Hemodynamic effects of alpha-adrenergic blockade during hypoxia in fetal sheep

Reuss, Mary Lynne; Parer, Julian T.; Harris, Joseph L.; Krueger, Terry R.

doi:10.1016/s0002-9378(16)32381-x

Cited by 78 publications

(17 citation statements)

References 10 publications

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“…It was demonstrated that acute hypoxia induced a decrease in intestinal blood flow at 0.9 of fetal gestation in both species (6,9). Because both administration of the ␣-adrenergic antagonist phenoxybenzamine (11) and chemical sympathectomy using 6-hydroxydopamine (6) blunted this reduction in intestinal blood flow, it was postulated that circulating catecholamines or sympathetic nerves may be involved in the control of intestinal arterial tone at this stage of fetal gestation. However, interpretation of these observations with respect to the regulation of intestinal arterial tone is hampered by the fact that in these studies intestinal blood flow was measured by means of a microsphere technique or flow probe instead of measuring the actual arterial diameter.…”

mentioning

confidence: 99%

Development of vasomotor responses in fetal mesenteric arteries

Rouwet

Mey²,

Slaaf

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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Changes in mesenteric arterial diameters were studied using intravital microscopy in chick fetuses at days 13 and 17 of incubation, corresponding to 0.6 and 0.8 fetal incubation time, both during 5 min of hypoxia followed by 5 min of reoxygenation and after topical administration of increasing concentrations (10(-6)-10(-2) M) of norepinephrine (NE) and acetylcholine (ACh). Baseline diameters of second-order mesenteric arteries increased from 56 microm at 0.6 incubation to 75 microm at 0.8 incubation. Acute hypoxia induced a reduction in arterial diameter to 87 +/- 4.4% of baseline at 0.6 incubation and to 44 +/- 6.7% at 0.8 incubation (P < 0.01). During reoxygenation, mesenteric arteries dilated to 118 +/- 6.5% and 121 +/- 7.5% of baseline at 0.6 and 0.8 fetal incubation time, respectively. Phentolamine did not affect the vasoconstriction during hypoxia at 0.6 incubation, whereas this alpha-adrenergic antagonist significantly attenuated the vasoconstrictor response at 0.8 incubation (to 93 +/- 2.7% of baseline, P < 0.01). Topical NE induced maximal vasoconstriction to 71 +/- 3% of baseline at 0.6 incubation and to 35 +/- 3.8% at 0.8 incubation (P < 0.01). Maximal vasodilation to topical ACh was 113 +/- 4.4% and 122 +/- 4.8% of baseline at 0.6 and 0.8 incubation, respectively. These in vivo findings show that fetal mesenteric arteries constrict in response to acute hypoxia and that the increase in magnitude of this vasoconstrictor response from 0.6 to 0.8 of fetal development results from an increase in adrenergic constrictor capacity.

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confidence: 99%

Development of vasomotor responses in fetal mesenteric arteries

Rouwet

Mey²,

Slaaf

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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“…These include catecholamines (Jones & Wei, 1985) and arginine vasopressin (Alexander et al 1974; Giussani et al 1994 a ). Treatment of sheep fetuses with adrenergic α 1 ‐ (Reuss et al 1982; Giussani et al 1993) or vasopressinergic V 1 ‐ (Perez et al 1989) receptor antagonists reduces the delayed peripheral vasoconstriction and attenuates the increase in fetal arterial blood pressure during acute hypoxaemia.…”

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confidence: 99%

Adrenergic and vasopressinergic contributions to the cardiovascular response to acute hypoxaemia in the llama fetus

Giussani

Riquelme

Sanhueza

et al. 1999

The Journal of Physiology

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The effects of fetal intravenous treatment with phentolamine or a vasopressinergic V1‐receptor antagonist on the fetal cardiovascular responses to acute hypoxaemia in the llama were investigated. Six llama fetuses were surgically prepared between 60 and 70% of gestation under general halothane anaesthesia with vascular catheters and transit‐time ultrasonic flow probes around a carotid artery and a femoral artery. At least 4 days after surgery all fetuses were subjected to a 3 h experiment: 1 h of normoxia, 1 h of hypoxaemia and 1 h of recovery while on slow i.v. infusion with saline. On separate days this experiment was repeated with fetal i.v. treatment with either phentolamine or a V1‐receptor antagonist dissolved in saline. During saline infusion all llama fetuses responded to acute hypoxaemia with intense femoral vasoconstriction. Phentolamine during normoxia produced hypotension, tachycardia and vasodilatation in both the carotid and the femoral circulations. During hypoxaemia, fetuses treated with phentolamine did not elicit the pronounced femoral vasoconstriction and all died within 20 min of the onset of hypoxaemia. A V1‐receptor antagonist produced a femoral vasodilatation during normoxia but did not affect the fetal cardiovascular responses to acute hypoxaemia. In conclusion, α‐adrenergic and V1‐vasopressinergic mechanisms contribute to a basal vasoconstrictor tone in the femoral circulation in the llama fetus. The enhanced femoral vasoconstriction during acute hypoxaemia in the llama fetus is not mediated by stimulation of V1‐vasopressin receptors, but is dependent on α‐adrenergic receptor stimulation. Such α‐adrenergic efferent mechanisms are indispensable to fetal survival during hypoxaemia in the llama since their abolition leads to cardiovascular collapse and death.

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“…The fetal peripheral vasoconstrictor response to acute hypoxaemia is mediated via carotid chemoreflex activation of the sympathetic nervous system, since both bilateral section of the carotid sinus nerves (Giussani et al 1993; Bartelds et al 1993) and α‐adrenergic blockade (Reuss et al 1982; Giussani et al 1993) markedly attenuate the increase in peripheral vascular resistance in response to hypoxaemia in the late gestation sheep fetus. As the hypoxaemic episode continues, plasma concentrations of catecholamines (Jones & Robinson, 1975; Jones & Wei, 1985) and NPY (Fletcher et al 2000) are increased in the fetal circulation, and act to maintain the peripheral vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Calcitonin gene‐related peptide antagonism attenuates the haemodynamic and glycaemic responses to acute hypoxaemia in the late gestation sheep fetus

Thakor

Bloomfield

Patterson

et al. 2005

The Journal of Physiology

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The fetal defence to acute hypoxaemia involves cardiovascular and metabolic responses, which include peripheral vasoconstriction and hyperglycaemia. Both these responses are mediated via neuroendocrine mechanisms, which require the stimulation of the sympathetic nervous system. In the adult, accumulating evidence supports a role for calcitonin gene-related peptide (CGRP) in the activation of sympathetic outflow. However, the role of CGRP in stimulated cardiovascular and metabolic functions before birth is completely unknown. This study tested the hypothesis that CGRP plays a role in the fetal cardiovascular and metabolic defence responses to acute hypoxaemia by affecting sympathetic outflow. Under anaesthesia, five sheep fetuses at 0.8 of gestation were surgically instrumented with catheters and a femoral arterial Transonic flow-probe. Five days later, fetuses were subjected to 0.5 h hypoxaemia during either I.V. saline or a selective CGRP antagonist in randomised order. Treatment started 30 min before hypoxaemia and ran continuously until the end of the challenge. Arterial samples were taken for blood gases, metabolic status and hormone analyses. CGRP antagonism did not alter basal arterial blood gas, metabolic, cardiovascular or endocrine status. During hypoxaemia, similar falls in P a,O 2 occurred in all fetuses. During saline infusion, hypoxaemia induced hypertension, bradycardia, femoral vasoconstriction, hyperglycaemia and an increase in haemoglobin, catecholamines and neuropeptide Y (NPY). In contrast, CGRP antagonism markedly diminished the femoral vasoconstrictor and glycaemic responses to hypoxaemia, and attenuated the increases in haemoglobin, catecholamines and NPY. Combined, these results strongly support the hypothesis that CGRP plays a role in the fetal cardiovascular and metabolic defence to hypoxaemia by affecting sympathetic outflow.

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Hemodynamic effects of alpha-adrenergic blockade during hypoxia in fetal sheep

Cited by 78 publications

References 10 publications

Development of vasomotor responses in fetal mesenteric arteries

Development of vasomotor responses in fetal mesenteric arteries

Adrenergic and vasopressinergic contributions to the cardiovascular response to acute hypoxaemia in the llama fetus

Calcitonin gene‐related peptide antagonism attenuates the haemodynamic and glycaemic responses to acute hypoxaemia in the late gestation sheep fetus

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