Vasopressin and prostanoid mechanisms in control of cerebral blood flow in hypotensive newborn pigs

1990 ◽  
Vol 258 (2) ◽  
pp. H408-H413 ◽  
Author(s):  
W. M. Armstead ◽  
C. W. Leffler ◽  
D. W. Busija ◽  
R. Mirro
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Vascular Resistance ◽  
Brain Regions ◽  
Cerebral Metabolic Rate ◽  
Cerebral Vasoconstriction ◽  
Newborn Pigs ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

The interaction between vasopressinergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious hypotensive newborn pig was investigated. Indomethacin treatment (5 mg/kg) of hypotensive piglets caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 52 and 198% 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.58 +/- 0.32 ml.100 g-1.min-1 to 1.01 +/- 0.12 and 0.29 +/- 0.08 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Treatment with the putative vascular (V1) receptor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid-2-(O-methyl)tyrosine]arginine vasopressin (MEAVP) had no effect on regional cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or during hemorrhagic hypotension. However, decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were blunted markedly in animals treated with MEAVP. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn pig, as reported previously, and implicate removal of vasopressinergic modulation by prostanoids as a potential mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.

Adrenergic and prostanoid mechanisms in control of cerebral blood flow in hypotensive newborn pigs

1988 ◽  
Vol 254 (4) ◽  
pp. H671-H677
Author(s):  
W. M. Armstead ◽  
C. W. Leffler ◽  
D. W. Busija ◽  
D. G. Beasley ◽  
R. Mirro
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Vascular Resistance ◽  
Brain Regions ◽  
Cerebral Metabolic Rate ◽  
Cerebral Vasoconstriction ◽  
Sympathetic Modulation ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

The interaction between adrenergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious, hypotensive newborn pig was investigated. Pretreatment with the selective alpha 1- and alpha 2-adrenoceptor antagonists prazosin and yohimbine, respectively, had no effect on cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or after hemorrhagic hypotension. Indomethacin treatment (5 mg/kg ia) of piglets following hemorrhage caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 54 and 177%, 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.42 +/- 0.28 to 1.45 +/- 0.28 ml.100 g-1.min-1 and to 1.0 +/- 0.28 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were the same as in animals pretreated with vehicle, prazosin, or yohimbine. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn, as reported previously. These data do not implicate removal of sympathetic modulation by prostanoids as a mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.

scholarly journals Opioids and the Prostanoid System in the Control of Cerebral Blood Flow in Hypotensive Piglets

1991 ◽  
Vol 11 (3) ◽  
pp. 380-387 ◽  
Author(s):  
William M. Armstead ◽  
Robert Mirro ◽  
David W. Busija ◽  
Charles W. Leffler
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Brain Regions ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Consumption ◽  
Cerebral Vascular Resistance ◽  
Indomethacin Treatment ◽  
Cerebral Vascular

The interaction between opioid and prostanoid mechanisms in the control of cerebral hemodynamics was investigated in the conscious hypotensive piglet. Radiomicrospheres were used to determine regional cerebral blood flow (rCBF) in piglets pretreated with the opioid receptor antagonist, naloxone, or its vehicle, saline, during normotension, hypotension, and after the administration of indomethacin, a cyclooxygenase inhibitor, during hypotension. Hemorrhage (30 ml/kg) decreased systemic arterial pressure from 68 ± 12 to 40 ± 10 mm Hg but did not decrease blood flow to any brain region. Indomethacin treatment (5 mg/kg) of hypotensive piglets decreased blood flow to all brain regions within 20 min; this decrease in CBF resulted from increases in cerebral vascular resistance of 65 and 281% at 20 and 40 min after treatment, respectively. In hypotensive piglets, cerebral oxygen consumption was reduced from 2.62 ± 0.71 to 0.53 ± 0.27 ml 100g−1 min−1 and to 0.11 ± 0.04 ml 100 g−1 min−1 at 20 and 40 min following indomethacin, respectively. Treatment with naloxone (1 mg/kg) had no effect on rCBF, calculated cerebral vascular resistance, or cerebral oxygen consumption of normotensive or hypotensive piglets. However, decreases in CBF and oxygen consumption and increases in cerebral vascular resistance upon treatment of hypotensive piglets with indomethacin were attenuated in animals pretreated with naloxone. These data indicate that the removal of prostanoid modulation of an opioid-mediated constrictor influence on the cerebral circulation is a potential mechanism for the increase in cerebral vascular resistance that follows indomethacin treatment of hypotensive piglets.

scholarly journals Interrelationships Among Regional Cerebral Blood Flow, Mean Transit Time, Vascular Volume and Cerebral Vascular Resistance

Stroke ◽  
1974 ◽  
Vol 5 (6) ◽  
pp. 719-724 ◽  
Author(s):  
YOSHIHIRO KURIYAMA ◽  
TAKASHI AOYAMA ◽  
KUNIHIKO TADA ◽  
SHOTARO YONEDA ◽  
TADAATSU NUKADA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Transit Time ◽  
Regional Cerebral Blood Flow ◽  
Mean Transit Time ◽  
Regional Cerebral Blood ◽  
Vascular Volume ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Hypothermia reduces cerebral metabolic rate and cerebral blood flow in newborn pigs

1987 ◽  
Vol 253 (4) ◽  
pp. H869-H873 ◽  
Author(s):  
D. W. Busija ◽  
C. W. Leffler
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Body Temperature ◽  
Metabolic Rate ◽  
Rectal Temperature ◽  
Cerebral Circulation ◽  
Radioactive Microspheres ◽  
Cerebrovascular Resistance ◽  
Cerebral Metabolic Rate ◽  
Newborn Pigs

We examined effects of hypothermia on cerebral metabolic rate and cerebral blood flow in anesthetized, newborn pigs (1-4 days old). Cerebral blood flow (CBF) was determined with 15-micronS radioactive microspheres. Regional CBF ranged from 44 to 66 ml . min-1.100 g-1, and cerebral metabolic rate was 1.94 +/- 0.23 ml O2.100 g-1 . min-1 during normothermia (39 degrees C). Reduction of rectal temperature to 34-35 degrees C decreased CBF and cerebral metabolic rate 40-50%. In another group of piglets, we examined responsiveness of the cerebral circulation to arterial hypercapnia during hypothermia. Although absolute values for normocapnic and hypercapnic CBF were reduced by hypothermia and absolute values for normocapnic and hypercapnic cerebrovascular resistance were increased, the percentage changes from control in these variables during hypercapnia were similar during normothermia and hypothermia. In another group of animals that were maintained normothermic and exposed to two episodes of hypercapnia, there was no attenuation of cerebrovascular dilatation during the second episode. We conclude that hypothermia reduces CBF secondarily to a decrease in cerebral metabolic rate and that percent dilator responsiveness to arterial hypercapnia is unaltered when body temperature is reduced.

Cerebral blood flow is increased during controlled ovarian stimulation

2007 ◽  
Vol 293 (6) ◽  
pp. H3265-H3269 ◽  
Author(s):  
Ori Nevo ◽  
Jean F. Soustiel ◽  
Israel Thaler
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Ovarian Stimulation ◽  
Follicular Phase ◽  
Controlled Ovarian Stimulation ◽  
Ovarian Suppression ◽  
Late Follicular Phase ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Estrogen appears to enhance cerebral blood flow (CBF). An association between CBF and physiologically altered hormonal levels due to menstrual cycle, menopause, or exogenous manipulations such as ovariectomy or hormone replacement therapy has been demonstrated. The purpose of this study was to determine the association between ovarian stimulation and CBF in vivo by measuring blood flow in the internal carotid artery (ICA) after pituitary suppression and during controlled ovarian stimulation in women undergoing in vitro fertilization treatment cycles. ICA volume flows were measured by angle-independent dual-beam ultrasound Doppler in 12 women undergoing controlled ovarian stimulation. Measurements were performed after pituitary/ovarian suppression, in the late follicular phase, and at midluteal phase. Blood flow in the ICA increased by 22.2% and 32% in the late follicular and midluteal phases compared with the respective values obtained during ovarian suppression ( P < 0.0005 and P < 0.0001, respectively). There was a significant correlation between increments in estrogen levels and increments in CBF when the late follicular phase was compared with the ovarian suppression period ( r = 0.8, P < 0.001). Mean blood flow velocity significantly increased (by 15.7% and 16.9%, respectively) and cerebral vascular resistance significantly decreased (by 17.6% and 26.5%) during the late follicular and midluteal phases compared with respective measures during ovarian suppression. There was a significant correlation between an increase in estrogen levels and a decrease in cerebral vascular resistance when the late follicular phase was compared with the ovarian suppression period ( r = −0.6, P < 0.05). These changes imply sex hormone-associated intracranial vasodilation leading to increased CBF during controlled ovarian stimulation.

Hyperthermia increases cerebral metabolic rate and blood flow in neonatal pigs

1988 ◽  
Vol 255 (2) ◽  
pp. H343-H346 ◽  
Author(s):  
D. W. Busija ◽  
C. W. Leffler ◽  
M. Pourcyrous
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Intravenous Injection ◽  
Neonatal Pigs ◽  
Cerebral Metabolic Rate ◽  
Resistance Vessels ◽  
Newborn Pigs ◽  
Cerebral Resistance

We examined effects of hyperthermia on cerebral metabolic rate for oxygen (CMRO2) and cerebral blood flow (CBF) in anesthetized, newborn pigs (2–5 days old). CBF and CMRO2 were measured during normothermia (38 degrees C) and during hyperthermia induced by body heating (42 degrees C). During normothermia, total CBF was 32 +/- 3 ml.min-1.100 g-1 (n = 9), and CMRO2 was 1.34 +/- 0.08 ml O2.100 g-1.min-1 (n = 7). During hyperthermia, total CBF increased by 97 +/- 23% and CMRO2 by 65 +/- 24%. We also examined whether cerebral resistance vessels were responsive under these conditions. During hyperthermia, total CBF was 63 +/- 6 ml.min-1.100 g-1, and CMRO2 was 2.13 +/- 0.27 ml O2.100 g-1.min-1. During sustained hyperthermia, intravenous injection of 5 mg/kg of indomethacin decreased total CBF by 45 +/- 7% (n = 9), and CMRO2 fell by 55 +/- 10% (n = 5). We conclude that 1) hyperthermia increases CBF and CMRO2, and 2) the dilated cerebrovascular bed during hyperthermia still is responsive to a constrictor stimulus.

Sympathetic regulation of the cerebral circulation by the carotid chemoreceptor reflex

1980 ◽  
Vol 238 (4) ◽  
pp. H594-H598 ◽  
Author(s):  
S. F. Vatner ◽  
L. L. Priano ◽  
J. D. Rutherford ◽  
W. T. Manders
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Cerebral Circulation ◽  
Sympathetic Nerves ◽  
Sodium Pentobarbital ◽  
Sympathetic Regulation ◽  
Reflex Stimulation ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

The effects of carotid chemoreceptor reflex stimulation (intracarotid injection of nicotine 0.2 microgram/kg) were examined in conscious dogs on the cerebral circulation, using the radioactive microsphere technique to measure cerebral blood flow. In intact dogs (n = 18) with ventilation controlled, carotid chemoreceptor reflex stimulation increased (P less than 0.01) mean arterial pressure by 36 +/- 5% (SE) and calculated cerebral vascular resistance by 58 +/- 13%, whereas cerebral blood flow fell by 7 +/- 6% (NS). After bilateral cervical sympathectomy (n = 9), carotid chemoreceptor reflex stimulation induced significantly different (P less than 0.01) effects on cerebral blood flow, which rose by 42 +/- 8%, and cerebral vascular resistance, which did not change. To determine whether the difference in effect was due to the sympathectomy or merely to the repetition of the stimulus, another group of dogs (sham; n = 6) that had intact sympathetic nerves were studied a second time. In "sham" dogs, the repeat response to carotid chemoreceptor stimulation also induced significantly different effects from those in dogs with sympathectomy. After general anesthesia with sodium pentobarbital, or after section of the ipsilateral carotid sinus nerve, carotid chemoreceptor stimulation with nicotine, 0.2 microgram/kg, failed to induce a detectable hemodynamic effect. Thus, in the conscious dog, stimulation of the carotid chemoreceptor reflex elicits significant sympathetically mediated vasoconstriction in cerebral vessels.

Cerebrovascular response to hypoxia in baroreceptor- and chemoreceptor-denervated dogs

1981 ◽  
Vol 241 (5) ◽  
pp. H724-H731 ◽  
Author(s):  
R. J. Traystman ◽  
R. S. Fitzgerald
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Section ◽  
Carotid Baroreceptor ◽  
Aortic Baroreceptors ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Cerebral hemodynamic responses to arterial hypoxemia were studied in anesthetized paralyzed dogs that were or that had undergone carotid baroreceptor denervation, carotid chemoreceptor denervation, vagotomy, or both vagotomy and carotid sinus nerve section. Arterial O2 content was lowered from control (19.0 vol%) to 9.6 vol% by either decreasing arterial O2 tension [hypoxic hypoxemia (HH)] or increasing carboxyhemoglobin saturation[carbon-monoxide hypoxemia (COH)] at normal O2 tension. In intact animals (composite control values from all groups) HH and COH resulted in similar increases in cerebral blood flow (to 205 and 197% of control, respectively). Cerebral vascular resistance decreased more with COH than with HH (to 42 vs. 60% of control). The response from carotid baroreceptor-denervated animals and from vagotomized animals did not differ from that of the intact animals. After carotid chemoreceptor denervation and combined carotid sinus nerve section and vagotomy, both HH and COH increased cerebral blood flow to 194% of control (same increase as in intact animals, carotid baroreceptor-denervated animals, and vagotomized animals) and produced equal reductions in cerebral vascular resistance (to 34% of control). These data show that the carotid and aortic chemoreceptors are not necessary for the increase in cerebral blood flow provoked by hypoxemia and that this response is not modified by the carotid and aortic baroreceptors.

scholarly journals Endothelium-Derived Relaxing Factor Inhibits Constrictor Responses of Large Cerebral Arteries to Serotonin

1992 ◽  
Vol 12 (3) ◽  
pp. 500-506 ◽  
Author(s):  
Frank M. Faraci ◽  
Donald D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Cerebral Arteries ◽  
Large Arteries ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Endothelium-derived relaxing factor [EDRF, nitric oxide (NO) or a NO-containing compound] influences basal tone of cerebral blood vessels and mediates vasodilation in response to several stimuli. It is not known whether EDRF also modulates responses to cerebral vasoconstrictor stimuli in vivo. Our goal was to determine whether formation of EDRF inhibits constrictor responses of large cerebral arteries to serotonin. We measured cerebral blood flow (microspheres) and pial microvascular pressure (servo null) in anesthetized rabbits and calculated resistance of large cerebral arteries. Responses to an inhibitor of NO formation, NG-nitro-l-arginine (l-NNA, 3 mg/kg i.v.), were examined. l-NNA produced an increase in resistance of large arteries and total cerebral vascular resistance of approximately 15% (p < 0.05 for both variables) and a small decrease in cerebral blood flow (35 ± 9 vs. 32 ± 7 ml min−1 100 g−1, mean ± SD, p < 0.05). Under control conditions, infusion of serotonin (10 μg kg−1 min−1, into the left atrium) produced an increase in resistance of large arteries. Following treatment with l-NNA, the change in resistance of large arteries in response to serotonin was increased more than twofold (0.20 ± 0.17 vs. 0.43 ± 0.21 mm Hg ml−1 min 100 g, p < 0.05). In contrast, l-NNA did not alter the increase in resistance of large arteries during hypocapnia. l-arginine inhibited the effects of l-NNA on baseline cerebral vascular resistance and on responses of large arteries to serotonin. Thus, formation of EDRF (NO) from l-arginine (a) has a modest influence on cerebral blood flow under basal conditions and (b) inhibits constriction of large cerebral arteries to serotonin, but not hypocapnia.

Sign in / Sign up

Export Citation Format

Share Document