Inhibitory effect of cardiac contraction on coronary collateral blood flow

1977 ◽  
Vol 233 (5) ◽  
pp. H541-H546 ◽  
Author(s):  
R. E. Russell ◽  
R. W. Chagrasulis ◽  
J. M. Downey
Keyword(s):  
Blood Flow ◽  
Left Coronary Artery ◽  
Constant Pressure ◽  
Inhibitory Effect ◽  
Cardiac Contraction ◽  
Collateral Blood Flow ◽  
Ischemic Region ◽  
Perfusion Apparatus ◽  
Collateral Vessels ◽  
Coronary Collateral Blood Flow

The present study was undertaken to determine the effect of contraction on overall flow in an area supplied by collateral vessels. Changes in the distribution of blood flow across the wall of ischemic and normally perfused regions of the left ventricle were observed during normal beating and during vagal arrest. The main left coronary artery was cannulated and perfused at constant pressure (125 mmHg) using a servo pump apparatus. An ischemic area supplied by collaterals was created by ligating the left anterior descending artery. Radiomicrospheres (15 micrometer) were injected into the perfusion apparatus during beating. Then spheres with a different label were administered to the same heart during arrest. The results revealed that beating caused a gradient of blood flow inhibition from near zero at the epicardium to about 50% at the endocardium in both zones. Inhibition to flow at the mid wall of the ischemic zone, 71%, was significantly greater than that seen at the corresponding depth in the normally perfused region, 33%. These results indicate that contraction not only inhibits collateral blood flow to an ischemic region, but also that the inhibition is actually magnified at the mid wall.

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.

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

1990 ◽  
pp. 267-278 ◽  
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

Is Isoflurane-induced Preconditioning Dose Related?

2002 ◽  
Vol 96 (3) ◽  
pp. 675-680 ◽  
Author(s):  
Franz Kehl ◽  
John G. Krolikowski ◽  
Boris Mraovic ◽  
Paul S. Pagel ◽  
David C. Warltier ◽  
...  
Keyword(s):  
Blood Flow ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Collateral Blood Flow ◽  
Area At Risk ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Coronary Collateral Blood Flow

Background Volatile anesthetics precondition against myocardial infarction, but it is unknown whether this beneficial action is threshold- or dose-dependent. The authors tested the hypothesis that isoflurane decreases myocardial infarct size in a dose-dependent fashion in vivo. Methods Barbiturate-anesthetized dogs (n = 40) were instrumented for measurement of systemic hemodynamics including aortic and left ventricular pressures and rate of increase of left ventricular pressure. Dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion and were randomly assigned to receive either 0.0, 0.25, 0.5, 1.0, or 1.25 minimum alveolar concentration (MAC) isoflurane in separate groups. Isoflurane was administered for 30 min and discontinued 30 min before left anterior descending coronary artery occlusion. Results Infarct size (triphenyltetrazolium staining) was 29 +/- 2% of the area at risk in control experiments (0.0 MAC). Isoflurane produced significant (P < 0.05) reductions of infarct size (17 +/- 3, 13 +/- 1, 14 +/- 2, and 11 +/- 1% of the area at risk during 0.25, 0.5, 1.0, and 1.25 MAC, respectively). Infarct size was inversely related to coronary collateral blood flow (radioactive microspheres) in control experiments and during low (0.25 or 0.5 MAC) but not higher concentrations of isoflurane. Isoflurane shifted the linear regression relation between infarct size and collateral perfusion downward (indicating cardioprotection) in a dose-dependent fashion. Conclusions Concentrations of isoflurane as low as 0.25 MAC are sufficient to precondition myocardium against infarction. High concentrations of isoflurane may have greater efficacy to protect myocardium during conditions of low coronary collateral blood flow.

Hyperglycemia reduces coronary collateral blood flow through a nitric oxide-mediated mechanism

2001 ◽  
Vol 281 (5) ◽  
pp. H2097-H2104 ◽  
Author(s):  
Judy R. Kersten ◽  
Wolfgang G. Toller ◽  
John P. Tessmer ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Blood Glucose ◽  
Blood Glucose Concentration ◽  
Collateral Blood Flow ◽  
Coronary Collateral ◽  
Retrograde Blood Flow ◽  
Flow Through ◽  
Blood Glucose Concentrations ◽  
Coronary Collateral Blood Flow

We tested the hypothesis that hyperglycemia alters retrograde coronary collateral blood flow by a nitric oxide-mediated mechanism in a canine Ameriod constrictor model of enhanced collateral development. Administration of 15% dextrose to increase blood glucose concentration to 400 or 600 mg/dl decreased retrograde blood flow through the left anterior descending coronary artery to 78 ± 9 and 82 ± 8% of baseline values, respectively. In contrast, saline or l-arginine (400 mg · kg−1 · h−1) had no effect on retrograde flow. Coronary hypoperfusion and 1 h of reperfusion decreased retrograde blood flow similarly in saline- orl-arginine-treated dogs (76 ± 11 and 89 ± 4% of baseline, respectively), but these decreases were more pronounced in hyperglycemic dogs (47 ± 10%). l-Arginine prevented decreases in retrograde coronary collateral blood flow during hyperglycemia (100 ± 5 and 95 ± 6% of baseline at blood glucose concentrations of 400 and 600 mg/dl, respectively) and after coronary hypoperfusion and reperfusion (84 ± 14%). The results suggest that hyperglycemia decreases retrograde coronary collateral blood flow by adversely affecting nitric oxide availability.

scholarly journals Atrial natriuretic peptide augments coronary collateral blood flow: A study during coronary angioplasty

1998 ◽  
Vol 21 (10) ◽  
pp. 737-742 ◽  
Author(s):  
Zenon S. Kyriakides ◽  
Eftihia Sbarouni ◽  
Aias Antoniadis ◽  
Efstathios K. Iliodromitis ◽  
Dimitrios Mitropoulos ◽  
...  
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Coronary Angioplasty ◽  
Collateral Blood Flow ◽  
Coronary Collateral ◽  
Coronary Collateral Blood Flow ◽  
Atrial Natriuretic

scholarly journals Evaluation of Procedures Designed to Enhance Coronary Collateral Blood Flow

1962 ◽  
Vol 10 (2) ◽  
pp. 142-147 ◽  
Author(s):  
Robert M. Berne ◽  
Richard D. Jones ◽  
Frederick S. Cross
Keyword(s):  
Blood Flow ◽  
Collateral Blood Flow ◽  
Coronary Collateral ◽  
Coronary Collateral Blood Flow
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