Cardiovascular responses to graded degrees of hypoxaemia in the llama fetus

1995 ◽  
Vol 7 (3) ◽  
pp. 549 ◽  
Author(s):  
AJ Llanos ◽  
RA Riquelme ◽  
FA Moraga ◽  
G Cabello ◽  
JT Parer
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Cardiovascular Response ◽  
Blood Gases ◽  
Cardiovascular Responses ◽  
Fetal Sheep ◽  
Severe Hypoxaemia ◽  
The Central Nervous System ◽  
Blood Flow Redistribution

The fetal llama exposed to an intense degree of hypoxaemia did not increase cerebral blood flow, but showed a marked peripheral vasoconstriction. The same cardiovascular response is observed in fetal sheep submitted to a extremely severe hypoxaemia, when the initial compensatory vasodilatory mechanisms in brain and heart fail. To investigate whether the fetal llama responses to acute hypoxaemia are adaptive, or whether they are the result of a breakdown of mechanisms of blood flow redistribution that favours the central nervous system, we studied seven fetal llamas (0.6-0.7 of gestation) chronically-catheterized during 1 h of graded and progressive hypoxaemia. Fetal ascending aorta blood gases and fetal cardiac output and its distribution (radiolabelled-microspheres) were measured after 60 min of normoxaemia (B) and at the end of 20 min (H20), 40 min (H40) and 60 min (H60) of hypoxaemia. Data were analysed by ANOVA and Newman-Keuls tests. Each treatment resulted in a lower (P < 0.05) percentage of haemoglobin saturation than hypoxaemia; H40 was lower than H20, and H60 was lower than H20 and H40. No statistical difference was observed among treatments for cardiac output or cerebral blood flow. These results demonstrate that fetal cardiac output and brain blood flow are maintained at all degrees of hypoxaemia, indicating that these cardiovascular responses are an adaptive response in the llama fetus, rather than an index of cardiorespiratory decompensation.

Indomethacin compromises hemodynamics during positive-pressure ventilation, independently of prostanoids

1993 ◽  
Vol 74 (4) ◽  
pp. 1672-1678 ◽  
Author(s):  
D. D. Malcolm ◽  
J. L. Segar ◽  
J. E. Robillard ◽  
S. Chemtob
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Airway Pressure ◽  
Regional Blood Flow ◽  
Blood Gases ◽  
Positive Pressure ◽  
Organ Blood Flow ◽  
Mean Airway Pressure ◽  
Airway Pressures

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)

Efficacy of Cushing response during development in sheep

1991 ◽  
Vol 261 (2) ◽  
pp. H575-H582
Author(s):  
J. E. Backofen ◽  
R. C. Koehler ◽  
A. P. Harris ◽  
M. C. Rogers ◽  
R. J. Traystman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Metabolic Demand ◽  
O2 Uptake ◽  
Fetal Sheep ◽  
Cushing Response ◽  
Near Term

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.

scholarly journals OP16.09: Cardiac output and placental perfusion in growth‐restricted fetuses with cerebral blood flow redistribution

2019 ◽  
Vol 54 (S1) ◽  
pp. 140-140
Author(s):  
S. Miyashita ◽  
C. Sakamoto ◽  
S. Ochiai ◽  
M. Watanabe ◽  
E. Motegi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Placental Perfusion ◽  
Blood Flow Redistribution

Acute cardiovascular response to isocapnic hypoxia. I. A mathematical model

2000 ◽  
Vol 279 (1) ◽  
pp. H149-H165 ◽  
Author(s):  
Mauro Ursino ◽  
Elisa Magosso
Keyword(s):  
Mathematical Model ◽  
Central Nervous System ◽  
Heart Rate ◽  
Blood Flow ◽  
Nervous System ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Stretch Receptors ◽  
The Central Nervous System ◽  
Lung Stretch

A mathematical model of the acute cardiovascular response to isocapnic hypoxia is presented. It includes a pulsating heart, the systemic and pulmonary circulation, a separate description of the vascular bed in organs with the higher metabolic need, and the local effect of O2 on these organs. Moreover, the model also includes the action of several reflex regulatory mechanisms: the peripheral chemoreceptors, the lung stretch receptors, the arterial baroreceptors, and the hypoxic response of the central nervous system. All parameters in the model are given in accordance with the physiological literature. The simulated overall response to a deep hypoxia (28 mmHg) agrees with the experimental data quite well, showing a biphasic pattern. The early phase (8–10 s), caused by activation of peripheral chemoreceptors, exhibits a moderate increase in mean systemic arterial pressure, a decrease in heart rate, a quite constant cardiac output, and a redistribution of blood flow to the organs with higher metabolic need at the expense of other organs. The later phase (20 s) is characterized by the activation of lung stretch receptors and by the central nervous system hypoxic response. During this phase, cardiac output and heart rate increase together, and blood flow is restored to normal levels also in organs with lower metabolic need. The model may be used to gain a deeper understanding of the role of each mechanism in the overall cardiovascular response to hypoxia.

Arginine vasopressin mediates cardiovascular responses to hypoxemia in fetal sheep

1989 ◽  
Vol 256 (5) ◽  
pp. R1011-R1018 ◽  
Author(s):  
R. Perez ◽  
M. Espinoza ◽  
R. Riquelme ◽  
J. T. Parer ◽  
A. J. Llanos
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Arginine Vasopressin ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Potent Vasoconstrictor

Acute hypoxemia results in hypertension, bradycardia, and cardiac output redistribution in fetal sheep. The blood flow redistribution is produced by differential changes in vascular resistance of various fetal organs. alpha-Adrenergic activity is one of the few vasoconstrictor mechanisms thus far identified in the hypoxemic fetal sheep. Arginine vasopressin (AVP) is a potent vasoconstrictor in adults. Since AVP administration to the normoxic fetus mimics some of the fetal cardiovascular responses to hypoxemia and fetal plasma AVP levels increase with hypoxemia, we examined the hypothesis that AVP modifies the fetal cardiovascular response to hypoxemia by changing the vascular resistance of some fetal vascular beds. To test this we determined fetal systemic arterial pressure and fetal cardiac output and its distribution during hypoxemia with and without the V1 AVP antagonist d(CH2)5-Tyr(Me)AVP. Fourteen fetal sheep (0.79-0.90 of gestation) were chronically catheterized. Five days after surgery fetal hypoxemia was induced by introducing a mixture of 95% N2-5% CO2 (10-20 l/min) into a maternal tracheal catheter. The hypoxemia was maintained for 40 min. Fetal heart rate, systemic arterial blood pressure, and combined ventricular output and its distribution (radiolabeled microspheres) were measured before hypoxemia, at 20 min of hypoxemia alone, and at 20 min of hypoxemia plus either AVP antagonist (n = 5) or NaCl 0.9% (n = 5, controls). Fetal hypertension and bradycardia were partially reversed after the AVP antagonist administration during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Lack of evidence for impaired preload or Bezold-Jarisch activation during brief umbilical cord occlusions in fetal sheep

2021 ◽  
Author(s):  
Christopher A. Lear ◽  
Laura Bennet ◽  
Benjamin S. A. Lear ◽  
Jenny A. Westgate ◽  
Alistair Jan Gunn
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Cardiovascular Responses ◽  
Diastolic Filling ◽  
Fetal Sheep ◽  
Blood Flows ◽  
Rapid Fall ◽  
Filling Time ◽  
Cervical Vagotomy ◽  
Femoral Blood

Impaired cardiac preload secondary to umbilical cord occlusion (UCO) has been hypothesized to contribute to intrapartum decelerations, brief falls in fetal heart rate (FHR), through the activation of the Bezold-Jarisch reflex. This cardioprotective reflex increases parasympathetic and inhibits sympathetic outflows triggering hypotension, bradycardia and peripheral vasodilation but its potential to contribute to intrapartum decelerations has never been systematically examined. In this study we performed bilateral cervical vagotomy to remove the afferent arm and the efferent parasympathetic arm of the Bezold-Jarisch reflex. 22 chronically instrumented fetal sheep at 0.85 of gestation received vagotomy (n=7) or sham-vagotomy (control, n=15), followed by three 1-min complete UCOs separated by 4-min reperfusion periods. UCOs in control fetuses were associated with a rapid fall in FHR and reduced femoral blood flow mediated by intense femoral vasoconstriction, leading to hypertension. Vagotomy abolished the rapid fall in FHR (p<0.001), and despite reduced diastolic filling time, increased both carotid (p<0.001) and femoral (p<0.05) blood flow during UCOs, secondary to carotid vasodilation (p<0.01) and delayed femoral vasoconstriction (p<0.05). Finally, vagotomy was associated with an attenuated rise in cortical impedance during UCOs (p<0.05), consistent with improved cerebral substrate supply. In conclusion, increased carotid and femoral blood flows after vagotomy are consistent with increased left and right ventricular output, which is incompatible with the hypothesis that labor-like UCOs impair ventricular filling. Overall, the cardiovascular responses to vagotomy do not support the hypothesis that the Bezold-Jarisch reflex is activated by UCO. The Bezold-Jarisch reflex is therefore mechanistically unable to contribute to intrapartum decelerations.

Relation of Hypoxemia and/or Hypocapnia to Lactic Acid Content of Brain and Cardiovascular Response

1958 ◽  
Vol 193 (2) ◽  
pp. 345-349 ◽  
Author(s):  
Clyde Biddulph ◽  
Donald D. Van Fossan ◽  
Dominic Criscuolo ◽  
Robert T. Clark
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Lactic Acid ◽  
Cardiovascular Response ◽  
Control Level ◽  
Tissue Level ◽  
Chemical Analyses ◽  
Lactic Acid Concentration ◽  
Determining Factors ◽  
Lactic Acid Content

The lactic acid concentration of brain was measured 3 hours after death in dogs which had been subject to hypocapnia, hypoxemia with hypocapnia, and hypoxemia without hypocapnia for 15 minutes. There was no elevation of brain lactic acid above the control level in those dogs subjected to hypocapnia or hypoxemia alone, however, when hypocapnia and hypoxemia were combined there was a significant increase. Cardiovascular and blood chemical analyses support the conclusion that variations in cerebral blood flow, availability of oxygen at the tissue level and interference with oxidative metabolism are important determining factors in brain lactic acid build-up. The results agree with those obtained in altitude-exposed animals, for they likewise show an elevation of brain lactic acid.

Dynamics of cerebral blood flow regulation explained using a lumped parameter model

2002 ◽  
Vol 282 (2) ◽  
pp. R611-R622 ◽  
Author(s):  
Mette S. Olufsen ◽  
Ali Nadim ◽  
Lewis A. Lipsitz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cardiovascular Response ◽  
Lumped Parameter Model ◽  
Initial Increase ◽  
Windkessel Model ◽  
Cerebrovascular Resistance ◽  
Posture Change ◽  
Lumped Parameter ◽  
Young Subjects

The dynamic cerebral blood flow response to sudden hypotension during posture change is poorly understood. To better understand the cardiovascular response to hypotension, we used a windkessel model with two resistors and a capacitor to reproduce beat-to-beat changes in middle cerebral artery blood flow velocity (transcranial Doppler measurements) in response to arterial pressure changes measured in the finger (Finapres). The resistors represent lumped systemic and peripheral resistances in the cerebral vasculature, whereas the capacitor represents a lumped systemic compliance. Ten healthy young subjects were studied during posture change from sitting to standing. Dynamic variations of the peripheral and systemic resistances were extracted from the data on a beat-to-beat basis. The model shows an initial increase, followed approximately 10 s later by a decline in cerebrovascular resistance. The model also suggests that the initial increase in cerebrovascular resistance can explain the widening of the cerebral blood flow pulse observed in young subjects. This biphasic change in cerebrovascular resistance is consistent with an initial vasoconstriction, followed by cerebral autoregulatory vasodilation.

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