scholarly journals Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

2014 ◽  
Vol 35 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Christopher K Willie ◽  
Philip N Ainslie ◽  
Ivan Drvis ◽  
David B MacLeod ◽  
Anthony R Bain ◽  
...  

The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral blood flow (CBF), arterial blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers ( n=17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing (‘clamp’) was then used to replicate an identical temporal pattern of decreasing arterial PO2 (PaO2) and increasing arterial PCO2 (PaCO2) while breathing. End-apnea PaO2 ranged from 23  to 37 mm Hg (30±7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54±24% versus 34±26%, respectively; however, CBF increased similarly between apnea and clamp (93.6±28% and 83.4±38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Blake R. Simon ◽  
Hana E. Baker ◽  
Conner C. Earl ◽  
Adam G. Goodwill ◽  
Sam Luebbe ◽  
...  

Background and Hypothesis: Prior studies have established that progressive increases in coronary blood flow are sufficient to maintain myocardial oxygen delivery in response to reductions in arterial oxygenation. However, the precise mechanisms responsible for anemic coronary vasodilation remain poorly understood. This investigation tested the hypothesis that autonomic neural pathways contribute to the maintenance of myocardial oxygen delivery in response to graded reductions in arterial hematocrit.  Experimental Design: Experiments were conducted in open-chest anesthetized swine while assessing coronary blood flow and coronary arterial and venous blood gases in response to progressive hemodilution. Isovolemic hemodilution was achieved via simultaneous removal of 250mL of arterial blood and addition of 250mL of a synthetic plasma expander (Hespan) in swine that received either vehicle or a combination of atropine (0.5mg/kg) and propranolol (1mg/kg) (Atro/Pro).  Results: Relative to vehicle control swine, treatment with Atro/Pro increased heart rate by ~50±4 beats/min and arterial pressure by ~10±1 mmHg.  However, Atro/Pro did not significantly alter increases in coronary blood flow in response to isovolemic hemodilution (hematocrits ranging from ~35±1% to ~15±1%). Coronary venous PO2, an index of myocardial oxygenation, was also unchanged by hemodilution in both vehicle and Atro/Pro treated swine.   Conclusion and Potential Impact: These data suggest that autonomic neural pathways do not play a significant role in the maintenance of myocardial oxygen delivery in response to graded reduction in arterial oxygen content. Understanding of how myocardial oxygen supply is ultimately sensed and regulated in response to reductions in tissue oxygenation remains elusive.  


2001 ◽  
Vol 280 (6) ◽  
pp. H2591-H2597 ◽  
Author(s):  
A. Rebel ◽  
C. Lenz ◽  
H. Krieter ◽  
K. F. Waschke ◽  
K. Van Ackern ◽  
...  

We addressed the question to which extent cerebral blood flow (CBF) is maintained when, in addition to a high blood viscosity (Bvis) arterial oxygen content (CaO2 ) is gradually decreased. CaO2 was decreased by hemodilution to hematocrits (Hct) of 30, 22, 19, and 15% in two groups. One group received blood replacement (BR) only and served as the control. The second group received an additional high viscosity solution of polyvinylpyrrolidone (BR/PVP). Bvis was reduced in the BR group and was doubled in the BR/PVP. Despite different Bvis, CBF did not differ between BR and BR/PVP rats at Hct values of 30 and 22%, indicating a complete vascular compensation of the increased Bvis at decreased CaO2 . At an Hct of 19%, local cerebral blood flow (LCBF) in some brain structures was lower in BR/PVP rats than in BR rats. At the lowest Hct of 15%, LCBF of 15 brain structures and mean CBF were reduced in BR/PVP. The resulting decrease in cerebral oxygen delivery in the BR/PVP group indicates a global loss of vascular compensation. We concluded that vasodilating mechanisms compensated for Bvis increases thereby maintaining constant cerebral oxygen delivery. Compensatory mechanisms were exhausted at a Hct of 19% and lower as indicated by the reduction of CBF and cerebral oxygen delivery.


1994 ◽  
Vol 266 (1) ◽  
pp. 1-1
Author(s):  
T. S. Rosenkrantz ◽  
I. Knox ◽  
E. L. Zalneraitis ◽  
J. R. Raye ◽  
P. J. Porte ◽  
...  

Pages R1262–R1269: T. S. Rosenkrantz, I. Knox, E. L. Zalneraitis, J. R. Raye, P. J. Porte, R. Cramer, R. Smoloski, and A. F. Philipps. “Cerebral metabolism and electrocortical activity in the chronically hyperglycemic lamb.” Page R1265: Several errors relating to significance of changes in arterial oxygen concentration, cerebral oxygen delivery, and cerebral oxygen uptake were introduced into Table 1 by the publisher. All of the information in the abstract and text are correct as originally printed. A corrected version of the table is reprinted below. Note that there were no changes in the fetal arterial oxygen content during any of the study periods, cerebral oxygen delivery rose during G2 (P = 0.06), and there was a significant increase in cerebral oxygen uptake during G2 (P < 0.05). It is hoped that this clarifies conflicting information in the text and the table concerning the metabolic changes that occur in the brain of the chronically hyperglycemic fetal lamb. (See PDF)


1994 ◽  
Vol 266 (3) ◽  
pp. 1-1
Author(s):  
T. S. Rosenkrantz ◽  
I. Knox ◽  
E. L. Zalneraitis ◽  
J. R. Raye ◽  
P. J. Porte ◽  
...  

Pages R1262–R1269: T. S. Rosenkrantz, I. Knox, E. L. Zalneraitis, J. R. Raye, P. J. Porte, R. Cramer, R. Smoloski, and A. F. Philipps. “Cerebral metabolism and electrocortical activity in the chronically hyperglycemic lamb.” Page R1265: Several errors relating to significance of changes in arterial oxygen concentration, cerebral oxygen delivery, and cerebral oxygen uptake were introduced into Table 1 by the publisher. All of the information in the abstract and text are correct as originally printed. A corrected version of the table is reprinted below. Note that there were no changes in the fetal arterial oxygen content during any of the study periods, cerebral oxygen delivery rose during G2 ( P = 0.06), and there was a significant increase in cerebral oxygen uptake during G2 ( P < 0.05). It is hoped that this clarifies conflicting information in the text and the table concerning the metabolic changes that occur in the brain of the chronically hyperglycemic fetal lamb. (See PDF)


1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.


1981 ◽  
Vol 1 (4) ◽  
pp. 413-417 ◽  
Author(s):  
Masahito Kusunoki ◽  
Kazufumi Kimura ◽  
Masaichi Nakamura ◽  
Yoshinari Isaka ◽  
Shotaro Yoneda ◽  
...  

The contribution of hematocrit (Ht) changes on cerebral blood flow (CBF) and brain oxygenation in ischemic cerebrovascular disease is still controversial. In the present study, effects of Ht variations on CBF and oxygen delivery were investigated in patients with ischemic cerebrovascular disease. CBF was measured by the Xe-133 intracarotid injection method in 27 patients, whose diagnoses included completed stroke, reversible ischemic neurological deficit, and transient ischemic attack. Ht values in the patients ranged from 31 to 53%. There was a significant inverse correlation between CBF and Ht in these Ht ranges. Oxygen delivery, i.e., the product of arterial oxygen content and CBF, increased with Ht elevation and reached the maximum level in the Ht range of 40–45% and then declined. The CBF-Ht and oxygen transport-Ht relations observed in our study were similar to those in the glass-tube model studies by other workers rather than to those in intact animal experiments. From these results, it is conceivable that in ischemic cerebrovascular disease, the vasomotor adjustment was impaired in such a manner that the relations among Ht, CBF, and oxygen delivery were different from those in healthy subjects. Further, an “optimal hematocrit” for brain oxygenation was also discussed.


2016 ◽  
Vol 120 (2) ◽  
pp. 282-296 ◽  
Author(s):  
Michael M. Tymko ◽  
Ryan L. Hoiland ◽  
Tomas Kuca ◽  
Lindsey M. Boulet ◽  
Joshua C. Tremblay ◽  
...  

Our aim was to quantify the end-tidal-to-arterial gas gradients for O2 (PET-PaO2) and CO2 (Pa-PETCO2) during a CO2 reactivity test to determine their influence on the cerebrovascular (CVR) and ventilatory (HCVR) response in subjects with (PFO+, n = 8) and without (PFO−, n = 7) a patent foramen ovale (PFO). We hypothesized that 1) the Pa-PETCO2 would be greater in hypoxia compared with normoxia, 2) the Pa-PETCO2 would be similar, whereas the PET-PaO2 gradient would be greater in those with a PFO, 3) the HCVR and CVR would be underestimated when plotted against PETCO2 compared with PaCO2, and 4) previously derived prediction algorithms will accurately target PaCO2. PETCO2 was controlled by dynamic end-tidal forcing in steady-state steps of −8, −4, 0, +4, and +8 mmHg from baseline in normoxia and hypoxia. Minute ventilation (V̇E), internal carotid artery blood flow (Q̇ICA), middle cerebral artery blood velocity (MCAv), and temperature corrected end-tidal and arterial blood gases were measured throughout experimentation. HCVR and CVR were calculated using linear regression analysis by indexing V̇E and relative changes in Q̇ICA, and MCAv against PETCO2, predicted PaCO2, and measured PaCO2. The Pa-PETCO2 was similar between hypoxia and normoxia and PFO+ and PFO−. The PET-PaO2 was greater in PFO+ by 2.1 mmHg during normoxia ( P = 0.003). HCVR and CVR plotted against PETCO2 underestimated HCVR and CVR indexed against PaCO2 in normoxia and hypoxia. Our PaCO2 prediction equation modestly improved estimates of HCVR and CVR. In summary, care must be taken when indexing reactivity measures to PETCO2 compared with PaCO2.


1957 ◽  
Vol 189 (3) ◽  
pp. 576-579 ◽  
Author(s):  
E. Allbaugh Farrand ◽  
R. Larsen ◽  
Steven M. Horvath

The changes in splanchnic blood flow and related metabolic functions which occurred as the result of the infusion of 0.1 µg/kg/min. of l-epinephrine and l-norepinephrine for 10 minutes were measured in anesthetized dogs. l-Epinephrine elicited a marked increase in estimated splanchnic blood flow and no change in mean arterial pressure. While a significantly increased mean arterial blood pressure was observed following the administration of l-norepinephrine, no change in estimated splanchnic blood flow occurred. Arterial oxygen content was increased significantly with both drugs. Utilization of oxygen by the splanchnic bed was not changed during the infusion of either drug but was increased during the postepinephrine infusion period.


2012 ◽  
Vol 113 (7) ◽  
pp. 1012-1023 ◽  
Author(s):  
Zafeiris Louvaris ◽  
Spyros Zakynthinos ◽  
Andrea Aliverti ◽  
Helmut Habazettl ◽  
Maroula Vasilopoulou ◽  
...  

Some reports suggest that heliox breathing during exercise may improve peripheral muscle oxygen availability in patients with chronic obstructive pulmonary disease (COPD). Besides COPD patients who dynamically hyperinflate during exercise (hyperinflators), there are patients who do not hyperinflate (non-hyperinflators). As heliox breathing may differently affect cardiac output in hyperinflators (by increasing preload and decreasing afterload of both ventricles) and non-hyperinflators (by increasing venous return) during exercise, it was reasoned that heliox administration would improve peripheral muscle oxygen delivery possibly by different mechanisms in those two COPD categories. Chest wall volume and respiratory muscle activity were determined during constant-load exercise at 75% peak capacity to exhaustion, while breathing room air or normoxic heliox in 17 COPD patients: 9 hyperinflators (forced expiratory volume in 1 s = 39 ± 5% predicted), and 8 non-hyperinflators (forced expiratory volume in 1 s = 48 ± 5% predicted). Quadriceps muscle blood flow was measured by near-infrared spectroscopy using indocyanine green dye. Hyperinflators and non-hyperinflators demonstrated comparable improvements in endurance time during heliox (231 ± 23 and 257 ± 28 s, respectively). At exhaustion in room air, expiratory muscle activity (expressed by peak-expiratory gastric pressure) was lower in hyperinflators than in non-hyperinflators. In hyperinflators, heliox reduced end-expiratory chest wall volume and diaphragmatic activity, and increased arterial oxygen content (by 17.8 ± 2.5 ml/l), whereas, in non-hyperinflators, heliox reduced peak-expiratory gastric pressure and increased systemic vascular conductance (by 11.0 ± 2.8 ml·min−1·mmHg−1). Quadriceps muscle blood flow and oxygen delivery significantly improved during heliox compared with room air by a comparable magnitude (in hyperinflators by 6.1 ± 1.3 ml·min−1·100 g−1 and 1.3 ± 0.3 ml O2·min−1·100 g−1, and in non-hyperinflators by 7.2 ± 1.6 ml·min−1·100 g−1 and 1.6 ± 0.3 ml O2·min−1·100 g−1, respectively). Despite similar increase in locomotor muscle oxygen delivery with heliox in both groups, the mechanisms of such improvements were different: 1) in hyperinflators, heliox increased arterial oxygen content and quadriceps blood flow at similar cardiac output, whereas 2) in non-hyperinflators, heliox improved central hemodynamics and increased systemic vascular conductance and quadriceps blood flow at similar arterial oxygen content.


Sign in / Sign up

Export Citation Format

Share Document