Electromagnetic Flowmeter Probe Research Articles

Hemodilution does not alter the aortic-to-femoral arterial pressure difference in dogs.

Distal arterial pressure normally differs from aortic pressure. This difference is modified by changes of vascular resistance. Hemodilution, due to decreased viscosity, decreases vascular resistance. Therefore, the difference between aortic and distal arterial pressures could be altered as well. We investigated whether acute hemodilution affected this difference in dogs. Eleven mongrel dogs weighing 16.6 +/- 4.4 kg were anesthetized with pentobarbital and sufentanyl and mechanically ventilated. Arterial presssure was recorded using Millar catheter-tipped pressure transducers in the proximal aorta and in the distal femoral artery. An electromagnetic flowmeter probe was placed around the aorta. Effective downstream pressure was estimated by extrapolation of exponential arterial pressure decay during 3-second occlusion of the proximal aorta. Hemodilution was effected by removal of 30 ml/kg of blood and replacement with 60 ml/kg of warmed saline. In addition, the effects of 1 microg/kg phenylephrine and 4 microg/kg of sodium nitroprusside were measured before and after hemodilution. Hemodilution decreased hematocrit from 39 +/- 11.2% to 25.6 +/- 4.95%. Systolic and mean pressures were unchanged but aortic diastolic pressure decreased significantly, from 86 +/- 17 to 79 +/- 15 mmHg (p < 0.005). Peak systolic pressure was 13.5 +/- 7.2 mmHg higher in the femoral artery than in the aorta before, and 16 +/- 8.7 mmHg after, hemodilution (p > 0.05). Nitroprusside decreased the femoral to aortic peak systolic pressure difference from 14.3 +/- 6.3 to 7.7 +/- 15.3 mmHg, p = 0.05 before hemodilution and from 14.3 +/- 8.8 to 2.5 +/- 11 mmHg, p < 0.005 afterwards. Hemodilution significantly decreased the effective downstream pressure, from 44 +/- 9 to 36 +/- 6.8 mmHg in the aorta (p < 0.05), and from 51 +/- 2 to 37 +/- 3.1 mmHg in the distal femoral artery (p < 0.05). Acute hemodilution did not alter the aortic-to-distal arterial pressure difference in dogs.

Effect of tPA on regional lung perfusion in unilobar canine pulmonary thromboembolism.

We investigated effects of tissue-type plasminogen activator (tPA) on regional pulmonary arterial hemodynamics in pulmonary thromboembolism (PTE) in a canine model of unilobar PTE. Ten beagle dogs were divided into two groups-tPA (n = 5) and control group (n = 5). In each dog an artificial blood circuit (ABC) consisting of a silicone tube and a cannulation-type electromagnetic blood flowmeter probe was placed at the left lower pulmonary artery. A unilobar PTE was induced by placing autologous clots into a metallic coil inside the ABC. The CO2 sampling tubes were positioned at the orifice of the left lower bronchus and the trachea, and the end-expiratory CO2 partial pressure (PET(CO2)) was measured. In the tPA group, blood flow at the left lower pulmonary artery (LL-flow) was improved to near baseline within approximately 30 min of receiving tPA, and PET(CO2) at the left lower bronchus (LL-PET(CO2)) increased in direct correlation with LL-flow. The hemodynamic improvement after tPA therapy correlated with the partial pressure of the regional pulmonary expiratory CO2. Moreover, it was suggested that changes in physiologic conditions in PTE were not determined by clot quantity alone.

Inhibition of cerebral metabolic and circulatory responses to nitrous oxide by 6-hydroxydopamine in dogs.

To determine whether cerebral metabolic and circulatory consequences of N2O result from activation of the sympathoadrenal system. The effects of pretreatment with intracisternal injection of 6-OHDA, which produces chemical sympathectomy, were studied in dogs. Seven days before measurement dogs were pretreated with intracisternal injection of either saline vehicle (sham-group) or 100 micrograms.kg-1 6-hydroxydopamine (6-OHDA, group). Cerebral blood flow (CBF) was measured using an electromagnetic flow-meter probe and cerebral metabolic rate for oxygen (CMRO2) was calculated as the product of CBF and arterial-sagittal sinus blood oxygen content difference [C(a-v)O2]. In the sham group, N2O (60%) increased CMRO2 from 6.11 +/- 0.21 ml.100 g-1.min-1 to 7.10 +/- 0.39 ml.100 g-1.min-1 and CBF from 63 +/- 5 ml.100 g-1.min-1 to 173 +/- 26 ml.100 g-1.min-1. In the 6-OHDA group, CMRO2, did not change during N2O exposure, whereas CBF increased from 61 +/- 3 ml.100 g-1.min-1 to 135 +/- 19 ml.100 g-1.min-1 but less then in the sham group. The 6-OHDA group displayed a reduction in cortical noradrenaline (NA) concentration from 263.2 +/- 35.6 ng.g-1 to 102.7 +/- 16.5 ng.g-1. Cortical dopamine (DA) concentration was not affected by 6-OHDA administration. These results suggest that most of the increase in CMRO2 and at least a part of the increase in CBF during N2O exposure in the sham-group are related to sympathoadrenal-stimulating effects of N2O.

Simultaneous Measurements of Cerebral Circulation with Electromagnetic Flowmetry and Doppler Ultrasound Velocity in the Newborn Pig

Cerebral blood flow measurement has been an important investigative tool in newborns at risk for perinatal brain damage. The validity of Doppler cerebral blood flow velocity measurements depends on a constant vessel diameter. We have validated Doppler against the electromagnetic flowmeter (EM) using a modified common carotid artery model in the 1-d-old piglet. Two sets of continuous and simultaneous recordings were performed: 1) the Doppler and EM probe on the same common carotid artery (extracerebral branches were ligated), and 2) the EM probe on the common carotid artery and the Doppler probe recording from an intracerebral artery through an artificial fontanel. Arterial partial pressure of carbon dioxide (PaCO2) was manipulated (2.8-7.4 kPa), as was arterial blood pressure (3.7-9.3 kPa). Simultaneous EM flow and estimated Doppler flow were compared. Ninety-three recordings were obtained with both transducers on the modified carotid artery, and 49 were obtained with the Doppler insonicating an intracerebral artery. A multiple regression model was used for statistical analysis. The correlation between EM and both sets of Doppler measurements for individual animals was > 0.95 and was unaffected by changes in arterial blood pressure or PaCO2. Thus, the common carotid and the intracerebral artery investigated did not change their diameter significantly in response to PaCO2 or arterial blood pressure. The relationships between EM and Doppler in the individual animal were all linear but revealed great variability in the slopes due to the unknown vessel diameter and angle of insonication.(ABSTRACT TRUNCATED AT 250 WORDS)

Relations entre la prise alimentaire et la consommation d'oxygène des organes drainés par la veine porte chez le porc éveillé

The intestinal absorption of glucose and alpha-amino nitrogen, the appearance of D-and L-lactic acids in the protal vein and the consumption of oxygen by the organs of the abdominal extrahepatic splanchnic area were studied simultaneously in pigs either during the postprandial period or during a fasting period of the same length. For this purpose, 5 growing pigs (59.4 +/- 3.5 kg live weight) were fitted with permanent catheters in the portal vein and carotid artery and with an electro-magnetic flowmeter probe around the portal vein. This device was used to measure the exchanges between the blood and the intestinal lumen. For a period of 1 wk, the animal received a semi-synthetic diet containing 6% purified cellulose (R6) and then during the next wk, a diet containing 16% purified cellulose (R16), the order of distribution being alternated from one animal to the next. During each of these 2 wk and after a fasting period of 16 h, they were subjected to 2 successive tests of 5 h, either after intake of an 800-g meal (R) (R6 or R16), or after no meal intake (J6 or J16). During these tests, blood samplings were made at 15 to 30-min intervals, the consumption of oxygen was recorded by an ABL3 radiometer and the afore mentioned nutrients and metabolites analysed in these samples. The consumption of oxygen was higher (P > 0.01) during the postprandial period (5.41 +/- 0.19 mmol/kg/h) than during the fasting period (4.64 +/- 0.19 mmol/kg/h) while the availability of oxygen only increased slightly (P < 0.05) (14.01 +/- 0.66 vs 13.08 +/- 0.76 mmol/kg/h). By contrast, the oxygen extraction coefficient did not significantly increase with meal intake. The appearance of L-lactic acid in the portal blood was higher (P < 0.001) during the postprandial period (3.83 +/- 0.32 g/h) than during the fasting period (1.23 +/- 0.23 g/h). The energy expenditure due to the aerobic metabolism of the organs drained by the portal vein ranged from 35.7 to 37.8 kcal/h after meal intake, ie 1-18% more than after fasting. The anaerobic metabolism only represented 0.3-0.4% (fasting) and 1.1-1.3% (postprandial period) of this aerobic metabolism. Oxygen consumption was not changed by the dietary cellulose content.

Transport des acides aminés dans l'aire splanchnique par le plasma sanguin et le sang chez le veau préruminant

Three preruminant calves were fitted with catheters in portal and hepatic veins and in a mesenteric artery. Two electromagnetic flowmeter probes were clipped around the portal vein and the hepatic artery. The calves were fed either a diet with a low (L) or a high (R) abomasal emptying rate for dietary proteins. Blood flow and free amino acid levels in plasma (P) and blood (S) were determined before the morning meal and during the following 7 h. In the portal vein, for most amino acids P/S ratios were correlated to the net amino acid balance of the digestive tract measured in plasma. By contrast in the hepatic vein, these ratios were mainly correlated to hepatic balance measured in whole blood. Correlations between digestive tract and hepatic balance calculated using either plasma or whole blood pool were different for some amino acids. This suggests that amino acid exchange between plasma and blood cells is low and absorbed amino acids are mainly transported to the liver by plasma, whereas whole blood rather than plasma is concerned in amino acid exchanges in the liver.

Physical and mechanical effects of cardioplegic injection on flow distribution and myocardial damage in hearts with normal coronary arteries

The physical and mechanical effects of injecting crystalloid cardioplegic solution under various pressures and flows was studied (in canine hearts) to establish a safe method for administering it in the presence of normal coronary arteries. A constant pressure system (300 mm Hg = 15 psi) was maintained in the solution reservoir, and flows and pressures were varied with the use of cannulas of different inner diameters: 0.8, 1.35, 1.6, 2.3, 2.58, and 2.80 mm. Cardioplegia distribution was measured by 15 microns radioactive microspheres. Peak flow rate, total flow, and mean flow rate per infusion were measured by an inline electromagnetic flowmeter probe. Direct aortic root pressure, time to standstill, and myocardial temperatures were recorded by continuous monitoring. Cardiac isoenzymes were measured in the coronary sinus, peripheral blood, and directly in the myocardial tissue. Histologic changes in the left ventricle were examined by light microscopy. The results showed that the higher the flow and pressure, the shorter the prearrest period, the better the flow distribution, and the faster the myocardial temperature drop. Mean aortic root pressures higher than 110 mm Hg and peak flow rates greater than 1500 ml/min caused a higher incidence of mechanical-physical trauma to the vascular endothelium and the endocardium, but cellular protection was good. Low pressure (less than 30 mm Hg) and peak flows (less than 125 ml/min) showed a higher incidence of cellular (myocardial) ischemia, focal necrosis, and uneven flow distribution. An aortic root pressure of 61 +/- 5 mm Hg, a mean peak flow rate of 622 +/- 52 ml/min, and a total flow of 600 ml for the first injection seem to offer the best cellular protection with minimal physical injury to the endothelium and endocardium for a mean canine heart weight of 236 gm.

Coronary Blood Flow During Exercise Following Nonselective and Selective α1Adrenergic Blockade with Indoramin

Studies were performed to compare the effects of alpha 1-adrenergic blockade with indoramin and nonselective alpha-adrenergic blockade with phentolamine on coronary blood flow and myocardial oxygen consumption during exercise. Nine dogs trained to run on a motor-driven treadmill were instrumented with electromagnetic flowmeter probes on the left circumflex coronary artery, and aortic and coronary sinus catheters for determination of myocardial arteriovenous oxygen difference. During control conditions, myocardial oxygen consumption and coronary blood flow increased as a direct function of heart rate during exercise. Phentolamine caused a significant decrease in blood pressure, while heart rate, coronary blood flow, and myocardial oxygen consumption were significantly increased at rest and during all exercise stages. Although alpha 1-adrenergic blockade with indoramin caused a similar reduction of arterial pressure, heart rate was unaltered both at rest and during exercise. Coronary blood flow and myocardial oxygen consumption were unchanged by alpha 1-adrenergic blockade at rest and during light exercise: however, during the heaviest exercise stages alpha 1-blockade caused a significant decrease in myocardial oxygen consumption. These findings are in agreement with the concept that phentolamine, by blocking presynaptic alpha 2-adrenoceptors which normally modulate norepinephrine release, increases sympathetic activity during exercise while indoramin, by acting as a selective alpha 1-adrenergic blocker, does not produce this effect.

Relaxations of Isolated Rabbit Coronary Artery by Purine Derivatives

The pharmacological nature of purinoceptors in the rabbit coronary artery was investigated by comparing the extent of vasorelaxation induced by various purine derivatives, with or without amino group at C6 and with or without ribose at N9 in the purine structure. These derivatives were grouped according to structure--adenosine, inosine, adenine, and hypoxanthine analogs. The vasorelaxations produced by adenosine analogs were inhibited by aminophylline, while relaxations produced by the other three groups were unaffected. In the case of adenosine analogs, modification of amino group at C6 to secondary amine resulted in reduction of the potency of the vasorelaxing effect. The order of potency was as follows: adenosine greater than N6-(L)-phenylisopropyladenosine greater than N6-(D)-phenylisopropyladenosine greater than N6-cyclohexyl-adenosine greater than N6-(2,5-dioxo-3-pyrrolidinyl)-adenosine greater than kinetine riboside greater than N6-methyladenosine. On the other hand, the aminophylline-resistant relaxations of adenine analogs were augmented by modification of amino group at C6 to secondary or to tertiary amine. The order of potency was as follows: 6-cyclohexylaminopurine greater than 6-dimethylaminopurine greater than kinetine greater than 6-methylaminopurine adenine. Of adenosine, N6-cyclohexyladenosine, adenine, C6-cyclohexylaminopurine, and inosine, N6-cyclohexylaminopurine was the most potent phosphodiesterase inhibitor of crude enzyme prepared from rabbit aorta. From the order of potency of relaxations produced by adenosine analogs, adenosine receptors in the rabbit coronary artery seem to be of the A2-subtype. The relaxation induced by aminophylline-resistant adenine analogs may be due to activation of an unknown but specific site, since there is a structure-activity relationship in the relaxations produced by this group. Such relaxations may be linked to inhibition of phosphodiesterase in the rabbit coronary artery.

Measurement of flow in large veins by the continuous thermodilution method.

Simple methods for measuring percutaneously blood flow in veins characterized by a large oscillatory component of flow are lacking. Therefore, a thermodilution technique with a constant infusion rate was used for the measurement of inferior vena cava flow in anesthetized dogs. The accuracy of the method was studied both in an artificial circuit and in in vivo experiments. The thermal catheter was introduced upstream in a flow of water ranging from 50 to 1,200 ml/min produced in an artificial circuit maintained at 37 degrees C. With a volume of cold injectate of 43 ml/20s, the correlation between the values obtained by direct measurement and by thermodilution technique was highly significant (r = 0.993; n = 37) with a slope practically equal to 1.0 (Y = 1.03 X + 2.42). With the thermal catheter introduced through the jugular vein and an electromagnetic flowmeter probe placed around the exposed vessel, volumetric flows were registered in the subhepatic vena cava, infrarenal vena cava, as well as renal and iliac veins of eight dogs. Comparison of the values obtained by the two techniques yielded a regression equation of Y = 0.96 X + 34.31 with a correlation coefficient r = 0.943 (range 50-1,000 ml/min; n = 40). The continuous injection method was as accurate at low flows as at high. Qualitatively, thermodilution curves were comparable to electromagnetic flowmeter curves, reproducing instantaneously the cyclic respiratory variations. The method is thus particularly suitable for use in those veins in which there is a large oscillatory component of flow.

Change in pulmonary and systemic circulation in acute ventricular septal defect.

The correlation between left to right ventricular (L-R) shunt flow and other hemodynamic changes was studied in 16 dogs with an acute ventricular septal defect (VSD) and normal pulmonary vascular bed. The interventricular shunt flow was measured directly with a specially designed electromagnetic flowmeter probe, where the area of the VSD was constant. The sudden presentation of VSD increased pulmonary arterial pressure, pulmonary flow and left ventricular end-diastolic pressure. L-R shunt flow was not changed significantly by atrial pacing except when the rate was increased to over 200/min. Dogs with a VSD were treated with isoproterenol and dextran to vary the shunt flow and hemodynamic parameters. L-R shunt flow was decreased by isoproterenol and increased by dextran loading. The percentage changes of L-R shunt flow from pre-drug values correlated well with the change in left ventricular end-diastolic pressure (r = 0.75) and the ratio of pulmonary to systemic vascular resistance (r = -0.73). Change in total pulmonary vascular resistance had a greater effect on L-R shunt flow than did a change in systemic vascular resistance, whereas a change in aortic flow had less effect (r = 0.35) on L-R shunt flow than did a change in preload and afterload. The time to peak LV dP/dt, as an index of cardiac contractility, and heart rate were not correlated with the relative change in L-R shunt flow. These results indicate that L-R shunt flow induced by the sudden presentation of a VSD varied with changes in the pulmonary and systemic circulation.

Coronary and Systemic Hemodynamic Effects of Tetramethylpyrazine in the Dog

The hemodynamic effects of tetramethylpyrazine were examined in 27 anesthetized open chest dogs with electromagnetic flowmeter probes on the left circumflex coronary artery and ascending aorta. Tetramethylpyrazine, 2-15 mg/kg i.v., caused prominent systemic and coronary vasodilation, with a maximum reduction of mean aortic pressure from 92 +/- 5 mm Hg during control conditions to 62 +/- 7 mm Hg (p less than 0.01), a peak increase in cardiac output from 3.0 +/- 0.4 to 4.1 +/- 0.7 L/min (p less than 0.05), and a peak reduction of systemic vascular resistance from 2,450 +/- 400 to 1,210 +/- 329 dyne X s X cm-5 (p less than 0.01). Simultaneously, heart rate increased from 143 +/- 9 to 174 +/- 8 beats/min (p less than 0.01), and maximum left ventricular dP/dt increased from 2,410 +/- 120 to 4,020 +/- 60 mm Hg/s (p less than 0.01). Dose-related increases of coronary blood flow occurred from 37.3 +/- 3.7 to a maximum of 74.1 +/- 6.6 ml/min (p less than 0.01), while mean coronary vascular resistance decreased from 1,770 +/- 240 to 700 +/- 260 dyne X s X cm-3 (p less than 0.01). Myocardial oxygen consumption increased in proportion to the increase in coronary blood flow. Following beta-adrenergic blockade with propranolol (1 mg/kg, i.v.), ganglionic blockade with hexamethonium, or catecholamine depletion with reserpine (1.0 mg/kg, i.p.), the systemic and coronary vasodilator effects of tetramethylpyrazine persisted, but the increases in heart rate, maximum left ventricular dP/dt, and myocardial oxygen consumption were markedly attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of indomethacin on coronary blood flow during graded treadmill exercise in the dog.

This study tested the hypothesis that metabolites of arachidonic acid may contribute to the coronary vascular response to physiological increases of myocardial O2 consumption that occur during exercise. Studies were performed in eight chronically instrumented dogs with electromagnetic flowmeter probes on the left circumflex coronary artery and aortic and coronary sinus catheters. Data were obtained at rest and during graded treadmill exercise during control conditions and after administration of the cyclooxygenase inhibitor indomethacin. During control conditions heart rate, aortic pressure, and coronary blood flow increased progressively during exercise; this was accompanied by a significant increase in myocardial O2 extraction, as evidenced by a decrease in coronary venous O2 tension (Po2) particularly during the first stage of exercise. Indomethacin (5 mg/kg iv) resulted in marked blunting of the coronary vasodilator response to intracoronary arachidonic acid in anesthetized open-chest dogs. After administration of indomethacin to awake dogs, resting heart rate, aortic pressure, and coronary venous Po2 were unaltered, and the response of these variables to exercise was not changed. The increase in coronary blood flow during exercise was also unchanged after indomethacin, so that the relationship between myocardial O2 consumption and coronary blood flow was unaltered by cyclooxygenase inhibition. Thus we were unable to demonstrate a significant effect of the prostaglandin system in mediating the coronary vascular response to exercise.

Circulatory Responses to Midazolam Anesthesia

Experiments were performed on nine dogs instrumented with pulmonary artery Swan-Ganz catheters and catheters placed into the distal aorta and posterior caval vein. Electromagnetic flowmeter probes were placed around the portal vein and hepatic artery, and the portal vein was cannulated. A week later, systemic and splanchnic circulatory variables were studied before and after 10 mg/kg of midazolam given intravenously. Three minutes after injection, heart rate increased 26% (P less than 0.006), cardiac index decreased 15% (P less than 0.001), portal flow increased 19% (P greater than 0.05), and hepatic arterial flow decreased slightly (P less than 0.002). Later, portal blood flow decreased 17% below baseline values (P less than 0.006). The biphasic response of portal blood flow to midazolam is probably related to redistribution of blood within the splanchnic system (blood mobilization from spleen and intestine). It is suggested that because maintenance of cardiac output during midazolam anesthesia depends on compensatory mechanisms, failure to increase cardiac output with compensatory increases in heart rate, contractility, and blood volume mobilization from the splanchnic circulation could result in decreased cardiac output.

Effect of nitroglycerin and nifedipine on subendocardial perfusion in the presence of a flow-limiting coronary stenosis in the awake dog.

SUMMARY. This study examined the effects of nitroglycerin and nifedipine on the transmural distribution of myocardial blood flow when ischemia-induced vasodilation of the distal coronary vasculature caused a proximal coronary stenosis to become flow-limiting. Studies were performed in chronically instrumented awake dogs with electromagnetic flowmeter probes and hydraulic occluders on the left circumflex coronary artery. Myocardial blood flow was estimated with 15|i radioactive microspheres. During control conditions, subendocardial (endo) flow significantly exceeded subepicardial (epi) flow (endo:epi = 1.33 ± 0.12). Following a 10-second coronary occlusion, reactive hyperemia occurred with excess arterial inflow resulting in 330 ± 37% blood flow debt repayment. This response was not altered by nitroglycerin (0.015 mg/kg, iv), but was decreased by nifedipine (0.01 mg/kg, iv) to 175 ± 38%, indicating depression of the coronary vasodilator response to a brief ischemic stimulus. When, following a 10-second occlusion, arterial inflow was limited to the preocclusion rate by a proximal stenosis, subepicardial flow increased at the expense of hypoperfusion of the subendocardium (endo/epi decreased to 0.50 ± 0.04; P < 0.01), and the continuing subendocardial ischemia resulted in augmentation of the subsequent reactive hyperemia (debt repayment = 556 ± 5%; P < 0.01). Both nitroglycerin and nifedipine abolished the augmentation of the reactive hyperemic response which occurred when a total occlusion was followed by an interval of coronary stenosis. This effect was associated with enhanced subendocardial blood flow during the interval of restricted inflow, suggesting that both of these agents alleviate the subendocardial hypoperfusion and ischemia which occur in the presence of a proximal flow-limiting coronary stenosis. (Ore Res 50: 678-687, 1982)

Effect of perfusion pressure distal to a coronary stenosis on transmural myocardial blood flow.

We tested the hypothesis that reductions of perfusion pressure distal to a flow-limiting coronary artery stenosis can directly impair perfusion of the subendocardial myocardium. Dogs were instrumented with an electromagnetic flowmeter probe and a variable occluder on the proximal left circumflex coronary artery. Coronary perfusion pressure was measured with a catheter distal to the occluder. Coronary autoregulation was abolished by intraarterial infusion of adenosine to produce maximal coronary vasodilation. The transmural distribution of myocardial blood flow was measured with radioactive microspheres during unimpeded arterial inflow, when the occluder was progressively narrowed to reduce distal coronary pressure to approximately 70%, 50% and 35% of the control coronary perfusion pressure, and during total coronary occlusion. Heart rate, left ventricular diastolic pressure and the fraction of coronary artery flow during systole remained constant throughout the study. Progressive reductions of coronary perfusion pressure were accompanied by direct reductions of the subendocardial/subepicardial blood flow ratio (r = 0.83). Examination of the relationship between myocardial blood flow and coronary perfusion pressure showed that blood flow decreased linearly with perfusion pressure, with flow ceasing at a positive pressure (zero-flow pressure). Blood flow data from four transmural myocardial layers from epicardium to endocardium showed that this zero-flow pressure increased progressively from 10 +/- 2.1 mm Hg in the subepicardium to 18 +/- 2.3 mm Hg in the subendocardium (p less than -.01). Consequently, as coronary pressure was reduced, the zero-flow pressure represented a progressively greater fraction of coronary pressure in the subendocardium than in the subepicardium. This effect appeared to account for the progressive redistribution of blood flow away from the subendocardium that occurred as coronary pressure was decreased. Myocardial vascular resistance did not change as a result of changes in coronary perfusion pressure.

Electromagnetic measurements of duodenal digesta flow in cannulated sheep.

Studies of duodenal digesta flow were made in sheep implanted with an electromagnetic flowmeter probe on the ascending and transverse duodenum and in sheep equipped in the ascending duodenum with a 'Y'-type or 'Ash'-type reentrant cannula or with a 'special simple' cannula. The flow of digesta was recorded between one week and 5 months after surgery. Patterns of the digesta flow through the individual systems of cannulation were compared with that of an implanted probe used as a reference. The order of similarity was Ash reentrant cannula less than Y reentrant cannula less than special simple cannula. The rate of digesta flow was similar for the probe, the Ash reentrant cannula with a one-way valve and the special simple cannula, but it was lower for the Y reentrant cannula due to frequent oscillation of the digesta. It was concluded that accurate quantitative electromagnetic measurements of duodenal digesta flow can now be performed in sheep fitted with the Ash-type reentrant cannula equipped with a one-way valve.

Transposition response, a cardiovascular response to change of habitat in the rat.

Aortic flow and arterial pressure were observed in conscious rats by means of an electromagnetic flowmeter probe implanted around the ascending aorta and an arterial cannula inserted into the abdominal aorta through a femoral artery. When the rat was transposed to a new box from its usual one, heart rate, cardiac output and peak flow acceleration were increased but arterial pressure remained unchanged. Total peripheral resistance was decreased. This response complex of the cardiovascular system to change of habitat was designated as "transposition response." After beta adrenoceptor blockade with propranolol, transposition no longer increased heart rate, cardiac output or peak flow acceleration but markedly increased arterial pressure and total peripheral resistance. The response was essentially unchanged by atropinization or adrenalectomy. Besides cardiac excitation and adrenergic vasoconstriction, the response includes a beta adrenergic vasodilatation, which is at least in part mediated by transmitters released at the sympathetic nerve endings and presumably equivalent to the cholinergic vasodilatation in the cat and dog.

Effects of nitroglycerin and propranolol on the distribution of transmural myocardial blood flow during ischemia in the absence of hemodynamic changes in the unanesthetized dog.

Chronically instrumented awake dogs were used to study the effects of nitroglycerin and propranolol on the transmural distribution of myocardial blood flow during transient ischemia. Studies were carried out 7-14 d after implantation of an electromagnetic flowmeter probe and balloon occluder on the left circumflex coronary artery, placement of epicardial minor axis sonar crystals, and implantation of left atrial, left ventricular, and aortic catheters. The occluder was inflated to completely interrupt flow for 10 s followed by partial release to reestablish flow at 60% of the preocclusion level. During this partial release, which served as the control for the study, regional myocardial blood flow was measured with 7- to 10-mum radioactive microspheres. After control measurements, seven dogs were given nitroglycerin (0.4 mg i.v.) and eight dogs propranolol (0.2 mg/kg i.v.). 5 min later the occlusion and partial release sequence was repeated, and regional myocardial blood flow was measured when heart rate, aortic and left ventricular end-diastolic pressure, and minor axis diameter were unchanged from control values.The data values were selected so that total flow to the ischemic region during partial release after nitroglycerin or propranolol administration was not significantly different from flow during the control partial release. After nitroglycerin administration, endocardial flow (endo) in the ischemic region increased from 0.46+/-0.07 to 0.59+/-0.06 ml/min per g (P < 0.006); epicardial flow (epi) decreased from 0.78+/-0.09 to 0.70+/-0.08 ml/min per g (P < 0.04). The endo:epi ratio increased from 0.65+/-0.07 to 0.92+/-0.10 (P < 0.05). In contrast, administration of propranolol produced no significant change in transmural flow (endo, 0.42+/-0.02 and 0.46+/-0.03 ml/min per g; epi, 0.71+/-0.06 and 0.70+/-0.07 ml/min per g) or in the endo:epi ratio (0.60+/-0.03, 0.66+/-0.06) in the ischemic region. Nitroglycerin and propranolol produce different effects on the transmural distribution of blood flow to ischemic myocardium. Nitroglycerin can increase blood flow to the underperfused endocardium in the absence of alterations in heart size, hemodynamic parameters, and total transmural flow to the ischemic region. Under similar conditions, propranolol has no significant effect on the transmural distribution of blood flow to an ischemic region.

Limits of sensitivity of radiopertechnetate flow studies in the detection of asymmetrical renal perfusion.

A canine model has been devised using electromagnetic flowmeter probes to study the sensitivity of radiopertechnetate renal angiography. Highly significant correlations were obtained when the measured flow rates were compared with normalized values of the peak activity and uptake slopes for each kidney. Analysis of the data suggests the unilateral renal disease associated with less then 20% difference in flow between the kidneys may not be diagnosed reliably from the pertechnetate perfusion test.