Blood Flow In Conscious Dogs Research Articles

Saline‐induced natriuresis and renal blood flow in conscious dogs: effects of sodium infusion rate and concentration

This study focused on static and dynamic changes in total renal blood flow (RBF) during volume expansion and tested whether a change in RBF characteristics is a necessary effector mechanism in saline-induced natriuresis. The aortic flow subtraction technique was used to measure RBF continuously. Identical amounts of NaCl (2.4 mmol kg(-1)) were given as slow isotonic (Iso, 120 min), slow hypertonic (Hyper, 120 min), and rapid isotonic loads (IsoRapid, 30 min). During Iso and IsoRapid, arterial blood pressure increased slightly (6-7 mmHg), and during Hyper it remained unchanged. Iso and Hyper increased sodium excretion (4 +/- 1 to 57 +/- 27 and 10 +/- 4 to 79 +/- 28 micromol min(-1), respectively) and decreased plasma renin activity (by 38% and 29%), angiotensin II (by 56% and 58%) and aldosterone (by 47% and 65%), while RBF remained unchanged. IsoRapid caused a similar increase in sodium excretion (to 72 +/- 19 micromol min(-1)), a similar decrease in renin system activity, but a 15% elevation of RBF (282 +/- 22 to 324 +/- 35 mL min(-1)). Selected frequency domain parameters of RBF autoregulation did not change in response to any load. In response to slow saline loading simulating daily sodium intake, the rate of sodium excretion may increase 10-20-fold without any change in mean arterial blood pressure or in RBF. Regulatory responses to changes in total body NaCl levels appears, therefore, to be mediated primarily by neurohumoral mechanisms and may occur independent of changes in arterial pressure or RBF.

Donitriptan, a Unique High‐Efficacy 5‐HT1B/1D Agonist: Key Features and Acute Antimigraine Potential

ABSTRACTWe hypothesized that the limited acute therapeutic effectiveness of tryptamine derivatives in alleviating migraine headache could be explained by the relatively low intrinsic activity of these agents at 5‐HT1B/1D receptors. Donitriptan is a novel arylpiperazide 5‐hydroxytryptamine (5‐HT) derivative which was designed to exploit the higher potency and efficacy properties of 5‐HT compared to tryptamine at 5‐HT1B/1D receptors. In vitro, donitriptan has subnanomolar affinity for nonhuman and human 5‐HT1B/1D receptors and micromolar affinity for the 5‐HTip subtype. Donitritpan potently inhibited forskolin‐induced cAMP formation and enhanced specific GTP35γS specific binding to a greater extent than tryptamine derivatives and equivalent to 5‐HT in C6 cells expressing human 5‐HT1B or 5‐HT1D receptors. Donitriptan produced more potent and larger amplitude increases in hyperpolarizing Ca2+‐dependent K+ current than sumatriptan in guinea pig isolated trigeminal ganglion neurons, and was more potent than tryptamine derivatives in eliciting contractile responses in rabbit isolated saphenous vein rings. In vivo, donitriptan evoked more potent, longer‐lasting and greater amplitude carotid vasoconstrictor responses than tryptamine derivatives in anesthetized pigs; and in contrast to sumatriptan, naratriptan or zolmitriptan, produced long‐lasting, dose‐dependent decreases in unilateral carotid blood flow in conscious dogs at doses from 0.63 mg/kg p.o. without affecting heart rate or behavior. Oral donitriptan also evoked hypothermic responses in guinea pigs suggesting that the compound gains access to the brain.Donitriptan is thus a selective, potent 5‐HT1B/1D receptor agonist which can be distinguished from tryptamine derivatives in consistently exerting high intrinsic activity at these receptors in a series of vascular and neuronal models relevant to migraine. Advantages in terms of therapeutic effectiveness in the acute relief of migraine headache over currently available triptans can be expected to include greater response rates and consistency of pain relief, a lower incidence of migraine recurrence and better tolerability. The acute anti‐migraine potential of the first high efficacy 5‐HT1B/1D agonist of its kind, donitriptan, is currently being investigated in man.

Effects of Prostaglandin E1 on Hepatic Blood Flow in Conscious Dogs with Chronic Biliary Obstruction

To evaluate the effects of prostaglandin E₁ (PGE₁) on the hepatic circulation in cholestasis, hepatic arterial blood flow (HAF), portal venous blood flow (PVF), cardiac output, and heart rate during PGE₁ infusions were investigated before and 2 weeks after biliary obstruction in conscious dogs by a transit-time ultrasonic flowmeter. In the control period, HAF and PVF increased dose dependently with the infusion of PGE₁ from 0.05 to 0.5 µg/kg/min. During the biliary obstruction period, a lower dose of PGE₁ increased HAF and PVF. The plasma concentration level of PGE₁ during the infusion of PGE₁ was significantly higher at each dose in the cholestatic animals. These results suggest that the metabolism of PGE₁ is attenuated by cholestasis. Plasma PGE₁ concentrations should be useful in deciding the optimal dose of PGE₁.

Effect of JTV-506, a novel vasodilator, on coronary blood flow in conscious dogs.

Coronary vasodilator and hemodynamic profiles of JTV-506, a newly synthesized 2,2-bis-methoxymethyl benzopyran-derivative potassium channel opener, were evaluated in conscious dogs. JTV-506 (2.5-10 microg/kg, i.v.) elicited dose-dependent increases in coronary blood flow (CBF) and heart rate (HR) but only slight changes in mean blood pressure (MBP). Other vasodilators such as levcromakalim, nicorandil, diltiazem, and nitroglycerin, when administered intravenously, elicited increases in CBF and HR and a decrease in MBP. When dosed orally JTV-506 (0.01-0.1 mg/kg), levcromakalim (0.01-0.1 mg/kg), nicorandil (1-10 mg/kg), and nifedipine (3-30 mg/kg) also elicited increases in CBF and HR and a decrease in MBP. JTV-506 caused a marked increase in CBF with slight changes in HR and MBP. In contrast to JTV-506, however, the changes caused by levcromakalim, nicorandil, and nifedipine were accompanied by a marked increase in HR and a marked decrease in MBP. These results suggest that the action of JTV-506 on hemodynamics is different from that of other vasodilators, including reference potassium channel openers, and that the profile of cardiovascular action of JTV-506 may be useful in the treatment of angina pectoris.

Autoregulation and non‐homeostatic behaviour of renal blood flow in conscious dogs.

1. Spontaneously occurring haemodynamic variations within 4 h affecting renal blood flow (RBF) were compared with externally induced short changes of renal artery pressure (RAP) in conscious resting dogs. 2. In all animals in which RAP was servo-controlled (n = 6), perfect autoregulation of RBF was observed. 3. In all 4 h recordings of spontaneous renal blood flow (n = 9), certain combinations of blood pressure and blood flow occurred remarkably frequently as indicated by three-dimensional frequency distributions. 4. Cluster analysis demonstrated significant differences between these areas of accumulation (P < 0.001). The average number of 'set points' per 4 h session was 3.1 +/- 0.3. 5. The shift from one set point to another is probably mediated by multiple control systems impinging on renal haemodynamics as suggested by 1/f fluctuations. 6. In seven dogs, an additional renal venous catheter allowed measurements of the arterial-venous (A-V) oxygen partial pressure (PO2) difference as an indicator of the renal metabolic demand. An inverse relationship between A-V PO2 difference and RBF (Y = X(-0.034) + 40.9, r = -0.9, P < 0.001) was found, indicating that the metabolic demands vary little (if at all) between the different set points. 7. The presented data suggest a modified view of renal homeostasis. There exist distinct combinations between RBF and RAP, which are very stable. Autoregulation merely buffers the fluctuations around these set points.

Effect of enkephalins on cardiac output and regional blood flow in conscious dogs

Page H1656: C. L. Rosen, A. Cote, and G. G. Haddad. “Effect of enkephalins on cardiac output and regional blood flow in conscious dogs.” Figures 5 and 6 should appear as follows. (See PDF)

Effect of enkephalins on cardiac output and regional blood flow in conscious dogs

Page H1656: C. L. Rosen, A. Cote, and G. G. Haddad. “Effect of enkephalins on cardiac output and regional blood flow in conscious dogs.” Figures 5 and 6 should appear as follows. (See PDF)

Effect of enkephalins on cardiac output and regional blood flow in conscious dogs

To investigate the effects of enkephalins on cardiac output and regional blood flow, we administered D-Ala-D-Leu-enkephalin (DADLE) intracisternally (ic) to 14 chronically instrumented unanesthetized dogs. Measurements were made at base line, 20, 45, and 75 min after DADLE (25 or 125 micrograms/kg) and 15 min after naloxone (5 micrograms/kg ic). After 125 micrograms/kg DADLE, all animals developed hypoventilation, bradycardia, and decreased O2 consumption without hypotension. Cardiac output decreased (-34%), but brain blood flow increased (+110%). Blood flow decreased to the diaphragm (-38%), heart (-21%), skeletal muscle (-40%), skin (-67%), pancreas (-79%), and gastrointestinal tract (-26%). After 25 micrograms/kg DADLE, there were no consistent changes in cardiac output or regional blood flow. Four additional animals (without DADLE) were exposed to altered inspired gases to reproduce the blood gas changes after DADLE. These animals developed hyperventilation without bradycardia and increased brain (+114%) and diaphragm (+649%) blood flow. We conclude that centrally administered enkephalins produce 1) a parallel decrease in ventilation, heart rate, O2 consumption, and cardiac output and 2) a major blood flow redistribution, primarily dictated by the effects of opioids on ventilation, heart rate, and metabolism.

Effects of Left Ventricular Receptor Stimulation on Coronary Blood Flow in Conscious Dogs

HomeCirculation ResearchVol. 61, No. 5_supplementEffects of Left Ventricular Receptor Stimulation on Coronary Blood Flow in Conscious Dogs Free AccessResearch ArticlePDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessResearch ArticlePDF/EPUBEffects of Left Ventricular Receptor Stimulation on Coronary Blood Flow in Conscious Dogs Irving H. Zucker, Kurtis G. Cornish, Johnnie Hackley and Kay Bliss Irving H. ZuckerIrving H. Zucker Search for more papers by this author , Kurtis G. CornishKurtis G. Cornish Search for more papers by this author , Johnnie HackleyJohnnie Hackley Search for more papers by this author and Kay BlissKay Bliss Search for more papers by this author Originally published3 Apr 2018https://doi.org/10.1161/res.61.5_supplement.ii-54Circulation Research. 1987;61:II-54–II-60 Previous Back to top Next FiguresReferencesRelatedDetailsCited ByKinugawa S, Post H, Kaminski P, Zhang X, Xu X, Huang H, Recchia F, Ochoa M, Wolin M, Kaley G and Hintze T (2003) Coronary Microvascular Endothelial Stunning After Acute Pressure Overload in the Conscious Dog Is Caused by Oxidant Processes, Circulation, 108:23, (2934-2940), Online publication date: 9-Dec-2003. November 1, 1987Vol 61, Issue 5_supplementArticle InformationMetrics Download: 7 © 1987 American Heart Association, Inc.https://doi.org/10.1161/res.61.5_supplement.ii-54 Originally publishedApril 3, 2018 PDF download

Effects of left ventricular receptor stimulation on coronary blood flow in conscious dogs.

The present study was undertaken to determine the effects of intracoronary administration of the veratrum alkaloid veratridine on coronary blood flow and resistance in conscious, chronically instrumented intact and sinoaortic denervated dogs. Ten dogs were instrumented with a Doppler flow probe on the left anterior descending coronary artery. A chronic catheter was placed in the left circumflex coronary artery and in the aorta and left atrium. A Konigsberg pressure cell was placed in the left ventricle, and pacing leads were attached to the left atrium and ventricle. While heart rate was kept constant, bolus intracoronary injections of veratridine (0.1-0.4 microgram/kg) were administered in the unblocked state after beta 1-receptor blockade, after alpha-receptor blockade, and after cholinergic blockade. In the unblocked state, late diastolic coronary resistance fell by 34.7 +/- 5.0%. The maximum response was achieved at a time when arterial pressure was not significantly different from control. After beta 1-blockade, coronary resistance fell by 29.1 +/- 7.9%. After combined alpha- and beta-blockade, coronary resistance fell by 25.4 +/- 6.5% in response to veratridine. The addition of atropine completely blocked the decrease in coronary resistance, changing it by an average of -0.10 +/- 2.5%. The responses in sinoaortic denervated dogs were similar to those in intact animals. The response was abolished by vagotomy. We conclude that cardiac receptor stimulation causes a reflex decrease in coronary resistance in the awake dog that is completely accountable by a cholinergic mechanism.

Effects of atrial natriuretic peptide on proximal epicardial coronary arteries and coronary blood flow in conscious dogs.

The effects of atrial natriuretic peptide (ANP) on proximal epicardial coronary artery dimensions and coronary blood flow were examined in 7 awake dogs chronically instrumented with miniature coronary dimension crystals and Doppler flow probes on the circumflex coronary artery. ANP (10, 50, and 150 micrograms) was infused as a bolus via the left atrial catheter. Aortic pressure, left ventricular end-diastolic pressure, heart rate, and dP/dt did not change significantly with any dose of ANP. ANP caused transient (1-5 minutes) dose-related increases in coronary blood flow; maximum increases were 28.1 +/- 6.9%, 40.2 +/- 6.2%, and 73.9 +/- 12.5% with the 10-, 50-, and 150-micrograms doses, respectively. ANP also induced prolonged (average 70.2 +/- 28.6 minutes with 150-micrograms dose) dose-related increases in coronary diameter; maximum increases were 3.1 +/- 1.0%, 3.9 +/- 1.5%, and 5.7 +/- 1.3% with the 10-, 50-, and 150-micrograms doses, respectively. The increase in diameter was not attenuated when the transient increase in blood flow was prevented by partial occlusion with a pneumatic snare. Combined autonomic blockade with propranolol (1 mg/kg), phentolamine (1 mg/kg), and atropine (0.06 mg/kg) attenuated the relative increase in coronary flow but did not alter the increases in epicardial coronary diameter produced by ANP. These data demonstrate that bolus injection of ANP effects preferential, sustained, dose-dependent, flow-independent increases in epicardial coronary dimensions and relatively brief dose-dependent increases in coronary blood flow. The vasodilator effects of ANP on epicardial vessels are direct and are not mediated via the autonomic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Diurnal changes in coronary blood flow in conscious dogs.

The purpose of the present study was to evaluate potential diurnal changes in resting coronary blood flow under conditions of comparable myocardial oxygen requirements. We studied 21 conscious, resting dogs instrumented for the measurement of coronary flow, left ventricular pressure, and regional myocardial segment length. Recordings were taken in the early morning and late afternoon. In the afternoon, left circumflex coronary blood flow was 12.8% higher than in the morning, without detectable changes in the major hemodynamic determinants of myocardial oxygen consumption, i.e., heart rate, left ventricular pressure, peak positive dP/dt, end-diastolic regional myocardial dimension, and regional myocardial stroke work. These results are consistent with a circadian variation of coronary vascular tone accompanied by compensatory alteration in myocardial oxygen extraction and may have clinical relevance, since the coronary vascular tone may change dynamically in patients with critical coronary stenosis.

Autoregulation of hind-limb blood flow in conscious dogs.

We evaluated the efficiency of blood flow autoregulation of the hind-limb vascular bed of eleven conscious dogs during: resting conditions; graded levels of treadmill exercise; and increases in oxygen consumption produced by the administration of 2,4-dinitrophenol (DNP). Blood flow to the left hind limb was measured with an electromagnetic flow probe on the left external iliac artery. Hind-limb perfusion pressure was measured from a catheter in the deep femoral artery and was controlled via an externally inflatable occlusion cuff positioned just distal to the flow probe. Arterial pressure was measured in the abdominal aorta. Experiments were performed 5-16 days after instrumentation. Hind-limb pressure-flow (P-F) relationships were evaluated by decreasing hind-limb perfusion pressure in 4-5 small sequential 'square-wave' steps of 10-15 mmHg each while measuring flow. Each step decrease in perfusion pressure was maintained for 2 min. The efficiency of autoregulation was quantified by calculating the closed-loop gain of flow regulation (Gc) at each decrement in perfusion pressure utilizing the equation: Gc = 1-[(F0-Fn/F0)/(P0-Pn/P0)] where F0 and P0 are the starting (control) flows and pressures prevailing prior to decreasing perfusion pressure, and Fn and Pn are the new flows and pressures at each decrement in perfusion pressure. A Gc value less than 0 indicates a predominantly passive P-F relationship, while a Gc of 1 is perfect autoregulation of flow. When the dogs were at rest, decrements in hind-limb perfusion pressure were accompanied by almost equivalent decreases in flow, i.e. no autoregulation occurred, and Gc averaged -0.177 +/- 0.044 over the pressure range from 100-40 mmHg. During all levels of treadmill exercise (on gradients of 0, 7, or 21%), however, positive Gc values were found that averaged from 0.258 +/- 0.046 at a gradient of 0% to 0.392 +/- 0.041 at a gradient of 21% and were significantly different from Gc values found during rest at perfusion pressure ranges from 90-40 mmHg. The administration of DNP directly into the hind-limb circulation increased hind-limb blood flow from 199 to 481 ml/min. In the presence of DNP, Gc values were positive over perfusion pressure ranges from 100-40 mmHg and averaged 0.473 +/- 0.054. These data demonstrate that hind-limb blood flow is not autoregulated in resting dogs, but that significant autoregulation is manifest during conditions that increase oxygen consumption.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of halothane on renal hemodynamics during normovolemia and acute hemorrhagic hypovolemia.

The effects of halothane on renal hemodynamics under both normovolemic and hypovolemic conditions were investigated in chronically instrumented conscious dogs whose homeostatic mechanisms were not altered by the presence of preexisting drugs. Renal blood flow and aortic pressure were assessed by prior implantation of Doppler ultrasonic flow probes on the renal artery and a catheter in the descending aorta. Administration of halothane to conscious normovolemic dogs (Group HN) resulted in 11-26% decreases in renal vascular resistance with no significant changes occurring in renal blood flow. In a second group of animals made hypovolemic while awake (Group AH), 30% of the blood volume was removed over one-half hour. In response to hemorrhage, these conscious animals' renal blood flow did not significantly change from the normovolemic control, and renal vascular resistance significantly decreased. With no further intervention, renal vascular resistance and renal blood flow remained unchanged from the level achieved after the 30% hemorrhage. A third group of animals (Group HH) was hemorrhaged in a manner similar to that of Group AH. They also showed no significant changes in renal blood flow and a significant decrease in renal vascular resistance in response to hemorrhage. Thereafter, administration of halothane, as in Group HN, to this group produced 11-23% decreases in renal vascular resistance with no significant decline in renal blood flow from the hypovolemic control levels established after hemorrhage. The author concludes the following: administration of halothane to normovolemic conscious dogs does not decrease renal blood flow; a moderate degree of acute hemorrhagic hypovolemia does not decrease renal blood flow in conscious dogs; and administration of halothane to acutely hypovolemic conscious dogs does not impair renal perfusion.

Corticotropin-releasing factor, sauvagine, and urotensin I: effects on blood flow.

Corticotropin-releasing factor (CRF), sauvagine (SVG), and urotensin I (UI) were tested for their effects on superior mesenteric blood flow in conscious dogs. Intravenous (iv) administration of CRF, SVG, and UI induced an immediate rise of mesenteric blood flow that was associated with a decrease in mean arterial pressure and an increase in heart rate. Intracerebroventricular (ICV) injection of SVG and UI, but not CRF, rapidly (within 5 min after injection) elicited a long (90 min) elevation of mesenteric blood flow. Central administration of these peptides induced a delayed rise in heart rate and slightly elevated mean arterial pressure. The finding that CRF given ICV did not increase mesenteric blood flow could not be explained by the release of vasoactive agents such as vasopressin, epinephrine, or norepinephrine. After injection of CRF, SVG, and UI, plasma concentrations of CRF-, SVG-, and UI-like immunoreactivity did not increase as determined by radioimmunoassay. These results indicate that SVG and UI, but not CRF, administered ICV produce a long increase of mesenteric blood flow in conscious dogs. Because iv SVG and UI decrease mean arterial pressure and ICV SVG and UI increase mean arterial pressure and do not cause an increase in SVG- and UI-like immunoreactivity in the peripheral circulation, it is proposed that SVG and UI injected into the third cerebral ventricle act within the central nervous system to increase superior mesenteric blood flow in the dog.

Exogenous serotonin and gastric mucosal blood flow in conscious dogs.

The effects of serotonin on pentagastrin- and bethanechol-stimulated gastric mucosal blood flow (GMBF) and acid secretion were evaluated. Conscious gastric fistula dogs were used, with neutral red clearance as the method to estimate the mucosal blood flow. Serotonin inhibited the acid secretion, with a counteracting effect of propranolol and methysergide. Serotonin inhibited the pentagastrin- and bethanechol-stimulated GMBF after 15 min of infusion. The ratio between GMBF and acid secretion was increased during serotonin infusion, which suggests primary and independent changes in both variables. Propranolol and methysergide counteracted the serotonin inhibition of the GMBF. It may be concluded from this study that the acid-inhibitory effect of serotonin is not mediated by changes in the GMBF. The actions of serotonin on acid secretion and GMBF are mediated by specific receptors.

Effect of nitroglycerin on regional myocardial blood flow following an experimental coronary spasm.

This study was designed to evaluate the effect of nitroglycerin (30 micrograms given as an i.v. bolus) on regional distribution of myocardial blood flow in conscious dogs, following an acute coronary occlusion similar to a coronary spasm. The left anterior descending (LAD) coronary artery was acutely occluded with a balloon cuff occluder. The distribution of blood flow between the endocardium and the epicardium of both the normal and ischemic area of the left ventricle was determined by means of the radioactive microsphere technique. Acute occlusion of the left anterior descending coronary artery produced a significant decrease of blood flow reaching the area irrigated by this artery; this decrease was of a lesser magnitude after administration of nitroglycerin. In addition, ischemia produced a disproportionate decrease in endocardial blood flow. This decrement was also of a lesser magnitude following administration of nitroglycerin. Blood perfusion to the non-ischemic myocardium was not altered. These results indicate that an intravenous bolus of nitroglycerin, given after a brief coronary occlusion simulating a coronary spasm, increases blood flow to the ischemic myocardium, induces a favorable redistribution of blood flow toward the ischemic endocardium and does not produce any decrement of blood perfusion to the non-ischemic myocardium.

Regulation by insulin of myocardial glucose and fatty acid metabolism in the conscious dog.

In vivo small doses of insulin inhibit lipolysis, lower plasma FFA, and stimulate glucose disposal. Lowering of plasma FFA, either in the absence of a change in insulin or during combined hyperglycemia and hyperinsulinemia, promotes glucose uptake by heart muscle in vivo. In the isolated perfused heart, large doses of insulin directly stimulate heart glucose uptake. To assess the effect of physiological elevations of plasma insulin upon myocardial glucose and FFA uptake in vivo independent of changes in plasma substrate concentration, we measured arterial and coronary sinus concentrations of glucose, lactate, and FFA, and coronary blood flow in conscious dogs during a 30 min basal and a 2 h experimental period employing three protocols: (a) euglycemic hyperinsulinemia (insulin clamp, n = 5), (b) euglycemic hyperinsulinemia with FFA replacement (n = 5), (c) hyperglycemic euinsulinemia (hyperglycemic clamp with somatostatin, n = 5). In group 1, hyperinsulinemia (insulin = 73 +/- 13 microU/ml) stimulated heart glucose uptake (7.3 +/- 4.4 vs. 28.2 +/- 2.8 mumol/min, P less than 0.002), lowered plasma FFA levels by 80% (P less than 0.05), and decreased heart FFA uptake (28.4 +/- 4 vs. 1.5 +/- 0.9, P less than 0.01). When the fall in plasma FFA was prevented by FFA infusion (group 2), hyperinsulinemia (86 +/- 10 microU/ml) provoked a lesser (P less than 0.05) stimulation of glucose uptake (delta = 8.2 +/- 4.2 mumol/min) than in group 1, and there was no significant change in FFA uptake (25.3 +/- 16 vs. 16.5 +/- 4). Hyperglycemia (plasma glucose = 186 +/- 8 mg/100 ml) during somatostatin infusion resulted in only a small rise in plasma insulin (delta = 12 +/- 7 microU/ml), and although plasma FFA tended to decline, heart glucose uptake did not rise significantly (delta = 5.5 +/- 3.2 mumol/min, P = NS). There was no significant change in coronary blood flow during any of the three study protocols. We conclude that, in the dog, insulin at physiologic concentrations: (a) stimulates heart glucose uptake, both directly and by suppressing the plasma FFA concentration, and (b) does not alter coronary blood flow. Hyperglycemia per se has little effect on heart glucose uptake.

Effect of atrial fibrillation on atrial blood flow in conscious dogs

This study was undertaken to examine the independent effects of atrial tachycardia, ventricular tachycardia, and atrial fibrillation (AF) on atrial and ventricular blood flow in conscious, heart-blocked dogs using radioactive microspheres. Atrial blood flow averaged 0.54 ± 0.08 ml/min/g during the control period at an atrial rate of 124 beats/min and a ventricular rate of 90 beats/min. Atrial flow increased to 0.72 ± 0.12 ml/min/g during atrial pacing at 236 beats/min, but was not significantly altered by ventricular pacing at 200 beats/min. AF at a ventricular rate of 90 beats/min resulted in atrial flow values of 0.91 ± 0.08 ml/min/g. The ratio of atrial flow to left ventricular flow during AF averaged 1.18 ± 0.08. Administration of a maximal vasodilating dose of adenosine during AF further increased atrial flow to 2.18 ± 0.16 ml/min/g. Atrial tachycardia or AF did not significantly affect ventricular blood flow. These data indicate (1) that atrial blood flow increases significantly during AF, reaching flow values per gram of tissue comparable to those of the left ventricle, and (2) that this flow is regulated by the metabolic needs of the atrial tissue and does not represent maximal vasodilation.

Bone blood flow in conscious dogs at rest and during exercise.

Using the microsphere technique bone blood flow was measured in different anatomical and functional regions in long bones in conscious dogs. The measurements were performed during physical exercise upon a treadmill, and the bone blood flow values were obtained as prework resting values after 1 and 2 hours of exercise and after 1 hour of rest. The perfusion rates increased 50 per cent from 1.6 to 2.5 ml X 100 g tissue-1 X min-1 in the femoral and tibial cortical bones during work. In the cancellous bone of the femoral head an increase from 12.6 to 20.6 ml X 100 g tissue-1 X min-1 was found. Equal flow responses were determined in the fat-filled tibia-condylar and femoral supracondylar bone. The increase took place after 2 hours' exercise, but nonstatistically verified increased perfusion was found after 1 hour's work. The alternation in bone blood flow suggests that bone has a capability of physical vasodilation during muscular work but the flow response is slow and therefore the vasodilatation seems mediated by a metabolically induced stimulus.