Effect of amrinone on diaphragm blood flow

1988 ◽  
Vol 65 (4) ◽  
pp. 1506-1513 ◽  
Author(s):  
R. J. Bundy ◽  
J. S. Arnold ◽  
A. F. DiMarco ◽  
F. Hussein ◽  
G. S. Supinski
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Isometric Force ◽  
Vena Cava ◽  
Force Transducer ◽  
Mechanically Ventilated ◽  
Before And After ◽  
Tension Time ◽  
Vascular Beds

The purpose of the present study was to examine the effect of amrinone, a drug known to augment cardiac output and dilate peripheral vascular beds, on diaphragm blood flow. Studies were performed on 12 anesthetized mechanically ventilated dogs in which strips of left costal diaphragm were developed in situ. Strip blood flow was assessed with a drop counter attached to a catheter tied into the phrenic veins' draining strips. Strip tension was measured with an isometric force transducer. Amrinone was administered as an intravenous bolus of 2 mg/kg followed by a continuous infusion of 25 micrograms.kg-1.min-1. Amrinone increased cardiac output and resting diaphragm blood flow [from 1.8 +/- 0.1 to 3.2 +/- 3 (SE) l/min and from 13 +/- 2 to 29 +/- 6 (SE) ml.100 g-1.min-1, respectively, P less than 0.001 for both comparisons]. Amrinone also increased blood flow during periods of rhythmic contraction (tension time indexes of 0.1-0.4, P less than 0.05 for comparisons of flow with and without amrinone at each tension time index) and increased the magnitude of the postcontraction hyperemia (P less than 0.02 for comparisons of hyperemic flow with and without amrinone at tension time indexes of 0.3 and 0.4). Graded occlusion of the inferior vena cava produced reductions in arterial pressure, cardiac output, and diaphragm blood flow both before and after amrinone. Both cardiac output and diaphragm blood flow were greater after amrinone, however, at all levels of blood pressure examined. These findings indicate that amrinone can override diaphragm vasoregulatory systems and augment diaphragm blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of inhaled and intravenous acetylcholine on bronchial blood flow in anesthetized sheep

1996 ◽  
Vol 80 (1) ◽  
pp. 341-344 ◽  
Author(s):  
M. Scuri ◽  
V. McCaskill ◽  
A. D. Chediak ◽  
W. M. Abraham ◽  
A. Wanner
Keyword(s):  
Blood Flow ◽  
Systemic Arterial Pressure ◽  
Bronchial Mucosa ◽  
Anatomic Site ◽  
Bronchial Wall ◽  
Mechanically Ventilated ◽  
Lung Resistance ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Increased Blood Flow

The reported effects of cholinergic agonists on bronchial blood flow (Qbr) have been inconsistent. The aim of the present study was to determine whether the inconsistency could be due to the mode of agonist administration (systemic vs. aerosol) or the anatomic site of blood flow in the bronchus (mucosal vs. deep wall). In 10 anesthetized mechanically ventilated adult sheep, we measured Qbr in main bronchi by color-coded microspheres, systemic and pulmonary arterial pressures, cardiac output, and lung resistance (RL) before and after acetylcholine (ACh) administered either as an aerosol (nebulized dose 100 micrograms) or as an intravenous bolus (2 micrograms/kg). Before drug administration, 72% of mean Qbr was distributed to the bronchial mucosa and the remainder was distributed to the deep bronchial wall. For a comparable increase in mean RL (150% for intravenous ACh and 205% for aerosol ACh), mean total Qbr normalized for systemic arterial pressure increased by 291% after intravenous ACh (P < 0.05) and decreased by 9% after aerosol ACh (not significant). Mucosal and deep wall Qbr increased proportionally. Atropine (0.2 microgram/kg) prevented the changes in Qbr and RL after intravenous ACh. Thus intravenous but not aerosol ACh increased blood flow in the mucosa and deep wall of extrapulmonary bronchi. This suggests that the muscarinic receptors mediating vasodilation are more accessible to intravascular than intrabronchial ACh.

Hemodynamic effects of leukotriene C4 in ovine fetus

1990 ◽  
Vol 259 (6) ◽  
pp. E851-E855
Author(s):  
B. A. Meyer ◽  
S. W. Walsh ◽  
V. M. Parisi
Keyword(s):  
Blood Flow ◽  
Vena Cava ◽  
Cardiovascular Effects ◽  
In Vivo Studies ◽  
Leukotriene C4 ◽  
Blood Flows ◽  
Before And After ◽  
Placental Blood ◽  
Near Term

Leukotrienes are synthesized during pregnancy and produce cardiovascular effects in adults. We hypothesized that leukotriene C4 would cause vasoconstriction in the fetus and placenta. Eight near-term, unanesthetized ovine fetuses were studied before and after infusion of 10 micrograms leukotriene C4 (LTC4) into the fetal vena cava. Cardiovascular monitoring of maternal and fetal arterial pressures and heart rates was performed. Fetal blood flows were measured by the radioactive-microsphere technique. Sustained elevations in systolic and diastolic blood pressure and decreased fetal heart rate began by 1 min and returned to baseline by 30 min. Arterial pH fell from 7.33 +/- 0.01 to 7.29 +/- 0.01 at 15 min (P less than 0.05) and to 7.29 +/- 0.01 at 30 min (P less than 0.05), with a significant increase in base deficit from 0.7 +/- 0.7 to 3.5 +/- 0.7 at 15 min (P less than 0.05) and to 2.9 +/- 1.0 at 30 min (P less than 0.05). Fetal PO2 and PCO2 were unchanged. Significant decreases in blood flow and resistance were seen in the umbilical placental circulation as well as in fetal skeletal muscle and intestine. Blood flow and resistance were unchanged in the renal and adrenal vascular beds. Fetal administration of LTC4 caused no changes in maternal cardiovascular parameters. These findings represent the first in vivo studies of the effects of a lipoxygenase metabolite on fetal-placental blood flow.

Application and In situ calibration of a pulsed-doppler flowmeter for blood flow measurement in crustaceans

1994 ◽  
Vol 74 (2) ◽  
pp. 455-458 ◽  
Author(s):  
C.N. Airriess ◽  
B.R. McMahon ◽  
I.J. McGaw ◽  
G.B. Bourne
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
The Body ◽  
Pulsed Doppler ◽  
Arterial Perfusion ◽  
Non Invasive ◽  
In Situ Calibration ◽  
Flow Through ◽  
Doppler Flowmeter

The pulsed-Doppler flowmeter permits continuous, non-invasive measurement of blood flow through several arteries simultaneously. Summation of volume flow rates through all arteries leaving the heart allows determination of cardiac output, stroke volume, and the percentage of cardiac output delivered to each region of the body. The use of this system for investigating changes in arterial perfusion as well as its calibration in situ are described.

EFFECTS OF PROSTAGLANDIN F2α ON OVARIAN BLOOD FLOW AND VASCULAR RESISTANCE IN THE PSEUDOPREGNANT RABBIT

1975 ◽  
Vol 79 (2) ◽  
pp. 337-350 ◽  
Author(s):  
Per Olof Janson ◽  
Ivan Albrecht ◽  
Kurt Ahrén
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Prostaglandin F2α ◽  
Interstitial Tissue ◽  
Corpora Lutea ◽  
Luteal Function ◽  
Direct Measurements ◽  
Before And After

ABSTRACT In the search for data supporting the hypothesis that the luteolytic effect of prostaglandins (PG) is initiated by a vascular mechanism, some haemodynamic parameters including ovarian blood flow and vascular resistance were measured in pseudopregnant anaesthetized rabbits before and after exogenous administration of PGF2α. The measurements were performed on days 5–10 of pseudopregnancy induced by 500 IU HCG iv. Infusion of 50 μg/kg PGF2α iv over a one-minute period caused significant falls in cardiac output, heart rate and blood pressure after 1–3 min. Blood pressure and cardiac output were normalized after 16–49 min. Blood flow in the ovarian vein (direct measurements) decreased and returned to initial values parallel to the blood pressure and no change in resistance in the vascular bed drained by the vein was noted. Total ovarian blood flow and resistance, as measured in surgically intact ovaries before and after PG infusion, using 35 or 15 μm 169Yb and 46Sc-labelled microspheres, changed and remained constant respectively, according to the same pattern as in the direct measurements. The distribution of blood flow between the corpora lutea and the interstitial tissue of the ovary measured by 15 μm radioactive microspheres. PGF2α caused an interstitial vasodilation whereas no significant change in luteal vascular resistance was noted. Since luteal blood flow represented a predominant part of total ovarian flow in the type of ovary studied, the interstitial vasodilatation caused only negligible changes in blood flow to the whole ovary. The present study does not support the hypothesis of a PG-induced luteal blood flow reduction preceding luteolysis. The possible significance of the interstitial vasodilatation for luteal function remains to be elucidated.

Hemodynamic and renal effects of cross-linked hemoglobin infusion

1997 ◽  
Vol 272 (3) ◽  
pp. R793-R799 ◽  
Author(s):  
A. Cases ◽  
J. M. Stulak ◽  
Z. Katusic ◽  
E. Villa ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Sodium Excretion ◽  
Calcium Ionophore ◽  
Urinary Flow ◽  
Binding Effect ◽  
Scavenging Effect ◽  
Before And After ◽  
Vascular Beds

It is well known that hemoglobin binds nitric oxide (NO) and produces a pronounced vasoconstriction in isolated arteries. However, it is debatable whether such an effect takes place in whole animals, because hemoglobin also catalyzes the formation of prostaglandins from arachidonic acid. Short-term studies were performed to evaluate the effects induced by intravenous infusion of cross-linked hemoglobin (XL-Hb) on blood pressure (BP) and renal, iliac, and mesenteric flows, and on renal function in six anesthetized dogs. A similar volume-matched expansion with 6% dextran was used as a control (n = 6). Glomerular filtration rate (GFR), urinary flow, and total and fractional sodium excretion were measured before and after XL-Hb or dextran infusion to evaluate possible renal function changes. XL-Hb administration resulted in a 29% elevation in BP and a significant decrease of blood flow (30-37%) to the three vascular beds. XL-Hb did not alter GFR or sodium excretion, despite the increase in BP. In contrast, the administration of dextran did not significantly alter BP but induced a significant increase (6-13%) of blood flow in the three vascular beds. These changes were accompanied by threefold increases in urinary flow and sodium excretion without alterations in GFR. The binding effect of XL-Hb on NO was studied in isolated renal arteries in organ chambers. These in vitro studies showed that XL-Hb blunted the endothelium-mediated vasodilator response to calcium ionophore A-23187 and to acetylcholine. Our results demonstrate that XL-Hb administration is followed by hypertension, vasoconstriction, and blunted natriuresis. All these effects are compatible with the scavenging effect on NO attributed to XL-Hb.

Hemodynimic effects of systemic and central administration of clonidine in the monkey

1975 ◽  
Vol 228 (4) ◽  
pp. 1276-1279 ◽  
Author(s):  
P Bolme ◽  
RP Forsyth ◽  
T Ishizaki ◽  
KL Melmon
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Systemic Arterial Pressure ◽  
Intraventricular Injection ◽  
Central Administration ◽  
New Information ◽  
Before And After ◽  
Microsphere Method ◽  
Radioactive Microsphere Method

Systemic and regional hemodynamic changes were measured in restrained, conscious rhesus monkeys with indwelling arterial and venous catheters before and after clonidine (5 and 15 mug/kg) was slowly infused intravenously or smaller doses (2 mug/kg) were injected into a lateral cerebral ventricle. Dye-dilution cardiac outputs and the complete distribution of cardiac output were obtained intermittently with the use of the radioactive microsphere method. After the higher intravenous dose and the intraventricular injection, systemic arterial pressure was significantly lowered for 30-45 min. Both of these groups had similar changes in the redistribution of cardiac output and blood flow that outlasted the hypotensive period. Blood flow was maintained or increased in the hepatic and renal arteries at the expense of skin; flow to skeletal muscle and brain also decreased during the first hour. These data support previous studies that indicate that the primary action of clonidine is in the central nervous system and, in addition, add new information about the regional blood flow changes evoked by clonidine.

Contribution of Stenosis Resistance to the Rise in total Peripheral Resistance during Experimental Renal Hypertension in Conscious Dogs

1981 ◽  
Vol 61 (6) ◽  
pp. 663-670 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner ◽  
J. A. Angus ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Plasma Renin Activity ◽  
Renal Artery ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Vascular Beds ◽  
Renal Vascular

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.

Changes in Arterial Pressure during Mechanical Ventilation

2005 ◽  
Vol 103 (2) ◽  
pp. 419-428 ◽  
Author(s):  
Frédéric Michard
Keyword(s):  
Mechanical Ventilation ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vena Cava ◽  
Cardiac Preload ◽  
Physical Sign ◽  
Aortic Blood Flow ◽  
Mechanically Ventilated ◽  
Aortic Blood ◽  
Cyclic Changes

Mechanical ventilation induces cyclic changes in vena cava blood flow, pulmonary artery blood flow, and aortic blood flow. At the bedside, respiratory changes in aortic blood flow are reflected by "swings" in blood pressure whose magnitude is highly dependent on volume status. During the past few years, many studies have demonstrated that arterial pressure variation is neither an indicator of blood volume nor a marker of cardiac preload but a predictor of fluid responsiveness. That is, these studies have demonstrated the value of this physical sign in answering one of the most common clinical questions, Can we use fluid to improve hemodynamics?, while static indicators of cardiac preload (cardiac filling pressures but also cardiac dimensions) are frequently unable to correctly answer this crucial question. The reliable analysis of respiratory changes in arterial pressure is possible in most patients undergoing surgery and in critically ill patients who are sedated and mechanically ventilated with conventional tidal volumes.

Regional blood flows and cardiac output distribution in rats during acute anemia or polycythemia

1980 ◽  
Vol 58 (4) ◽  
pp. 411-415 ◽  
Author(s):  
U. Ackermann ◽  
A. T. Veress
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Output ◽  
Metabolic Factors ◽  
Nervous Control ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Normovolemic Anemia ◽  
Flow Changes ◽  
Vascular Beds

Radioactively labelled microspheres (15 μm diameter) were used to measure cardiac output (CO) distribution and blood flows in spleen, kidneys, and skeletal muscle before and after normovolemic anemia or polycythemia in anesthetized rats. Hematocrits were changed from 45 to 33% or from 45 to 59% by an exchange transfusion of homologous plasma or packed cells. Anemia was accompanied by a 39% increase in CO while polycythemia showed a 25% decrease. Following hemodilution the spleen as well as skeletal muscle received greater than normal fractions of CO and in each the flow increase was greater than expected from the fall in viscosity. The renal fraction of CO was unchanged. Following hemoconcentration "greater-than-normal" fractions of CO were distributed towards spleen and kidney. In these tissues the changes in flow were significantly greater than the change in resistance due to viscosity. Skeletal muscle flow changes appeared to have been due mostly to increased viscosity. These observations imply that during acute, isovolemic changes in hematocrit, the flow changes of individual vascular beds cannot be explained by viscosity changes alone but the importance of nervous control or of local metabolic factors remains to be investigated.

Regulation of blood flow in adipose tissue: involvement of the cholinergic system

2015 ◽  
Vol 309 (1) ◽  
pp. E55-E62 ◽  
Author(s):  
Richard Sotorník ◽  
Jean-Patrice Baillargeon ◽  
Maude Gagnon-Auger ◽  
Julie Ménard ◽  
Pascal Brassard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Cholinergic System ◽  
Control Site ◽  
Healthy Individuals ◽  
Vasoactive Agents ◽  
Before And After ◽  
Subcutaneous Adipose

Acetylcholine (Ach) has vasodilatory actions. However, data are conflicting about the role of Ach in regulating blood flow in subcutaneous adipose tissue (ATBF). This may be related to inaccurate ATBF recording or to the responder/nonresponder (R/NR) phenomenon. We showed previously that healthy individuals are R (ATBF increases postprandially by >50% of baseline BF) or NR (ATBF increases ≤50% postprandially). Our objective was to assess the role of the cholinergic system on ATBF in R and NR subjects. ATBF was manipulated by in situ microinfusion of vasoactive agents (VA) in AT and monitored by the 133Xenon washout technique (both recognized methods) at the VA site and at the control site. We tested incrementally increasing doses of Ach (10−5, 10−3, and 10−1 mol/l; n = 15) and Ach receptor antagonists (Ra) before and after oral administration of 75-g glucose using atropine (muscarinic Ra; 10−4 mol/l, n = 13; 10−5 mol/l, n = 22) and mecamylamine (nicotinic Ra; 10−3 mol/l, n = 15; 10−4 mol/l, n = 10). Compared with baseline [2.41 (1.36–2.83) ml·100 g−1·min−1], Ach increased ATBF dose dependently [3.32 (2.80–5.09), 6.46 (4.36–9.51), and 10.31 (7.98–11.52), P < 0.0001], with no difference between R and NR. Compared with control side, atropine (both concentrations) had no effect on fasting ATBF; only atropine 10−4 mol/l decreased post-glucose ATBF [iAUC: 1.25 (0.32–2.91) vs. 1.98 (0.64–2.94); P = 0.04]. This effect was further apparent in R. Mecamylamine had no impact on fasting and postglucose ATBF in R and NR. Our results suggest that the cholinergic system is implicated in ATBF regulation, although it has no role in the blunting of ATBF response in NR.

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