal, anti-inflammatory drug which inhibits cyclooxygenase, the major enzyme in the PG and TxA synthetic pathway (15–19).

Clinical Utility of Quantitative Cerebral Blood Flow Measurements during Internal Carotid Artery Test Occlusions

Neurosurgery ◽  
2002 ◽  
Vol 50 (5) ◽  
pp. 996-1005 ◽  
Author(s):  
Randolph S. Marshall ◽  
Ronald M. Lazar ◽  
William L. Young ◽  
Robert A. Solomon ◽  
Shailendra Joshi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Clinical Utility ◽  
Internal Carotid ◽  
Flow Measurements ◽  
Blood Flow Measurements

Doppler Blood Flow Measurements in Chronic Animal Preparations

1975 ◽  
Vol 49 (3) ◽  
pp. 17P-17P
Author(s):  
Maurice R. Cross ◽  
Clive Weller ◽  
E. B. Raftery
Keyword(s):  
Blood Flow ◽  
Flow Measurements ◽  
Blood Flow Measurements

Duplex Sonography of Normal Renal Allografts

1989 ◽  
Vol 30 (1) ◽  
pp. 53-56 ◽  
Author(s):  
B. Schwaighofer ◽  
F. Kainberger ◽  
F. Fruehwald ◽  
P. Huebsch ◽  
N. Gritzmann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Resistive Index ◽  
Duplex Sonography ◽  
Invasive Technique ◽  
Flow Measurements ◽  
Renal Allografts ◽  
Significant Difference ◽  
Main Renal Artery ◽  
Long Term Follow Up ◽  
Blood Flow Measurements

Thirty-five patients with normal renal allografts as well as 10 healthy volunteers with normal native kidneys were examined by duplex sonography. Blood flow measurements were performed in the main renal artery as well as in segmental, interlobar and arcuate arteries. In both groups the normal range of variation in blood flow was defined by using the resistive index (RI). Doppler wave forms and RI of main renal arteries were both similar to those of their branches. In renal allografts as well as in native kidneys the blood flow pattern showed a rapid up-slope in systole followed by a gradual down-slope in early diastole, with a persistent flow throughout diastole. In addition, there was no significant difference in the RI between allografted and native kidneys. The interobserver variability was less than 10 per cent. The mean RI was 0.68 using all data points. Vascular rejection in 11 patients could be discriminated significantly (p<0.001). Duplex sonography is useful in evaluating renal blood flow. This simple and non-invasive technique seems to be useful in long-term follow-up of renal allograft recipients.

Sign in / Sign up

Export Citation Format

Share Document