Differences in regional oxygen supply, oxygen consumption and blood flow during the onset of E. coli sepsis.
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Animals↗
Biomedical subjects
H J Beijer
Publications and source records attributed to H J Beijer.
Control of O2 supply to the pancreas during a cholecystokinin-induced increase in metabolism.
In the anesthetized dog, the pancreatic excretion of enzymes and the pancreatic blood flow were stimulated by a cholecystokinin (CCK) shot of 1 U/kg iv. The question raised was: is this augmented blood flow a metabolically controlled hyperemia or is it independent of the metabolic performance. After the administration of CCK, blood flow as well as O2 consumption were increased, while O2 extraction initially remained unchanged but later it increased. Capillary density, mitochondrial O2 consumption, capillary PO2 and cellular PO2 were calculated, using the model of the metabolic control of tissue oxygenation. The changes mentioned above could be simulated rather exactly. These simulations revealed that during the CCK stimulation of the pancreas is able to control its O2 supply through a fast decrease of the arteriolar resistance and a slow capillary recruitment. Thus, by a metabolic control the oxygen is sufficiently supplied to the pancreatic tissue.
Animals↗
Control of O2 supply to the pancreas during a vasopressin-induced vasoconstriction.
In the anesthetized dog, the metabolic level of the pancreas was elevated by a secretin infusion (1.2 U/kg/hr iv), displaying a metabolic control of tissue oxygenation and blood flow. Question was raised how this system would response to a decrease in O2 supply, as induced by increasing doses of vasopressin (2-131 mU/kg, iv). These vasopressin administrations progressively diminished blood flow (down to 20%), as well as secretory rate (down to 7%) and O2 consumption (down to 33%). The O2 extraction was increased up to 227%. Capillary density, mitochondrial O2 consumption, capillary PO2 and cellular PO2 were calculated by simulating these data with the model of the metabolic control of tissue oxygenation. The changes mentioned above could be simulated adequately. These simulations revealed that a. in the pancreas vasopressin primarily increases arteriolar resistance; the inhibition of metabolism is secondary to the vasopressin-induced vasoconstriction. b. The pancreas responds with a small compensatory capillary recruitment (up to 29%), which in itself would increase tissue oxygenation. c. The main consequence of the lowering of blood flow is a dramatic decrease of mean capillary PO2 (down to 38%), as well as a lowering in mean cellular PO2 (down to 41%). This lowering of O2 supply to the tissue will slow down the metabolic rate, as evidenced by the decrease of the volume of the excretion.
Animals↗
Feto-placental circulatory competence.
Doppler assessment of the pulsatility index (PI) of umbilical artery blood velocities offers promise as a simple, non-invasive method for early diagnosis of placental failure. The present report identifies the hemodynamic factors determining this PI, based on current knowledge of feto-placental physiology. It is postulated that the umbilical artery PI is mainly determined by the ratio of capillary to arterial resistances in the fetal placental circulation. However, the biological PI variations on a minute by minute basis are caused by short-term variations in blood pressure pulsatility. The ratio of resistances declines markedly with advancing pregnancy, indicating that the site of predominant resistance determining the volume of placental blood flow gradually migrates from the peripheral capillary to the arterial compartment. After 28 wk of gestation, umbilical artery PI values decrease below 1, reflecting the normal reserve capacity of the functional capillary bed of the placenta. PI values above 1 in the last trimester reflect a critical enhancement of placental capillary resistance, which must impede blood flow to functional chorionic villi. It is concluded that this Doppler technique may provide a simple method for clinical assessment of placental circulatory competence.
Aorta↗
Control of O2 supply to the stimulated exocrine pancreas.
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Animals↗
Antidiuretic effect of ritodrine with and without beta-adrenergic blockade.
Dose-related effects of ritodrine and ritodrine combined with metoprolol on urinary excretion rate were studied in anesthetized dogs. Urine production was abruptly reduced after a total dose of 4 micrograms.kg-1 of ritodrine. This effect could not be antagonized by metoprolol, although the ritodrine-induced decrease of mean arterial pressure and renal arterial blood flow was significantly inhibited. The possible role of fluid retention during tocolytic treatment, even with beta-adrenergic blockade, in the etiology of pulmonary edema is discussed with a review on recent literature.
Adrenergic beta-Antagonists↗
Cholinergic and pancreatic actions of purified porcine and synthetic vasoactive intestinal peptide (VIP).
In this study the vascular effects of VIP were studied in connection with its secretory performances in the pancreas and the liver. In anesthetized dogs pancreatic blood flow was measured parallel with measurement of bile and pancreatic secretion. VIP was injected intravenously at intervals of 1 minute in amounts of 1-2048 ng.kg-1. Striking conductance increases were observed in the pancreatic vascular beds ranging from an increase of 400% (pancreatic branch of splenic a.) to an increase of 80% (inferior pancreatic duodenal a.). Pancreatic secretion increased from 0 to 408 microliters.min-1 and bile secretion from 95 to 145 microliters.min-1. VIP has powerful vasodilating effects on pancreatic vascular beds accompanying pancreatic secretion and bile secretion. Porcine VIP and 2 synthetic VIP analogues exhibited similar hemodynamic and metabolic actions. Although a correlation between vascular and metabolic effects possibly exists, the effects of VIP on gut vessels and pancreatic secretory cells are most probably separate events: at low VIP doses increase in conductance was observed without a concomitant increased secretion. A possible role of VIP maintaining an adequate blood supply to the pancreas is discussed.
Animals↗
Cardiovascular effects of ritodrine are blocked by metoprolol in the anesthetized dog.
Inhibition of ritodrine-induced cardiac and peripheral vascular effects by the beta 1-adrenergic blocker metoprolol, was studied by electromagnetic flow measurements in anesthetized dogs. As expected, metoprolol inhibited the ritodrine-induced/increased cardiac workload and heart rate. Metoprolol also inhibited ritodrine-induced peripheral vasodilation. This leads to questions about the cardiac beta 1-adrenergic selectivity of metoprolol. Regarding earlier studies showing no interference in labor inhibition, the combination of ritodrine and metoprolol might be useful in treatment of preterm labor, while economizing cardiovascular performance centrally as well as peripherally.
Anesthesia↗
Pancreatic O2 consumption and CO2 output during secretin-induced, exocrine secretion from the pancreas in the anesthetized dog.
Secretin stimulates pancreatic water and CO2 excretion as well as pancreatic blood flow. It has been questioned whether the production (i.e. water and CO2 excretion) is reflected in the input-output difference of nutrients. In pentobarbital anesthetised dogs, pancreatic exocrine secretion was stimulated by secretin (Karolinska), 1 U/kg injected as an i.v. bolus. Secretion was maximally increased at 2 min after the secretin shot and returned to a basal value at between 16 and 32 min after secretin. Blood flow was also maximally increased at 2 min, but decreased to the basal value at between 8 and 16 min. O2 extraction first decreased (at 2 min) and then gradually increased until it was higher than the basal value (at 16 min) and then returned to the basal level (at 32 min). O2 consumption increased quickly, reached a plateau, lasting from 1 to 16 min, and then decreased to the basal level (32 min). CO2 transfer from blood to tissue reached a maximum at 4 min and then decreased to the basal value (at between 16 and 32 min). The curves for CO2 transfer from tissue to pancreatic secretion and for CO2 in the secretion had the same shape. It is concluded that the curve of production (of water and CO2 excretion) parallels the curve of O2 consumption fairly well. The O2 consumption curve did not correlate either with the blood flow curve or with the O2 extraction curve. About one quarter of the excreted CO2 originated from pancreatic metabolism and the remaining three quarters were transferred from blood, through the pancreatic tissue into the secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia, General↗
A vasopressin-induced decrease in pancreatic blood flow and in pancreatic exocrine secretion in the anesthetized dog.
Vasopressin decreases blood flow as well as secretory flow in the pancreas. The question raised was whether the blood flow decrease is the determinant of the decrease in secretion or quite the reverse. In pentobarbital anesthetized dogs, secretory flow was first increased to a steady level by infusion of secretin. At this steady state, O2 consumption and O2 extraction were increased, while blood flow remained at the control level, indicating an increase in the area available for exchange i.e. an increase in capillary density. At increasing doses of vasopressin, secretory flow decreased, arterial flow decreased, and O2 extraction increased, while O2 consumption decreased and venous-arterial CO2 concentration difference was not changed. At the same time CO2 transport decreased, CO2 concentration in the secretion was unchanged and CO2 output in the secretion was decreased. The decrease in blood flow was always seen about 25 s before the decrease in secretory flow, strongly suggesting that the decrease in blood flow induced the decrease in secretory flow. A higher dose of vasopressin was required to decrease the O2 consumption (i.e. this effect was less sensitive) than to increase O2 extraction. The decrease in secretory flow and the decrease in blood flow showed an intermediate sensitivity. So O2 consumption seems to be preserved at a high level by the increase in O2 extraction. It is concluded that the vasopressin-induced decrease in blood flow is the determinant of the decrease in secretory flow. This phenomenon is discussed in terms of the model for metabolic control of tissue oxygenation.
Anesthesia, General↗
Characteristics of flow velocities in the umbilical arteries, assessed by Doppler ultrasound.
Measuring blood velocities by Doppler ultrasound has introduced a new noninvasive technique into obstetrical diagnostics. This study evaluates the information about fetoplacental hemodynamics that can be extracted from Doppler signals obtained from umbilical arteries. The most significant blood flow characteristic is blood flow pulsatility expressed as pulsatility index (PI). The PI is the difference between systolic and diastolic velocity, divided by the mean velocity. The PI strongly correlates with downstream impedance to flow. It is demonstrated that sophisticated spectral analysis of the Doppler signals has no practical advantages over the simple zero-crossing technique for establishing PI values, since blood flow in umbilical arteries has a blunt-to-flat profile. This study shows that the PI is a gestational-age-related, intra- and inter-observer-reproducible variable. The significant decrease of PI values with advancing gestational age reflects a progressive reduction of placental vascular resistance to umbilical blood flow. The PI holds promise as a simple method for early diagnosis of impaired umbilical circulation.
Blood Flow Velocity↗
Effects of furosemide on biliary secretion, pancreatic blood flow, and pancreatic exocrine secretion.
The effects of furosemide on biliary secretion and on pancreatic hemodynamics and exocrine function were studied by quantitative flowmetry and timed collections of biliary and pancreatic exocrine secretion in the anesthetized dog. Biliary flow and the output of its components (Na+, K+, Ca, Mg, 3-OH bile salts, and bilirubin) increased significantly following a furosemide injection of 0.6 mg/kg and rose progressively to 75-150 per cent above basal levels as the furosemide dose was increased to 9.6 mg/kg. Pretreatment with secretin had no influence on furosemide-induced biliary secretion. Furosemide doses of 4.8 and 9.6 mg/kg increased blood flow in the superior pancreaticoduodenal arterial bed by 30-60 per cent but did not alter flow in the inferior pancreaticoduodenal arterial bed or the pancreatic branch of the splenic artery. However, small increases were seen in flow in the latter two arterial beds after furosemide when secretin administration preceded furosemide. Basal pancreatic secretion was not affected by furosemide, but pretreatment with a submaximal sustaining infusion of secretin uncovered a furosemide action to increase pancreatic exocrine flow and the outputs of Na+, K+, Ca, Mg, and enzymes by 25-35 per cent. These data extend previous studies of the gastrointestinal vasodilator effects of furosemide to the pancreatic circulation and previous data demonstrating furosemide-induced ionic transport in nonrenal systems to biliary, pancreatic acinar, and ductular transport in both organs. Whether the augmentation of pancreatic blood flow is secondary to enhanced ion transport in the exocrine pancreas or to an effect on ionic cotransport in vascular smooth muscle is unknown.
Animals↗
The effect of norepinephrine, isoprenaline and acetylcholine on the testicular and epididymal circulation in the pig.
Blood flow to the testis and epididymis of 7 anaesthetized male pigs was measured using electromagnetic blood flow sensors. An average blood flow to the testis of 12 ml/min/100 g and in the epididymal arteries of 19 ml/min/100 g was measured. The effect of intravenously administered norepinephrine, isoprenaline and acetylcholine on alpha and beta 2 adrenergic and cholinergic receptor sites, respectively, was investigated. As neither norepinephrine nor isoprenaline, nor acetylcholine changed vascular conductance of the testis, we could not demonstrate adrenergic and cholinergic receptor activity. The possibility of autonomic regulation by the nonvascular smooth muscles of the spermatic cord and the inner layer of the tunica albuginea has been discussed.
Acetylcholine↗
Hemodynamic splanchnic and renal changes associated with administration of arginine-hydrochloride in dogs.
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Abdomen↗
Hemodynamic actions of pentagastrin.
Pentagastrin (Peptavlon, ICI 50123) is known as a powerful stimulator of gastric acid secretion. Several authors have demonstrated a close relationship between gastric acid secretion and gastric blood flow. In this study the general hemodynamic properties of pentagastrin were investigated qualitatively and quantitatively. The study was performed on anesthetized mongrel dogs. Blood flow was assessed with non-cannulating electromagnetic flow probes. Pentagastrin was injected intravenously at intervals of 2 min in amounts between 1 ng and 8192 ng/kg, following a logarithmic scale. Pentagastrin dose-dependently increased splanchnic blood flow in a reversed U-shaped manner. The major vasoactivity occurred in two organ areas--the gastric area and the pancreatico-duodenal area. Pentagastrin increased blood flow in these areas to 300% and 350% of initial value, respectively, at a dose of 2-4 microgram/kg. Since heart rate, cardiac output, and arterial pressure were not influenced, pentagastrin had no general hemodynamic effect. This was confirmed by blood flow measurements in the renal a., common carotid a., and femoral a. It was therefore concluded that the splanchnic blood flow increase was due to an extreme decrease of splanchnic vascular resistance.
Animals↗
Time course and sensitivity of secretin-stimulated pancreatic secretion and blood flow in the anesthetized dog.
Time-effect relationship and sensitivity of pancreatic exocrine secretion and pancreatic blood flow were established, to test the supposition that blood flow to the pancreas is controlled by the secretory process. Pancreatic exocrine secretion rate was stimulated by incremental iv doses of secretin (Karolinska, 0.001--4 U/kg) in pentobarbital anesthetized dogs. Arterial pancreatic blood flow was measured by electromagnetic flowmeters; secretion rate was determined by measurement of frequency of consecutive secretory drops. Exocrine secretion rate and blood flow increased markedly. Secretion responded at a dose level 3-7 times lower than blood flow did. So at low secretory performance, the pancreas seemed to be well provided with basal blood supply. At moderate and high secretory levels blood flow did increase, but the flow increase was seen 16-22 sec before the secretion increase. So the additional support of blood flow in the secretory process occurred during the cellular preparation and during the start of the secretion increase. This suggests that secretion increase and blood flow increase are mediated by independent processes or receptors, but these processes seem to cooperate in processing the pancreatic juice.
Animals↗
The effect of secretin on peripheral arterial blood flow.
Arterial blood flow was measured in 18 arteries leading to nearly all major organs in the anesthetized dog, to obtain information about the specificity of the blood flow effects caused by secretin. This gastro-intestinal hormone was administered intravenously in a sequence of bolus injections (0.001--4 U/kg). Blood flow increase in the pancreatico-duodenal arteries was highest of all arteries observed. This flow increase in the superior pancreatico-duodenal artery was also found in its truncal artery (gastroduodenal a.), but to a less extend: the effect was diluted by the other--less reacting--branch (right gastro-epiploic a.) of the same truncal artery. We conclude that secretin preferentially increased blood flow in the pancreatico-duodenal arteries. Since secretin effects on heart rate and arterial pressure were but small, the flow increase in the pancreatico-duodenal area were caused by a lowering of the resistance of the pancreatico-duodenal vasculature. Comparison between the flow responses, elicited by secretin (Boots) and secretin (Karolinska), is discussed.
Animals↗
alpha- and beta-receptor blockade of isoproterenol- and norepinephrine-induced effects on regional blood flow and blood flow acceleration.
The effects of the beta-receptor blocking agent propranolol (100 microgram/kg i.v.) and of the alpha-receptor blocking agent dihydroergotamine (50 microgram/kg i.v.) on hemodynamic responses to isoproterenol and norepinephrine (both 1--1024 ng/kg) were investigated in anesthetized dogs. The effects studied were: (1) flow in the ascending aorta and the coronary, common hepatic, gastroduodenal, splenic, cranial mesenteric, renal and femoral arteries: (2) maximal flow acceleration in the splenic, cranial mesenteric and femoral arteries; (3) maximal rate of change of left ventricular pressure (LV dP/dt max). Propranolol shifted the dose-response curves for the isoproterenol-induced flow increases in the common hepatic, gastro-duodenal, and cranial mesenteric arteries to the right. It did not influence the flow responses to isoproterenol in the ascending aorta or the coronary, splenic, renal and femoral arteries. Propranolol prevented the decrease of arterial pressure evoked by isoproterenol. Propranolol shifted the isoproterenol-induced increase of LV dP/dt max and maximal blood flow to the same extent. Propranolol blocked the flow to the liver and gastrointestinal tract to a greater extent than the LV dP/dt max and maximal flow acceleration. Propranolol had no effect on the norepinephrine-induced increases in flow in the splenic, femoral and coronary arteries, but blocked the norepinephrine-evoked increases of flow accelerations and LV dP/dt max to the same extent. Dihydroergotamine inhibited the norepinephrine-induced increase in flow in the femoral artery and the decreases in flow in the hepatic, splenic, cranial mesenteric and renal arteries, and reversed the reduction of flow in the gastroduodenal artery. It is argued that dihydroergotamine may inhibit the increase in femoral flow through two mechanisms: (1) blocking the flow reduction to norepinephrine in the abdomen, and thereby passively shunting blood from the abdomen in preference to the femoral bed; (2) attenuating the norepinephrine-evoked reflexogenic femoral vasodilatation. It is concluded that: (1) propranolol is a beta-receptor blocking agent with a preference for blockade of isoproterenol-induced vascular effects; (2) norepinephrine-induced flow increases are not direct actions on vascular beta-receptors; (3) the increase of maximal blood flow accelerations after isoproterenol and norepinephrine is mediated by stimulation of cardiac beta-receptors; (4) dihydroergotamine is an alpha-receptor blocking agent particularly in the splanchnic vascular region.
Adrenergic alpha-Antagonists↗