Collateral-dependent Blood Flow Research Articles

Heparin increases exercise-induced collateral blood flow in rats with femoral artery ligation.

The potential for heparin to enhance the training-induced increase in collateral-dependent blood flow to the distal hind-limb muscles was evaluated after bilateral femoral artery ligation in adult male rats (approximately 350 g). Rats received either saline (n = 34) or heparin (n = 36) injections and were kept sedentary (limited to cage activity) or exercised on a treadmill 5 days per week up a 15% incline by one of two protocols: (1) exercise at a constant moderate speed (20 m/min) for approximately 6 wks or (2) exercise at a progressively increased speed for 7 to 8 weeks (started at 20 m/min, increased at 15 minutes to 25 m/min, and then increased at 30 minutes to 30 m/min). Heparin- and saline-treated rats, exercised by the moderate-speed protocol, were run for the same time each day. Collateral-dependent blood flow to the distal limb tissue was determined by using 15-microns 85Sr-labeled microspheres in an isolated hindquarter preparation perfused in the descending aorta at 100 mm Hg. For comparison with the above groups, sedentary animals with acute femoral artery ligation and without femoral obstruction were included. Exercise tolerance increased from approximately 7 minutes initially to 30 to 40 minutes per bout; tolerance was greater in the heparin-injected rats than in the saline-injected rats (P < .05). Muscle performance of the gastrocnemius-plantaris-soleus muscle group (GPS) during isometric contractions in situ improved with training, was further increased by heparin administration (P < .001), and generally scaled with recovery of blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-converting enzyme inhibition increases collateral-dependent muscle blood flow

The purpose of this study was to evaluate the effect of angiotensin-converting enzyme (ACE) inhibition on collateral-dependent blood flow (BF) during exercise. Adult male Sprague-Dawley rats (approximately 320 g) were fed zabicipril, an ACE inhibitor, mixed with powdered food at 0.0, 0.3, and 3.0 mg.kg-1 x day-1 (n = 12/group) for 5-7 days. Under ketamine-acepromazine anesthesia, the carotid and caudal arteries were catheterized for BF determination, and both femoral arteries were ligated to remove the primary route for BF to the distal limb tissue. Later on the same day, collateral-dependent hindlimb BF was determined at two treadmill speeds (15 and 25 m/min at 15% grade) with 85Sr- and 141Ce-labeled 15-microns microspheres. Zabicipril ingestion induced 50 and 65% inhibition of plasma ACE activity in the low- and high-dose group, respectively (P < 0.001). ACE inhibition did not affect body weight, blood pressure, or heart rate of the rats during exercise. However, BFs to the total hindlimb were 44 and 36% higher (P < 0.001) in zabicipril-treated animals than in the zero-dose controls (approximately 45 ml.min-1 x 100 g-1). Furthermore, BFs to the proximal hindlimb, distal hindlimb, and gastrocnemius-plantaris-soleus group were 33-44% greater in drug-treated than in control animals (P < 0.025). Higher speed (25 m/min) failed to further increase muscle BF; therefore peak BFs were likely achieved. These results indicate that collateral-dependent BF was improved by ACE inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Response of collateral-dependent myocardium to vasopressin release during prolonged intense exercise.

We hypothesized that vasopressin concentrations during exercise attenuate the increase in collateral-dependent blood flow leading to left ventricular dysfunction in Ameroid-occluded miniswine. An Ameroid occluder was placed around the proximal left circumflex coronary artery (LCX) of 19 miniswine. Ten weeks later V1 receptor blockade with the use of [d(CH2)5Tyr-(Me)]arginine vasopressin (10-12 micrograms/kg iv) increased resting transmural flow (radioactive microspheres) in the LCX region, indicating the presence of V1 receptors. Neither injection of lysine vasopressin (125 pmol/kg) after V1 receptor blockade nor injection of two specific V2 receptor agonists caused changes in mean arterial pressure, heart rate, or left anterior descending coronary arterial flow velocity, indicating that V2 receptors mediate no appreciable vasodilation in the swine coronary circulation. Next the ratio of collateral to noncollateral flow and regional systolic wall thickening (sonomicrometer dimension gauges) were measured at rest and after 20 min of prolonged, intense treadmill exercise (85-90% of heart rate reserve) in the presence and absence of V1 receptor antagonism. This degree of exertion increased plasma lysine vasopressin from 6.2 +/- 1.0 at rest to 21.0 +/- 7.0 pg/ml (P < 0.05) during the unblocked run. However, the decrease in transmural blood flow ratio (collateral to noncollateral flow) from rest was similar during exercise before and after V1 receptor blockade (0.78 +/- 0.07 and 0.80 +/- 0.05, respectively; P < 0.05 vs. rest). Likewise, percent systolic wall thickening in the collateral-dependent region decreased from rest to exercise in the absence and presence of V1 receptor antagonism (35.9 +/- 4.5 and 39.5 +/- 3.8%, respectively; P < 0.05 vs. rest).(ABSTRACT TRUNCATED AT 250 WORDS)