Total and regional cerebral blood flow during moderate and severe exercise in miniature swine

1976 ◽  
Vol 40 (2) ◽  
pp. 191-195 ◽  
Author(s):  
D. L. Foreman ◽  
M. Sanders ◽  
C. M. Bloor

To determine the influence of exercise on cerebral blood flow, we ran 14 swine at 3–6 mph and at 0–10% grades on a treadmill for 30 min at moderate and severe levels of exercise. Measuring heart rate, cardiac output, and aortic pressure via implanted probes, we injected 15-mum radiolabeled microspheres via the left atrium before and during exercise. We measured their distribution by gamma spectrometry, determining total cerebral blood flow, regional blood flow, and ratio of flow to gray and white matter. Heart rate, cardiac output, and aortic pressure rose progressively with increasing exercise. Total cerebral flow resembled that reported in humans, i.e., it did not change significantly with exercise. Regional flow distribution also failed to change significantly with exercise. The ratio of gray to white matter flow did not change except to the cerebellum where it rose significantly from resting values at both moderate and severe exercise. Gray matter received more flow than white matter during all three conditions of observation. Cerebral blood flow was remarkably constant during even severe exercise.

1989 ◽  
Vol 256 (3) ◽  
pp. H779-H788
Author(s):  
R. C. Koehler ◽  
J. E. Backofen ◽  
R. W. McPherson ◽  
M. D. Jones ◽  
M. C. Rogers ◽  
...  

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.


1993 ◽  
Vol 74 (4) ◽  
pp. 1672-1678 ◽  
Author(s):  
D. D. Malcolm ◽  
J. L. Segar ◽  
J. E. Robillard ◽  
S. Chemtob

We examined whether prostanoids contribute to the impaired cardiac function and decrease in regional blood flow induced by increasing mean airway pressure. Using microspheres, we measured cardiac output and major organ blood flow and assayed prostaglandin E2, 6-ketoprostaglandin F1 alpha, and thromboxane B2 in blood at mean airway pressures of 5–25 cmH2O in mechanically ventilated newborn piglets treated with ibuprofen (40 mg/kg, n = 6), indomethacin (0.3 mg/kg, n = 6), or vehicle (n = 6). Blood gases and pH were stable throughout the experiments. Prostanoid levels remained constant with increasing mean airway pressure in vehicle-treated pigs and were unchanged by indomethacin. However, ibuprofen decreased the prostanoid levels at all mean airway pressures studied (P < 0.01). As ventilatory pressure was progressively increased, cardiac output decreased gradually and similarly by 42–45% (P < 0.05) in all groups. At the highest mean airway pressure, blood flow decreased to the kidneys by 37–57%, to the ileum by 58–74%, and to the colon by 53–71% (P < 0.05) in all groups. Cerebral blood flow remained constant at all ventilatory pressures regardless of the treatment. There was no difference in cardiac output and regional hemodynamics between ibuprofen- and vehicle-treated animals. However, after indomethacin, ileal blood flow at the higher ventilatory pressures was 41–46% lower and cerebral blood flow at all mean airway pressures was 14–25% lower than after the other treatments (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 168 (1) ◽  
pp. 161-175 ◽  
Author(s):  
SUSANNE HOLMGREN ◽  
MICHAEL AXELSSON ◽  
ANTHONY P. FARRELL

The effects of adrenaline, noradrenaline, substance P and vasoactive intestinal polypeptide (VIP) on dorsal aortic blood pressure, coeliac artery blood flow and heart rate were studied in unrestrained dogfish, Squalus acanthias. Changes in the coeliac vascular bed were calculated from these variables. Perfused tail preparations were used to study the effects of the various drugs on the somatic vascular bed. Corrosion casts were made to study the gross architecture of the coeliac vascular bed. Adrenaline and noradrenaline increased dorsal aortic pressure and reduced the coeliac artery blood flow. Adrenaline caused a small increase in heart rate while noradrenaline caused a small decrease. Both drugs increased the resistance in the coeliac vascular bed. VIP increased dorsal aortic pressure, heart rate and resistance in the coeliac vascular bed. Substance P caused an increase in heart rate, cardiac output and, in particular, in coeliac artery blood flow; dorsal aortic pressure was simultaneously reduced. Voluntary swimming or fright immediately caused a pronounced reduction in blood flow in the coeliac artery, even though cardiac output and dorsal aortic pressure increased. It is concluded that adrenergic mechanisms and possibly VIP are involved in reducing the blood flow to the gut, while substance P increases the flow to the gut.


1989 ◽  
Vol 66 (5) ◽  
pp. 2101-2108 ◽  
Author(s):  
M. D. McKirnan ◽  
C. G. Gray ◽  
F. C. White

Cardiovascular, metabolic, and thermoregulatory responses were studied in eight male miniature swine during a prolonged treadmill run. Each animal underwent 8–10 wk of exercise training, thoracic surgery, and 3 wk of retraining before the experimental run. This regimen enabled the animals to run at 65% of the heart rate range (210–220 beats/min) for approximately 100 min. Skin wetting and a fan were used to cool the pigs during the run. Regional blood flow was significantly altered with the onset of exercise; however, hindlimb muscle and total gastrointestinal blood flow were unchanged throughout the exercise period. Compared with 5-min values, heart rate and cardiac output were significantly elevated by 17 beats/min and 31 ml.min-1.kg-1 at 60 min and by 20 beats/min and 33 ml.min-1.kg-1 at end exercise, respectively. Core temperatures increased between 5 and 30 min of exercise (39.4 vs. 39.9 degrees C) but then remained unchanged to the end of exercise. Mean arterial pressure, O2 consumption, and blood lactate did not change during the exercise bout. These data indicate that limiting increases in core temperature during prolonged exercise was associated with a plateau in active muscle blood flow.


2009 ◽  
Vol 111 (5) ◽  
pp. 988-1000 ◽  
Author(s):  
Tenille E. Ragoonanan ◽  
W Scott Beattie ◽  
C David Mazer ◽  
Albert K.Y. Tsui ◽  
Howard Leong-Poi ◽  
...  

Background Perioperative beta-blockade and anemia are independent predictors of increased stroke and mortality by undefined mechanisms. This study investigated the effect of beta-blockade on cerebral tissue oxygen delivery in an experimental model of blood loss and fluid resuscitation (hemodilution). Methods Anesthetized rats were treated with metoprolol (3 mg x kg) or saline before undergoing hemodilution with pentastarch (1:1 blood volume exchange, 30 ml x kg). Outcomes included cardiac output, cerebral blood flow, and brain (PBrO2) and kidney (PKO2) tissue oxygen tension. Hypoxia inducible factor-1alpha (HIF-1alpha) protein levels were assessed by Western blot. Systemic catecholamines, erythropoietin, and angiotensin II levels were measured. Results Hemodilution increased heart rate, stroke volume, cardiac output (60%), and cerebral blood flow (50%), thereby maintaining PBrO2 despite an approximately 50% reduction in blood oxygen content (P &lt; 0.05 for all). By contrast, PKO2 decreased (50%) under the same conditions (P &lt; 0.05). Beta-blockade reduced baseline heart rate (20%) and abolished the compensatory increase in cardiac output after hemodilution (P &lt; 0.05). This attenuated the cerebral blood flow response and reduced PBrO2 (50%), without further decreasing PKO2. Cerebral HIF-1alpha protein levels were increased in beta-blocked hemodiluted rats relative to hemodiluted controls (P &lt; 0.05). Systemic catecholamine and erythropoietin levels increased comparably after hemodilution in both groups, whereas angiotensin II levels increased only after beta-blockade and hemodilution. Conclusions Cerebral tissue oxygen tension is preferentially maintained during hemodilution, relative to the kidney, despite elevated systemic catecholamines. Acute beta-blockade impaired the compensatory cardiac output response to hemodilution, resulting in a reduction in cerebral tissue oxygen tension and increased expression of HIF-1alpha.


1976 ◽  
Vol 230 (1) ◽  
pp. 85-89 ◽  
Author(s):  
RJ McRitchie ◽  
SF Vatner ◽  
D Boettcher ◽  
GR Heyndrickx ◽  
TA Patrick ◽  
...  

The role played by the major arterial baroreceptor reflexes in the cardiovascular response to exercise was examined by comparing the responses of untethered conscious dogs instrumented for the measurement of aortic pressure and cardiac output with those of dogs with total arterial barorecptor denervation (TABD). Moderately severe levels of exercise (12 mph) in intact dogs increased cardiac output from 111 +/- 17 ml/kg per min, increased heart rate from 101 +/- 5 to 265 +/- 8 beats/min, and reduced total peripheral resistance from 0.039 +/- 0.003 to 0.015 +/- 0.002 mmHg/ml per min. Dogs with TABD responded in a very similar fashion; exercise increased cardiac output from 119 +/- 8 to 356 /+- 23 ml/kg per min, increased heart rate from 122 +/- 7 to 256 +/- 5 beats/min, and decreased total peripheral resistance from 0.042 +/- 0.005 to +/- 0.015 +/- 0.001 mmHg/ml per min. The reflex heart rate responses to intravenous bolus doses of methoxamine were also examined in intact animals, both at rest and during exercise. Methoxamine caused striking bradycardia at rest, but little bradycardia during exercise. These results suggest that the arterial baroreceptor reflex is normally turned off during severe exercise and thus does not modify significantly the cardiovascular response to exercise.


1991 ◽  
Vol 261 (2) ◽  
pp. H575-H582
Author(s):  
J. E. Backofen ◽  
R. C. Koehler ◽  
A. P. Harris ◽  
M. C. Rogers ◽  
R. J. Traystman ◽  
...  

Mean aortic pressure (MAP) increases (Cushing response) when intracranial pressure (ICP) approaches MAP. We elevated ICP to levels equivalent to normal baseline MAP with infusion of mock cerebrospinal fluid (CSF) into the lateral cerebral ventricles and contrasted responses in near-term fetal sheep, 1-wk-old lambs, and adult sheep anesthetized with pentobarbital sodium. With CSF infusion 1-wk-old lambs and adults produced sustained increases in MAP of 16 +/- 1 and 22 +/- 2 mmHg, respectively, over a 40-min period. However, cerebral blood flow fell 66 and 57%, and cerebral O2 uptake fell 34 and 37%, respectively. In the near-term fetus, MAP increased by 11 +/- 1 mmHg and cerebral blood fell 49% at 3 min of elevated ICP. However, by 15 min MAP had increased further (+17 +/- 2 mmHg) and cerebral blood flow was nearly restored. In contrast to postnatal sheep, cerebral O2 uptake was maintained throughout in the fetus. The mechanism of increased MAP differed among groups. In adults total peripheral resistance fell significantly, whereas in the fetus and lamb it remained constant. Cardiac output increased in each group, but, because of the fall in peripheral resistance, increased cardiac output was relatively more important to the rise in MAP in adults. In addition, marked vasoconstriction occurred in intestines and skin in the fetus. The Cushing response is well-developed in near-term fetal sheep. After birth it may lose its effectiveness in providing for the basal metabolic demand of the brain.


1983 ◽  
Vol 54 (6) ◽  
pp. 1641-1652 ◽  
Author(s):  
C. M. Parks ◽  
M. Manohar

Transmural distribution of myocardial blood flow and coronary vasodilator reserve (15-microns-diam radionuclide-labeled microspheres) was studied in 11 adult, healthy ponies at rest and during moderate and severe exercise performed on a treadmill (heart rate 56 +/- 4, 154 +/- 3, and 225 +/- 7 beats . min-1, respectively.). Exercise resulted in a marked increase in cardiac output, mean aortic pressure, right ventricular (RV) systolic and end-diastolic pressure, left ventricular (LV) end-diastolic pressure, and the maximum rate of rise of LV pressure LV (dP/dtmax). Accompanying these changes was a pronounced increase in transmural myocardial perfusion. During severe exercise, subendocardial/subepicardial (endo/epi) perfusion ratio for the LV (0.99 +/- 0.02) decreased significantly from control value (1.27 +/- 0.03) but it was not significantly different from 1.00. With adenosine infusion during severe exercise, transmural myocardial blood flow throughout the cardiac ventricles was able to increase significantly further (delta from severe exercise to severe exercise with adenosine, 75% for LV, 68% for septum, and 57% for RV) despite the fact that heart rate, aortic pressure, and RV and LV end-diastolic pressures were unaltered. During severe exercise with adenosine, endo:epi perfusion ratios were 1.11 +/- 0.15 and 1.32 +/- 0.10 for LV and RV, respectively. In the LV, the coronary vasodilator reserve was found to be the least in papillary muscles, where the increment in blood flow during severe exercise with adenosine was only 46% above severe exercise without adenosine. Coronary vasodilator reserve was largest in the middle layers of the LV myocardium (88%). With adenosine infusion during severe exercise, coronary vascular resistance in both LV and RV decreased significantly from that observed during severe exercise alone (27 +/- 2 and 30 +/- 2 mmHg . ml-1 . min . g, respectively) to levels observed during maximal coronary vasodilation induced by adenosine infusion at rest (20 +/- 2 and 18 +/- 2 mmHg . ml-1 . min . g, respectively). These data clearly demonstrate that there remains a marked coronary vasodilator reserve transmurally in the pony myocardium during severe exercise.


1989 ◽  
Vol 256 (6) ◽  
pp. H1651-H1658
Author(s):  
C. L. Rosen ◽  
A. Cote ◽  
G. G. Haddad

To investigate the effects of enkephalins on cardiac output and regional blood flow, we administered D-Ala-D-Leu-enkephalin (DADLE) intracisternally (ic) to 14 chronically instrumented unanesthetized dogs. Measurements were made at base line, 20, 45, and 75 min after DADLE (25 or 125 micrograms/kg) and 15 min after naloxone (5 micrograms/kg ic). After 125 micrograms/kg DADLE, all animals developed hypoventilation, bradycardia, and decreased O2 consumption without hypotension. Cardiac output decreased (-34%), but brain blood flow increased (+110%). Blood flow decreased to the diaphragm (-38%), heart (-21%), skeletal muscle (-40%), skin (-67%), pancreas (-79%), and gastrointestinal tract (-26%). After 25 micrograms/kg DADLE, there were no consistent changes in cardiac output or regional blood flow. Four additional animals (without DADLE) were exposed to altered inspired gases to reproduce the blood gas changes after DADLE. These animals developed hyperventilation without bradycardia and increased brain (+114%) and diaphragm (+649%) blood flow. We conclude that centrally administered enkephalins produce 1) a parallel decrease in ventilation, heart rate, O2 consumption, and cardiac output and 2) a major blood flow redistribution, primarily dictated by the effects of opioids on ventilation, heart rate, and metabolism.


1988 ◽  
Vol 64 (4) ◽  
pp. 1493-1499 ◽  
Author(s):  
N. Imai ◽  
C. K. Stone ◽  
P. D. Woolf ◽  
C. S. Liang

To determine whether endogenous opiates have a role in circulatory regulation during mild to moderate exercise, 11 chronically instrumented dogs were exercised on a treadmill up a 6% incline at 2.5 and 5.0 mph, each for 20 min, after treatment with either the opiate receptor antagonist naloxone (1 mg/kg bolus and 20 micrograms.kg-1.min-1 infusion) or normal saline. Naloxone increased plasma beta-endorphin and adrenocorticotropic hormone at rest but had no effect on resting heart rate, aortic pressure, cardiac output, left ventricular time derivative of pressure (dP/dt) and ratio of dP/dt at a developed pressure of 50 mmHg and the developed pressure (dP/dt/P), or plasma catecholamines. Plasma beta-endorphin and adrenocorticotropic hormone increased during exercise. In addition, graded treadmill exercise produced proportional increases in heart rate, cardiac output, aortic pressure, left ventricular dP/dt and dP/dt/P, and blood flow to exercising muscles, right and left ventricular myocardium, and adrenal glands. However, there were no differences in the circulatory responses to exercise between animals receiving naloxone and normal saline. Thus the endogenous opiate system probably does not play an important role in regulating the systemic hemodynamic and blood flow responses to mild and moderate exercise.


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