Flow In Dogs Research Articles

Effect of glomerulopressin on ovarian blood flow in dogs.

The present study showed that glomerulopressin decreased ovarian blood flow in normal dogs and that this effect could be inhibited by treatment with indomethacin. In addition diabetic dogs had a high plasma level of glomerulopressin and a low ovarian blood flow that was shown to increase after treatment with indomethacin. This suggests that the low ovarian blood flow in diabetis might be due to a prostaglandin synthesizing effect of glomerulopressin.

The role of cyclic AMP in canine secretin-stimulated bile flow

Cyclic nucleotide secretion rates in bile during the physiologic stimulation of ductular bile flow in dogs was evaluated by measurement of bile cyclic AMP concentration during the stimulation of secretin release by infusion of acid into the duodenum of dogs with chronic bile fistulas. The effects of PGA 1 and theophylline on secretin-stimulated bile flow and cyclic AMP secretin rates were also evaluated. Endogenous secretin stimulated bicarbonate-rich bile flow and decreased bile cyclic AMP concentration. PGA 1 significantly decreased secretin-stimulated bile flow but not bile cyclic AMP secretion. Theophylline did not alter secretin-stimulated bile flow or cyclic AMP secretion rates. These data indicate that based on cyclic AMP content in bile, secretin-stimulated ductular bile flow is unrelated to cyclic AMP metabolism.

Vagal control of coronary blood flow in dogs.

The experiments were performed on open-chest mongrel dogs, the hearts being paced at a constant rate. Both vagi were cut in the neck and the peripheral ends were stimulated with frequencies of 1, 5, 10, 15, 20, 25, 30, 35, 40 and 50 cycles per sec (30 sec, 8 V, 2 msec). Adrenergic beta-receptors were blocked with propranolol and adrenergic alpha-receptors with dihydroergotamine. Coronary flow was measured with electromagnetic flowmeters on the descending branch of the left coronary artery. A significant increase in coronary flow was observed with rising frequency of stimulation. This increase was 15 percent with 30 Hz and decreased with higher frequencies. The total coronary resistance reached its lowest level at the frequency of 30 cycles per sec. The results clearly indicate the parasympathetic control of myocardial blood flow.

Effects of acute ischaemia induced by atrial pacing on coronary blood flow in dogs.

Five anaesthetized open chested dogs were studied by measuring left anterior descending (LAD) coronary blood flow, at rest, after atrial pacing and after Isoprenaline infusion. The LAD was then stenosed in order to reduce the hyperaemic response and then the study was repeated. During the control situation LAD flow was shown to increase with the increase in heart rate. Although the partial occlusion did not drop resting coronary flow, it actually fell under stress conditions to 68 % of the control values. The importance of this observation is that although one might expect flow in a stenosed vessel to increase to a maximum limited by the stenosis, this in fact does not happen. lt appears that with increasing stress, local ischaemia produces a rise in coronary resistance. Such a mechanism may explain the occurrence of myocardial infarction without proximal occlusion of coronary vessels and may explain the discrepancy between the time course of myocardial infarction as observed following experimental coronary ligation and that seen in man.

Myocardial blood flow and hemodynamic responses to exercise training in dogs

ARTICLESMyocardial blood flow and hemodynamic responses to exercise training in dogsA. A. Bove, P. B. Hultgren, T. F. Ritzer, and R. A. CareyA. A. Bove, P. B. Hultgren, T. F. Ritzer, and R. A. CareyPublished Online:01 Mar 1979https://doi.org/10.1152/jappl.1979.46.3.571MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByThe coronary circulation in exercise trainingM. Harold Laughlin, Douglas K. Bowles, and Dirk J. Duncker1 January 2012 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 302, No. 1Regulation of Coronary Blood Flow During ExerciseDirk J. Duncker, and Robert J. Bache1 July 2008 | Physiological Reviews, Vol. 88, No. 3Explosives detection by sniffer dogs following strenuous physical activityApplied Animal Behaviour Science, Vol. 81, No. 2Effects of exercise training on left ventricular filling at rest and during exercise in patients with ischemic cardiomyopathy and severe left ventricular systolic dysfunctionAmerican Heart Journal, Vol. 132, No. 1Intravenous cocaine causes epicardial coronary vasoconstriction in the intact dogAmerican Heart Journal, Vol. 121, No. 6Coronary blood flow in dogs with contractile dysfunction due to experimental volume overload.Circulation, Vol. 83, No. 3Abnormal subendocardial blood flow in pressure overload hypertrophy is associated with pacing-induced subendocardial dysfunction.Circulation Research, Vol. 65, No. 6Epicardial coronary artery constriction with intravenous ethanolInternational Journal of Cardiology, Vol. 22, No. 3Ethanol causes epicardial coronary artery vasoconstriction in the intact dog.Circulation, Vol. 78, No. 1Effects of hypertrophy on the coronary circulationProgress in Cardiovascular Diseases, Vol. 30, No. 6Physiologic, Biochemical^ and Coronary Adaptation to Exercise ConditioningCardiology Clinics, Vol. 5, No. 2Proximal coronary vasomotor reactivity after exercise training in dogs.Circulation, Vol. 71, No. 3Reduced myocardial blood flow resulting from dynamic changes in coronary artery stenosisInternational Journal of Cardiology, Vol. 4, No. 3Tachycardia induced reduction in coronary blood flow distal to a stenosisInternational Journal of Cardiology, Vol. 2, No. 1 More from this issue > Volume 46Issue 3March 1979Pages 571-578 Copyright & PermissionsCopyright © 1979 the American Physiological Societyhttps://doi.org/10.1152/jappl.1979.46.3.571PubMed438029History Published online 1 March 1979 Published in print 1 March 1979 Metrics

Revasculization of Acute Cerebral Infarction and the Regional Cerebral Blood Flow in Dogs

Revasculization of Acute Cerebral Infarction and the Regional Cerebral Blood Flow in Dogs

Role of large arteries in regulation of cerebral blood flow in dogs.

Previous studies have demonstrated a significant pressure gradient from carotid artery to pial or middle cerebral arteries. This pressure gradient suggests that large cerebral arteries contribute to cerebral resistance. We have tested the hypothesis that large cerebral arteries contribute to regulation of cerebral blood flow during changes in blood gases and arterial pressure. Microspheres were used to measure brain blood flow in anesthetized dogs. Resistance of large cerebral arteries was estimated by determining the pressure gradient between common carotid and wedged vertebral artery catheters. Systemic hypercapnia and hypoxia dilated large cerebral arteries, and hypocapnia constricted large cerebral arteries. Resistance of large arteries was 0.6+/-0.1 (mean +/- SE) mm Hg per ml/min per 100 g during normocapnia. During hypercapnia and hypoxia, large artery resistance decreased significantly to 0.2 +/- 0.03 and 0.3 +/- 0.05, respectively. During hypocapnia large artery resistance increased significantly to 1.0 +/- 0.1. In other experiments, we found that large cerebral arteries participate in auto-regulatory responses to hemorrhagic hypotension. When arterial pressure was reduced from 110 to 58 mm Hg, autoregulation maintained cerebral blood flow constant, and resistance of large cerebral arteries decreased significantly from 1.0 +/- 0.2 to 0.6 +/- 0.1 mm Hg per ml/min per 100 g. In absolute terms, we calculated that 20-45% of the change in total cerebral resistance during these interventions was accounted for by changes in large artery resistance. These studies indicate that large cerebral arteries, as well as arterioles, participate actively in regulation of cerebral blood flow during changes in arterial blood gases and during autoregulatory responses to hemorrhagic hypotension.

Radiolabeled microsphere measurements of alveolar bone blood flow in dogs.

Radiolabeled microspheres were injected into the left cardiac ventricle in healthy adult dogs to quantify blood flow in maxillary and mandibular alveolar bone. Heart rate, arterial blood pressure and pulse contour were monitored throughout each experiment.Blood flow in maxillary alveolar bone was more than 30 % greater (p < .001) than in mandibular alveolar bone. Alveolar bone blood flow (mean ± S.D.) measured as ml/min per gram was 0.12 ± .02 in the maxilla compared to 0.09 ± .02 in the mandible. The cardiovascular paramenters monitored were constant immediately prior to the injection of microspheres and remained unchanged during and following injection.It is possible that radiolabeled microspheres can be used to quantify the circulatory changes in alveolar bone during the development of destructive periodontal disease in dogs.

Biliary spasmolytic action of 3-(2,4,5-triethoxybenzoyl)propionic acid (AA-149) in dogs

The spasmolytic action of 3-(2,4,5-triethoxybenzoyl)propionic acid (AA-149) on the biliary tract was investigated i in anesthetized dogs. Intravenous administration of AA-149 at 2 mg/kg and higher doses produced a dose- dependent reduction in passage resistance through the choledochoduodenal junction and in gallbladder pressure, and a dose-dependent increase in bile flow. AA-149, like cholecystokinin, decreased biliary ductal pressure in spite of increasing the bile flow in dogs with ligation of the cystic duct of the gallbladder, whereas taurocholate increased the pressure as well as the bile flow. Moreover, the spasmic response of the choledochoduodenal junction to morphine was depressed strongly by AA-149, but not consistently by atropine. The effects of AA-149 were not influenced by pretreatment with atropine, phentolamine or propranolol. These findings strongly suggest that AA-149 releaxed the biliary tract and depressed the morphine-induced spasm by a mechanism different from those of anticholinergic and sympathomimetic agents.

Spatial distribution of pulmonary blood flow in dogs in increased force environments

Spatial distribution of pulmonary blood flow (SDPBF) during 2- to 3-min exposures to 6-8 Gy acceleration was studied, using radioactive microspheres in dogs, and compared to previously reported 1 Gy control distributions. Isotope distributions were measured by scintiscanning individual 1-cm-thick cross sections of excised, fixed lungs. Results indicate: 1) the fraction of cardiac output traversing left and right lungs did not change systematically with the duration and magnitude of acceleration; but 2) the fraction is strongly affected by the occurrence or absence of fast deep breaths, which cause an increase or decrease, respectively, in blood flow through the dependent lung; and 3) Gy acceleration caused a significant increase in relative pulmonary vascular resistance (PVR) in nondependent and dependent regions of the lung concurrent with a decrease in PVR in the midsagittal region of the thorax. Result 3 may be mediated primarily by changes in regional alveolar volume and geometry in the nondependent hemithorax conbined with hydrostatic effects of extravascular fluid and active hypoxic response in the dependent region and is superimposed on, and may override, hydrostatic effects of perfusion pressures on SDPBF during acceleration.

Parasympathetic cholinergic control of cerebral blood flow in dogs.

SUMMARY We studied the effects of cholinergic receptor activation on cerebral blood flow in dogs anesthetized with chloralose. Continuous measurements of cerebral blood flow, arterial and cerebral spinal fluid pressure, heart rate, and respiratory carbon dioxide tension were made during parasympathetic nerve stimulation and during intraarterial infusion of acetylcholine. Multiple samples of arterial and cerebral venous blood were taken before, during, and after cholinergic vasodilation and analyzed for oxygen tension, carbon dioxide tension, and pH. Dose-response curves obtained by intra-arterial infusion of acetylcholine at 0.27-1,080 /ig/min and stimulation frequency-response curves obtained by excitation of the major petrosal nerve at 2-40 Hz demonstrated a dose or frequency-dependent cerebral vasodilation. The maximum cerebral vasodilation (171% of control flow) was obtained with an acetylcholine infusion of 1,080 /xg/min. During infusion of 27 /tg of acetylcholine/min arterial blood gases showed little or no change and thus could not have produced the observed change in cerebral blood flow. The changes in cerebral venous blood were all consistent with the observed increase in cerebral blood flow; oxygen tension rose from 30.4 to 36.0 mm Hg, carbon dioxide tension fell from 45.7 to 42.3 mm Hg, and pH rose from 7.342 to 7.360. Ipsilateral stimulation of the major petrosal nerve at 10 Hz, with a 3-msec pulse duration and 60-second stimulation period, produced an increase in cerebral blood flow to 111% of control flow. Cholinergic receptor blockade with atropine (1 mg/kg, i.v.) completely eliminated the cerebral vasodilation produced by acetylcholine infusion at 27 figlmin and significantly reduced the vasodilation resulting from major petrosal nerve stimulation. We conclude that the cerebral circulation has the capacity for significant cholinergic vasodilation. THE ABUNDANT anatomical evidence demonstrating the existence of nerve fibers on the cerebral vessels has recently been reviewed. 1 The sympathetic autonomic component of this innervation has been shown to have the capacity for marked cerebral vasoconstriction via an aadrenergic receptor mechanism. 2 - 3 A parasympathetic cerebral vasodilator mechanism was suggested by early workers when they observed pial vessel in response to cranial nerve stimulation. 4 More recently, intravertebral atropine was shown to suppress the resulting from inhalation of 5% CO2, 5 and intravertebral neostigmine enhanced cerebral vasodilator reactivity to CO2. (i Atropine was also shown to eliminate autoregulatory dilation in unanesthetized rabbits. 7 Each of these observations is consistent with a parasympathetic cholinergic vasodilator mechanism for the cerebral circulation. None of these studies demonstrates a parasympathetic cholinergic increase in cerebral blood flow. A cholinergic vasodilator mechanism to compliment the adrenergic vasoconstrictor mechanism has, therefore, not been clearly defined for the control of cerebral blood flow. In the present study, parasympathetic nerve stimulation and intra-arterial infusion of a cholinergic agonist, acetylcholine, were used to test for a possible parasympathetic cholinergic cerebral vasodilator mechanism.

Atraumatic measuring of pulmonary capillary blood flow in dogs.

Pulmonary capillary blood flow (Qc) was measured by a nitrous oxide uptake technique using a capacitance-plethysmograph to measure pulmonary volume changes. One hundred and four paired Qc and total cardiac outputs (Qt) were measured in 13 normal mongrel dogs. The mean Qc was 0.101 +/- 0.020 1-min -1-kg-1 while the mean Qt, measured by dye dilution, was 0.117 +/- 0.025 1-min-1-kg-1. This technique minimizes subject trauma and provides a method for repeated pulmonary capillary blood flow determinations in acute or chronic studies.

Sympathetic regulation of cephalic blood flow.

Blood flow to bilateral tissues (cranial and extracranial) was studied by means of the particle distribution method in two groups of anesthetized dogs (five using 25-mu radioactive microspheres, six using 15-mu microspheres) and five anesthetized stumptail Macaques monkeys (8-mj spheres) during unilateral sympathetic stimulation. The stimulatory parameters were adjusted to produce maximum pupillary dilatation. In the five dogs hemispheric and regional cerebral blood flow decreased but not significantly. Flow to the extracranial tissues decreased 82%. Hemispheric brain blood flow averaged 0.70 ml/min/gm for Paco2 of 40 mm Hg. In the six dogs sympathetic stimulation did not significantly decrease cerebral blood flow but decreased flow to extracranial tissues (72.3%). At an average Paco2 of 33.2 mm Hg, hemispheric blood flow to the unstimulated side averaged 0.51 ml/min/gm. In the five monkeys findings were essentially the same as those observed in the dogs. The hemispheric blood flow averaged 0.36 ml/min/gm on the nonstimulated side for an average Paco2 of 36.6 mm Hg. Under the conditions studied, electrical stimulation of the cervical sympathetic nerves does not appear to modify regional or total brain blood flow in dogs and Macaques monkeys. The vascular response in oral and other extracranial tissues is very dramatic, however.

Intrarenal blood flow in dogs with normal and spontaneously elevated blood pressure.

SummaryIntrarenal blood flow distribution was evaluated in 60 dogs with radiola-beled microspheres. The range of mean arterial blood pressure (BP) was 90 to 180 mm Hg, with an average of 137 mm Hg± 20 (SE). A poor but significant inverse correlation was found between renal blood flow (RBF) per gram kidney weight and the spontaneously occurring mean systemic pressure (r = −0.24, P < 0.001). Analysis of blood flow rates per gram inner and outer cortex showed substantially lower inner cortical flows in dogs with elevated blood pressure compared to dogs with lower blood pressures; outer cortical flow was essentially equivalent in the 60 animals. The correlation coefficient between inner cortical flow and BP was −0.534 (P < 0.001). Both inner and outer cortical resistance to flow increased significantly with pressure (P < 0.001). Electrolyte excretion rates (Na+ and K+) did not vary substantially in this population of dogs. These results demonstrate that spontaneously elevated blood pressure is associated with...

Effect of nonachlazine and oxyfedrine on the coronary blood flow in dogs

The coronary blood flow in anesthetized and unanesthetized dogs was measured by means of an ultrasonic Doppler radiotelemetric apparatus. The ultrasonic transducer was placed on the upper third of the descending branch of the left coronary artery. Nonachlazine was shown to increase the coronary blood flow considerably in both anesthetized and unanesthetized dogs. However, the action of the substance lasted only 2–3 min and depended on changes in cardiac activity. Oxyfedrine increased the coronary bllod flow by a lesser degree than nonachlazine but for a longer time (mean 20 min). Considering the high effectiveness of the two substances in clinical practice the authors conclude that the increase in the coronary blood flow is not the main course of action when attempting to obtain an antianginal effect in patients with ischemic heart disease.

Effect of 13‐NLE‐motilin on gastric secretion, serum gastrin level and mucosal blood flow in dogs.

1. In dogs with gastric fistulas and vagally innervated fundic and antral pouches, 13-norleucine-motilin (13-nle-motilin), a synthetic analogue of motilin, infused intravenously in graded doses produced a dose-dependent increase in gastric acid and pepsin outputs. 2. The motilin-induced stimulation of gastric secretion occurred independently of antral pH and was not accompanied by any alteration in the serum gastrin level suggesting that motilin did not affect the release of gastrin. 3. When infused intravenously in a constant dose against a constant background stimulation with pentagastrin or histamine 13-nle-motilin inhibited both acid and pepsin secretion from the main stomach and fundic pouch. 4. The inhibitory effect of 13-nle-motilin was always associated with a marked reduction in mucosal blood flow but without any change in the ratio of aminopyrine concentration in the gastric juice and blood plasma indicating that this peptide primarily affected gastric secretion but did not limit the gastric mucosal microcirculation.

Effects of fendilin hydrochloride (sensit) on systemic and coronary hemodynamics and on retrograde coronary blood flow in dogs.

Fendilin hydrochloride was tested in 9 normal anesthetized dogs and in 7 anesthetized dogs with acute coronary artery occlusion. The compound (1 mg/kg i.v.) caused a slight short lasting increase in coronary blood flow together with an increase in cardiac metabolic rate for oxygen of similar magnitude. There was no measurable effect on collateral conductance. No noteworthy effects on systemic hemodynamics were observed.

The haemodynamic effects of nitrous oxide anaesthesia on myocardial blood flow in dogs.

The effects of ventilation with nitrous oxide in oxygen on myocardial blood flow any oxygen metabolism were investigated in 31 mongrel dogs. The results of this study showed that, compared with controls, hyperoxic nitrous oxide mixtures did not cause any great changes in myocardial haemodynamics, despite a decrease in cardiac output and an increase in systemic vascular resistance. Normoxic nitrous oxide mixtures produced an increase of the coronary blood flow due to decreased coronary vascular resistance. To what extent this coronary vasodilatation resulted from a increased myocardial metabolism or from a direct effect of nitrous oxide on the coronary vascular bed cannot be quantified from the present results.

Effect of the histamine (H2) inhibitor metiamide on histamine-stimulated bile flow in dogs.

The effects of the histamine H2-receptor inhibitor metiamide on histamine-stimulated canine bile flow and gastric hydrogen ion output were evaluated. Histamine was found to stimulate bile volume in doses comparable to those that stimulated gastric hydrogen ion output; both responses appeared to have the same maximal response dose, 150 mug/kg per h. Metiamide alone did not alter hepatic bile flow. Administration of metiamide, 2 mg/kg per h, along with various doses of histamine demonstrated that the H2-receptor antagonist decreased bile volume and gastric hydrogen ion output from values obtained with histamine administration alone. The D50 of histamine for bile flow was 16.3 mug/kg per h and the D50 for hydrogen ion output was 44.2 mug/kg per h, Kinetic analysis suggests that the decrease in histamine-stimulated hydrogen ion output produced by metiamide is the result of competitive inhibition; the decrease in histamine-stimulated bile volume by metiamide which is different from the hydrogen ion inhibition, suggests noncompetitive inhibition. These data indicate that the mechanism of histamine choleresis is different from the mechanism of histamine-stimulated gastric acid output and that histamine-stimulated bile flow may not be the result of direct hormone-receptor interaction.

Continuous imaging of regional myocardial blood flow in dogs using krypton-81m.

The unique physical properties of the freely diffusible gas krypton-81 m allowed continuous imaging of regional myocardial blood flow in dogs when infused into the aortic root. Regional changes in myocardial perfusion related to transient coronary artery occlusion were demonstrated both as high resolution gamma camera images and as a quantitative strip chart record.