Coronary lymph: specific activities in interstitial fluid during uptake of 42K.
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Animals↗
Biomedical subjects
H F Downey
Publications and source records attributed to H F Downey.
Depletion of strontium from calves by hemodialysis.
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Animals↗
Coronary artery occlusion extends perfusion territory boundaries through microvascular collaterals.
Simultaneous in vivo infusions of two different colored 10 microns microsphere suspensions into the left anterior descending (LAD; red spheres) and left circumflex (LCx; blue spheres) coronary arteries of nine anesthetized dogs identified a specific region of canine myocardium perfused by both arterial branches. Subsequently, the LAD was ligated and a third (green) set of micropheres was infused into the patent LCx artery. Analysis of 40 microns serial sections of tissue revealed interface zones with capillaries perfused by both arteries. The first zone, defined as the Interface Transistion Zone (ITZ) was formed by an intermingling of microvessels supplied by the parent arteries of the adjacent perfusion territories; it separated tissue containing only one or the other colored microspheres. Another zone, defined as the Boundary Watershed Zone was located within the ITZ and had capillaries containing both red and blue microspheres. The width of ITZ was 53377 +/- 817 microns (mean +/- SD), and the width of the BWZ was 3358 +/- 618 microns. Green microspheres, infused into the LCx following coronary occlusion were also found in the ITZ and BWZ. Furthermore, capillaries perfused exclusively by the LAD before occlusion (tissue with red but not blue microspheres) adjacent to the perfusion interface contained green microspheres as well as red/green aggregates, indicating lateral extension of the LCx perfusion territory. This extension of the LCx territory was quantitated by comparing the location at which densities of green microspheres or green/red aggregates decreased abruptly compared to the location of the original ITZ and BWZ boundaries, respectively. Results showed that LAD occlusion caused a 24% expansion of the ITZ and a 48% expansion of the BWZ. In addition, all expansions were significantly greater in subepicardial compared to subendocardial regions (p < 0.001). These results clearly demonstrate the capability of microvascular anastomoses in providing blood flow to the periphery of an ischemic region. Furthermore, the perfusion interface is labile and might be amenable to manipulation.
Animals↗
Colored microspheres reveal interarterial microvascular anastomoses in canine myocardium.
While the presence of microvascular intercommunication within an individual myocardial arterial bed is well documented, there is a paucity of data to support the existence of anastomoses emanating from independent arterial beds. Simultaneous in-vivo infusion of two different colored microsphere suspensions into the left anterior descending (LAD) and left circumflex (LCx) coronary arteries identified a specific interface region of canine myocardium that was perfused by both arterial branches. Subsequent microscopic/morphometric analysis of 40 microns serial sections in eight hearts revealed clustering of microspheres in their respective perfusion territories (red microspheres in the LAD region away from the interface, blue microspheres in the LCx field away from the interface), along with a mutually perfused borderzone. In each tissue section, two regions within this zone were identified and their maximum widths measured. One region was defined as the Interface Transition Zone (ITZ) (mean width = 5251 +/- 770 microns; mean +/- SD). This region was formed by an intermingling of microvessels supplied by the parent arteries of the adjacent perfusion territories; it separated tissue containing only one or the other colored microspheres. The second region was defined as the Boundary Watershed Zone (BWZ) (mean zone width = 3151 +/- 611 microns; mean +/- SD). This region was formed by capillaries containing sphere aggregates of both colors; it was located exclusively within the ITZ. In addition, the ITZ and BWZ were significantly wider in subepicardial than in subendocardial regions (p less than 0.001).
Animals↗
Myocardial oxygen consumption and blood flow during nicotine infusion: effect of combined alpha- and beta-adrenergic blockade.
The effect of combined alpha- and beta-adrenergic blockade with phenoxybenzamine and propranolol, respectively, on changes in left ventricular myocardial oxygen consumption and blood flow during nicotine administrations (36 micrograms/kg/min, i.v.) was evaluated in anesthetized, open-chest dogs. Myocardial blood flow was estimated by injection of 8 to 10 micrometers diameter radioactive microspheres into the left atrium, and myocardial oxygen consumption was computed from the Fick principle. Before adrenergic blockade, nicotine caused a market (+151%) elevation in myocardial oxygen consumption and a parallel increase in myocardial blood flow. The increase in myocardial blood flow was uniform transmurally. These cardiac changes were accompanied by elevations in systemic arterial and left atrial pressures, peripheral vascular resistance, and heart rate, but by no change in aortic flow or in myocardial contractility. After adrenergic blockade, nicotine caused somewhat lesser, though still marked, elevations in myocardial oxygen consumption (+60%) and blood flow (+43%). Again, myocardial blood flow increases were uniform transmurally. Also, nicotine-induced increases in systemic arterial and left atrial pressure and in peripheral vascular resistance persisted after adrenergic blockade, whereas heart rate remained constant and aortic flow and myocardial contractility declined. The results indicate that nonadrenergic mechanisms contribute significantly to the increase in myocardial oxygen demand during nicotine infusion.
Animals↗
Regional myocardial blood flow during nicotine infusion after chronic coronary artery occlusion: effect of beta-adrenergic blockade.
In eight dogs a portion of the left ventricular free wall (LVFW) was rendered collateral-dependent (CD) by gradual occlusion of the left anterior descending coronary artery with a surgically implanted Ameroid constrictor. Six to 8 weeks later, the dogs were anesthetized and regional myocardial blood flow was measured with 7-10-micron radioactive microspheres during (a) control conditions, (b) nicotine alone (24 micrograms/kg/min i.v.), and (c) nicotine (24 micrograms/kg/min i.v.) after beta-adrenergic blockade with propranolol. During control conditions, mean transmural flow was similar in CD, border, and normal regions of the LVFW. Nicotine alone increased flow in all regions of the LVFW, with normal (+ 104%) greater than CD (+ 56%). These changes in flow were accompanied by increases in mean arterial pressure (+ 34%) and mean aortic flow (+ 54%). Nicotine after beta-adrenergic blockade appreciably raised mean arterial pressure (+ 83%) and mean left atrial pressure (+ 307%), but caused no increase in flow to any region of the LVFW. The results indicate (a) that the nicotine-induced increase in flow is blunted in a CD region, and that (b) beta-adrenergic blockade unmasks coronary vasoconstrictor mechanisms during nicotine infusion which prevent increases in flow to either normal or CD regions despite increased perfusion pressure and augmented myocardial oxygen demands.
Adrenergic beta-Antagonists↗
Pressure-induced changes in coronary flow and volume during reperfusion in canine hearts.
1. The effects of coronary artery occlusion and reperfusion on pressure-induced changes in coronary blood flow and blood volume were investigated. 2. The left anterior descending coronary artery (LAD) of canine hearts was cannulated and perfused independently with arterial blood by a controlled pressure system. LAD flow was measured continuously with an electromagnetic flowmeter and LAD volume was measured in the steady-state by indicator dilution. Measurements were made with perfusion pressure at 100 mmHg (control), 50 mmHg, and 150 mmHg before and after 2 h of LAD occlusion followed by 2 h of reperfusion. 3. With perfusion pressure at control, occlusion-reperfusion reduced LAD flow 19%, but had no significant effect on LAD volume. 4. Steady-state LAD flow and volume always varied directly with changes in perfusion pressure; after occlusion-reperfusion these variations were accentuated. 5. Analysis of transient and steady-state flow responses indicated diminished capability of arteriolar resistance vessels for active, autoregulatory adjustments in lumenal calibre following changes in perfusion pressure. 6. The results of this study demonstrate that occlusion-reperfusion causes derangement to pressure-volume and pressure-flow control mechanisms in the coronary circulation.
Animals↗
Perfusion with non-oxygenated Tyrode solution causes maximal coronary vasodilation in canine hearts.
1. Coronary vasodilator effects of non-ischaemic hypoxia (perfusion with non-oxygenated Tyrode solution) and ischaemic hypoxia (coronary occlusion) were compared. 2. The left anterior descending coronary artery (LAD) of six in situ canine hearts was perfused selectively at controlled pressure with normal arterial blood or with non-oxygenated Tyrode solution. LAD flow was measured continuously with an electromagnetic flowmeter. Reactive hyperaemic blood flow responses following 3 min Tyrode perfusion were compared with responses following 3 min complete coronary occlusion. 3. Control LAD blood flow was 26.9 +/- 4.6 ml/min. A 3 min period of Tyrode perfusion caused a peak reactive hyperaemic blood flow of 151 +/- 31 ml/min, which was not significantly different from that caused by 3 min occlusion, 123 +/- 17 ml/min. The duration and total volume of reactive hyperaemia flow following Tyrode perfusion were smaller than values following occlusion. 4. The present findings demonstrate that myocardial hypoxia per se is a sufficient vasodilatory stimulus to account for the peak reactive hyperaemic flow following 3 min occlusion, but that the prolonged reactive hyperaemic response depends on vasodilator metabolites which accumulate in ischaemic myocardium.
Animals↗
Regional blood flow in canine brain during nicotine infusion: effect of autonomic blocking drugs.
Radioactive microspheres (15 mu) were used to measure regional cerebral blood flow during intravenous infusion of nicotine (36 micrograms/kg/min) in anesthetized, open chest dogs. Experiments were conducted with uncontrolled mean aortic pressure and intact autonomic receptors (Series I; n = 9), and in four groups of dogs with mean aortic pressure held constant (Series II); 1) with intact autonomic receptors (n = 6), 2) after beta adrenergic blockade (n = 8), 3) after alpha and beta adrenergic blockade (n = 6), 4) after alpha and beta adrenergic and cholinergic blockade (n = 4). In Series I, nicotine raised mean aortic pressure (+ 72%) and increased flow in cerebral cortex (+ 67%), cerebellum (+ 38%), pons (+ 46%), medulla (+ 39%), and spinal cord (+ 48%). In all regions, but cortex, increases in vascular resistance limited nicotine-induced increases in flow. In Series II, nicotine changed flow only in cortex. Without blockade, nicotine increased cortical flow (+ 38%); but beta blockade abolished this increase in flow. After alpha and beta blockade nicotine again raised cortical flow (+ 29%), and additional cholinergic blockade had no effect on this response. It is concluded that nicotine causes predominant beta receptor mediated vasodilation in cerebral cortex, although it also activates alpha (vasoconstrictor) receptors and a non-adrenergic, non-cholinergic vasodilator mechanism in this region of brain.
Adrenergic alpha-Antagonists↗
Regional blood flow in canine brain during nicotine infusion: pentobarbital vs. chloralose anesthesia.
We compared vasoactive effects of intravenous nicotine (36 micrograms/kg/min) in regional cerebral circulations under pentobarbital and chloralose anesthesia. Experiments were conducted in three groups of dogs: Group I, pentobarbital anesthesia with fixed ventilation; Group II, chloralose anesthesia with fixed ventilation; Group III, chloralose anesthesia with free breathing. Values for regional cerebral blood flow measured with 15 mu radioactive microspheres were used to compute regional cerebral vascular resistance (rCBR). In Group I, nicotine had no effect on rCVR in cerebral cortex, and it increased significantly rCVR in cerebellum (+17%), pons (+13%), medulla (+23%), and spinal cord (+19%). Using chloralose instead of pentobarbital in dogs with fixed ventilation (Group II), caused a significant reduction in rCVR in the cerebral cortex during nicotine, although it did not alter significantly nicotine-induced changes in rCVR in other regions of the brain. Hypocapnic alkalosis during nicotine-induced hyperventilation (Group III) resulted in significant increases in rCVR in all regions of the brain; however, the increases in rCVR in non-cortical regions more than doubled those in the cerebral cortex. The present results indicate: Nicotine-induced vasodilation in cerebral cortex was blunted by pentobarbital anesthesia. Nicotine-induced vasodilation in cerebral cortex under chloralose anesthesia was sufficient to nullify in part the potent vasoconstrictor effect of hypocapnic alkalosis.
Anesthesia↗