EFFECT OF THE NEW ALPHA2-ADRENERGIC AGONIST MIVAZEROL ON METABOLISM AND BLOOD FLOW OF ISCHEMIC MYOCARDIUM IN ANESTHETIZED DOGS

1994 ◽  
Vol 81 (SUPPLEMENT) ◽  
pp. A758
Author(s):  
P. M. H.J. Roekaerts ◽  
F. W. Prinzen ◽  
H. W. W. Willigers ◽  
S. De Lange
Keyword(s):  
Blood Flow ◽  
Ischemic Myocardium ◽  
Adrenergic Agonist ◽  
Anesthetized Dogs

Dopamine-1 receptor stimulation impairs intestinal oxygen utilization during critical hypoperfusion

2003 ◽  
Vol 284 (2) ◽  
pp. H668-H675 ◽  
Author(s):  
Jorge A. Guzman ◽  
Ariosto E. Rosado ◽  
James A. Kruse
Keyword(s):  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Control Group ◽  
Oxygen Utilization ◽  
Hemorrhage Control ◽  
Receptor Stimulation ◽  
Anesthetized Dogs ◽  
Group 2 ◽  
Increased Susceptibility ◽  
Group 1

Effects of a dopamine-1 (DA-1) receptor agonist on systemic and intestinal oxygen delivery (D˙o 2)-uptake relationships were studied in anesthetized dogs during sequential hemorrhage. Control ( group 1) and experimental animals ( group 2) were treated similarly except for the addition of fenoldopam (1.0 μg · kg−1 · min−1) in group 2. Both groups had comparable systemic criticalD˙o 2(D˙o 2crit), but animals in group 2 had a higher gut D˙o 2crit(1.12 ± 1.13 vs. 0.80 ± 0.09 ml · kg−1 · min−1, P < 0.05). At the mucosal level, a clear biphasic delivery-uptake relationship was not observed in group 1; thus oxygen consumption by the mucosa may be supply dependent under physiological conditions. Group 2 demonstrated higher peak mucosal blood flow and lack of supply dependency at higher mucosalD˙o 2 levels. Fenoldopam resulted in a more conspicuous biphasic relationship at the mucosa and a rightward shift of overall splanchnic D˙o 2crit despite increased splanchnic blood flow. These findings suggest that DA-1 receptor stimulation results in increased gut perfusion heterogeneity and maldistribution of perfusion, resulting in increased susceptibility to ischemia.

Inhibition of nitric oxide synthesis attenuates pressure-induced natriuretic responses in anesthetized dogs

1993 ◽  
Vol 264 (1) ◽  
pp. F79-F87 ◽  
Author(s):  
D. S. Majid ◽  
A. Williams ◽  
L. G. Navar
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Synthesis Inhibition ◽  
Fractional Excretion Of Sodium ◽  
Anesthetized Dogs ◽  
Pressure Natriuresis

Inhibition of nitric oxide (NO) synthesis by intrarenal administration of nitro-L-arginine (NLA) leads to decreases in urinary sodium excretion (UNaV) in association with the increases in renal vascular resistance (RVR). In the present study, we examined the ability of the kidney to alter its sodium excretion in response to acute changes in renal arterial pressure (RAP) in anesthetized dogs before and during intrarenal infusion of NLA (50 micrograms.kg-1.min-1). NO synthesis inhibition in 11 dogs increased RVR by 32 +/- 4% and decreased renal blood flow (RBF) by 25 +/- 3%, outer cortical blood flow by 25 +/- 6%, urine flow by 37 +/- 14%, UNaV by 71 +/- 5%, and fractional excretion of sodium (FENa) by 71 +/- 4%. Glomerular filtration rate was not significantly changed during NLA infusion. As previously reported, there was suppression of the RBF autoregulation plateau during NO synthesis inhibition. In addition, there was a marked attenuation of urine flow and UNaV responses to reductions in RAP (150 to 75 mmHg), with significant reductions in the slopes of the relationships between RAP vs. UNaV and RAP vs. FENa during NLA infusion. Similar responses were observed in nine other dogs treated with the angiotensin receptor antagonist losartan, indicating that an augmented activity of the renin-angiotensin system is not responsible for attenuation of the slope of the pressure-natriuresis relationship during NLA infusion. These data suggest that NO may participate in the mediation of the pressure-natriuresis response.

Vascular responses of dura mater

1989 ◽  
Vol 257 (1) ◽  
pp. H157-H161 ◽  
Author(s):  
F. M. Faraci ◽  
K. A. Kadel ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Substance P ◽  
Dura Mater ◽  
Sympathetic Nerves ◽  
Vascular Headache ◽  
Vascular Responses ◽  
Anesthetized Dogs ◽  
High Level ◽  
The Brain ◽  
Increased Blood Flow

The goal of this study was to examine vascular responses of the dura mater. Microspheres were used to measure blood flow to the dura and brain in anesthetized dogs. Under control conditions, blood flow to the dura was 38 +/- 3 (SE) ml.min-1.100 g-1. Values for blood flow to the dura obtained with simultaneous injection of 15- and 50-microns microspheres were similar, which suggests that shunting of 15-microns spheres was minimal. Left atrial infusion of substance P (100 ng.kg-1.min-1) and serotonin (40 micrograms.kg-1.min-1), two agonists that have been reported to increase vascular permeability in the dura, increased blood flow to the dura two- to threefold. Adenosine (iv) produced vasodilatation in the dura. Adenosine and serotonin did not affect cerebral blood flow, but substance P increased blood flow to the brain by approximately 40%. Seizures, which produce pronounced dilatation of cerebral vessels despite activation of sympathetic nerves, produced vasoconstriction in the dura. Thus 1) the dura is perfused at a relatively high level of blood flow under normal conditions and is very responsive to vasoactive stimuli, and 2) substance P and serotonin, which have been implicated in the pathogenesis of vascular headache, produce pronounced vasodilator responses in the dura mater.

Stimulation of renal sodium reabsorption by angiotensin II

1977 ◽  
Vol 232 (4) ◽  
pp. F298-F306 ◽  
Author(s):  
M. D. Johnson ◽  
R. L. Malvin
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Flow Rate ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Filtration Fraction ◽  
Water Diuresis ◽  
Urinary Osmolality ◽  
Anesthetized Dogs ◽  
Renal Sodium Reabsorption

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.

Effect of Irsogladine Maleate on NSAID-Induced Reduction of Gastric Mucosal Blood Flow in Anesthetized Dogs

Digestion ◽  
2009 ◽  
Vol 79 (2) ◽  
pp. 73-78 ◽  
Author(s):  
Motonori Sato ◽  
Noriaki Manabe ◽  
Jiro Hata ◽  
Manabu Ishii ◽  
Tomoari Kamada ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Irsogladine Maleate ◽  
Anesthetized Dogs

Relationship of pyruvate and lactate during anaerobic metabolism. V: Coronary adequacy

1961 ◽  
Vol 200 (6) ◽  
pp. 1169-1176 ◽  
Author(s):  
William E. Huckabee
Keyword(s):  
Blood Flow ◽  
Coronary Flow ◽  
Cardiac Tissue ◽  
Anaerobic Metabolism ◽  
Constant Ratio ◽  
Blood Concentrations ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Relationship Of ◽  
The Relationship

Veno-arterial differences of pyruvate and lactate across the myocardium in chloralose-anesthetized dogs were very variable; in any one animal they changed continually with time despite constant blood flow and arterial blood concentrations. There was a systematic tendency of v-a lactate to vary with v-a pyruvate, as expressed in the calculated "Δ excess lactate," which remained nearly constant (or, if blood flow changed, bore a constant ratio to (a-v)O2). No change in Δ excess lactate from control values occurred in nonhypoxic experiments despite marked changes in v-a differences, arterial blood composition, and coronary flow. Cardiac Δ excess lactate became positive in most animals breathing 10% O2 in N2; output of excess lactate was also observed in all those in which moderate muscular exercise was induced. This anaerobic metabolism, or change in the relationship between pyruvate and lactate exchanges, was interpreted as an indication that O2 delivery response was not adequate to meet cardiac tissue requirements during such mild stresses when judged by the standards of adequacy of the basal state.

Role of adenosine in postprandial and reactive hyperemia in canine jejunum

1992 ◽  
Vol 263 (4) ◽  
pp. G487-G493 ◽  
Author(s):  
D. R. Sawmiller ◽  
C. C. Chou
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Adenosine Deaminase ◽  
Reactive Hyperemia ◽  
Concentration Difference ◽  
Adenosine Concentration ◽  
Anesthetized Dogs ◽  
Series Of Experiments ◽  
Increased Blood Flow

The role of adenosine in postprandial jejunal hyperemia was investigated by determining the effect of placement of predigested food into the jejunal lumen on blood flow and oxygen consumption before and during intra-arterial infusion of dipyridamole (1.5 microM arterial concn) or adenosine deaminase (9 U/ml arterial concn) in anesthetized dogs. Neither drug significantly altered resting jejunal blood flow and oxygen consumption. Before dipyridamole or deaminase, food placement increased blood flow by 30-36%, 26-42%, and 21-46%, and oxygen consumption by 13-22%, 21-22%, and 26-29%, during 0- to 3-, 4- to 7-, and 8- to 11-min placement periods, respectively. Adenosine deaminase abolished the entire 11-min hyperemia, whereas dipyridamole significantly enhanced the initial 7-min hyperemia (45-49%). Both drugs abolished the initial 7-min food-induced increase in oxygen consumption. Dipyridamole attenuated (14%), whereas deaminase did not alter (28%), the increased oxygen consumption that occurred at 8-11 min. Adenosine deaminase also prevented the food-induced increase in venoarterial adenosine concentration difference. In separate series of experiments, luminal placement of food significantly increased jejunal lymphatic adenosine concentration and release. Also, reactive hyperemia was accompanied by an increase in venous adenosine concentration and release. This study provides further evidence to support the thesis that adenosine plays a role in postprandial and reactive hyperemia in the canine jejunum.

Ventilation-perfusion inequality during constant-flow ventilation

1987 ◽  
Vol 62 (3) ◽  
pp. 1255-1263 ◽  
Author(s):  
P. T. Schumacker ◽  
J. I. Sznajder ◽  
A. Nahum ◽  
L. D. Wood
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Lung Volume ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Asymmetric Distribution ◽  
Constant Flow ◽  
Arterial Pco2 ◽  
Continuous Stream ◽  
Anesthetized Dogs

Previous work by Lehnert et al. (J. Appl. Physiol. 53:483–489, 1982) has demonstrated that adequate alveolar ventilation can be maintained during apnea in anesthetized dogs by delivering a continuous stream of inspired ventilation through cannulas aimed down the main-stem bronchi. Because an asymmetric distribution of ventilation might introduce ventilation-perfusion (VA/Q) inequality, we compared gas exchange efficiency in nine anesthetized and paralyzed dogs during constant-flow ventilation (CFV) and conventional ventilation (intermittent positive-pressure ventilation, IPPV). Gas exchange was assessed using the multiple inert gas elimination technique. During CFV at 3 l X kg-1 X min-1, lung volume, retention-excretion differences (R-E*) for low- and medium-solubility gases, and the log standard deviation of blood flow (log SD Q) increased, compared with the findings during IPPV. Reducing CFV flow rate to 1 l X kg-1 X min-1 at constant lung volume improved R-E* and log SD Q, but significant VA/Q inequality compared with that at IPPV remained and arterial PCO2 rose. Comparison of IPPV and CFV at the same mean lung volume showed a similar reversible deterioration in gas exchange efficiency during CFV. We conclude that CFV causes significant VA/Q inequality which may be due to nonuniform ventilation distribution and a redistribution of pulmonary blood flow.

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