Biomedical subjects

R Mirro

Publications and source records attributed to R Mirro.

At least 55 records · Page 3Linked to original sources

PubMed1989

Influence of endothelin on piglet cerebral microcirculation.

The purpose of this study was to determine responses of the newborn pig cerebral microcirculation to endothelin. Pial arterioles were observed directly using a closed cranial window in chloralose-anesthetized piglets. Topical application of endothelin derived from porcine endothelial cells produced increases in pial arteriolar diameter at the lowest concentration (0.1 ng/ml) (159 +/- 6 to 180 +/- 8 microns) and concentration-dependent decreases in pial arteriolar diameter at higher concentrations (141 +/- 6, 127 +/- 5, and 110 +/- 4 microns at 1, 10, and 100 ng/ml, respectively). Indomethacin (5 mg/kg iv) and aspirin (50 mg/kg iv) blocked dilator responses to endothelin and attenuated constrictor responses. Endothelin produced concentration-dependent increases in cortical periarachnoid cerebrospinal fluid levels of 6-ketoprostaglandin (6-keto-PG) F1 alpha, PGE2, PGF2 alpha, and thromboxane B2. Thus endothelin can produce either dilation or constriction of cerebral arterioles in newborn pigs, depending on concentration. Furthermore, prostanoids appear to mediate vasodilation induced by the lowest concentration of endothelin and contribute to constriction induced by higher concentrations of endothelin.

Animals↗

PubMed1989

Blood-induced superoxide anion generation on the cerebral cortex of newborn pigs.

Pigs were equipped with closed cranial windows to measure superoxide anion generation in response to blood placed on the cerebral cortex. Superoxide dismutase (SOD)-inhibitable nitro blue tetrazolium (NBT) reduction was measured in the presence of 1) artificial cerebrospinal fluid (CSF), 2) homologous nonheparinized blood (blood), and 3) blood after treatment with indomethacin. SOD-inhibitable NBT reduction was increased significantly in the blood group compared with control, whereas piglets pretreated with indomethacin had significantly less SOD-inhibitable NBT reduction. This suggests that superoxide anion is generated by extravascular blood and that this superoxide anion generation can be inhibited by indomethacin. To investigate the cellular origin of superoxide anion generation, SOD-inhibitable NBT reduction was measured during incubation with piglet whole blood or its components in vitro. The SOD-inhibitable NBT reduction of nonheparinized whole blood was 30 +/- 5.7 nmol.ml-1.20 min-1. This decreased to 2.5 +/- 1.3 nmol.ml-1.20 min-1 in the presence of indomethacin. SOD-inhibitable NBT reduction of ADP-stimulated platelet-rich plasma was 25.6 +/- 2.9 nmol.400 X 10(6) cells-1.20 min-1 and was decreased significantly (6.8 +/- 3.0 nmol.400 X 10(6) cells-1.20 min-1) in the presence of indomethacin. SOD-inhibitable NBT reduction by granulocytes was significant but unchanged by indomethacin. Similarly, SOD-inhibitable NBT reduction by lymphocytes and monocytes was unaffected by indomethacin. Reduction by the red cell fraction was small. These results suggest that substantial quantities of superoxide anion are generated via the platelet cyclooxygenase pathway of arachidonic acid metabolism.

Animals↗

PubMed1989

Effects of ischemia on brain blood flow and oxygen consumption of newborn pigs.

Brain circulation after 20 min of total brain ischemia was examined in unanesthetized newborn pigs. Except in the cerebrum, reactive hyperemia was observed throughout the brain, peaking by 5 min and subsiding by 20 min of reperfusion. Brain blood flow after 15 min of reperfusion matched the control. Blood flow to the cerebrum then decreased at 40 and 90 min reperfusion, while the rest of the brain was unaffected. Blood flow to the cerebrum returned to control by 24 h. Cerebral vascular resistance doubled by 15 min reperfusion, remained elevated at 90 min reperfusion, but returned to control by 24 h. Cerebral oxygen consumption followed a pattern similar to blood flow. Ninety minutes postischemia, hypercapnia-induced hyperemia was greatly attenuated in the cerebrum, reduced modestly in the diencephalon-mesencephalon, but unaffected in the rest of the brain. Thus 20 min of global brain ischemia in piglets does not produce reactive hyperemia in the cerebrum that is detectable at 5 min reperfusion but does in the remainder of the brain. Subsequent hemodynamic abnormalities apparently are confined to the cerebrum. Blood flow throughout the brain returns to normal by 24 h. Thus cerebral hemodynamic effects of total global ischemia are regionally dependent.

Animals↗

PubMed1989

Vascular responses to vasopressin are tone-dependent in the cerebral circulation of the newborn pig.

The effects of lysine vasopressin (LVP) on pial arteriolar diameter and cortical periarachnoid fluid prostanoid concentrations were investigated in newborn pigs. Chloralose-anesthetized piglets were equipped with closed cranial windows over the parietal cortex for observation of pial arterioles and collection of cerebrospinal fluid (CSF) passing over the cerebral surface. Prostanoids in the CSF were determined by radioimmunoassay. LVP (10-1,000 microU/ml) elicited concentration-dependent increases in pial arteriolar diameter associated with increased levels of 6-keto-prostaglandin (PG)F1 alpha, PGE2, thromboxane B2, and PGF2 alpha. LVP-induced pial arteriolar dilation was unchanged after intravenous indomethacin (5 mg/kg). Conversely, LVP constricts pial arterioles previously dilated by physiological (hemorrhagic hypotension) and pharmacological (topically applied PGE2 or isoproterenol) intervention. This constriction is potentiated by indomethacin. Vascular and biochemical changes elicited by LVP were blocked by intravenous [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid),2,(O-methyl)-Tyr-AVP] (5 micrograms/kg), a putative V1 receptor antagonist, whereas vascular effects of norepinephrine and U46619, a thromboxane A2 mimic, were unchanged. Therefore, the degree of vascular tone appears to influence responses of the newborn pig cerebral circulation to LVP.

Animals↗

PubMed1989

Postischemic cerebral microvascular responses to norepinephrine and hypotension in newborn pigs.

We examined the effects of 20 minutes' cerebral ischemia on cerebral microcirculatory responses to topical norepinephrine and systemic hypotension in three groups (sham-operated control, 2-3 hours postischemia, and 24 hours postischemia) of anesthetized newborn pigs equipped with closed cranial windows. Cerebral ischemia may eliminate the prostanoid vasodilator system from the cerebral circulation. Norepinephrine (10(-4) M) decreased pial arteriolar diameters similarly in all three groups (27%, 28%, and 21%, respectively), but only the sham-operated group exhibited pial arteriolar dilation in response to hypotension (28% at 33 mm Hg). Two-three and 24 hours after cerebral ischemia, hypotension decreased pial arteriolar diameters (21% and 17%, respectively). In sham-operated piglets, norepinephrine and hypotension increased cortical periarachnoid cerebrospinal fluid prostanoid concentrations. However, neither norepinephrine nor hypotension altered cerebral prostanoid production 2-3 or 24 hours after cerebral ischemia. Therefore, we conclude that after cerebral ischemia, autoregulatory pial arteriolar dilation in response to hypotension is absent, while vasoconstriction in response to norepinephrine is intact.

Administration, Topical↗

PubMed1989

Ischemia alters cerebral vascular responses to hypercapnia and acetylcholine in piglets.

Effects of ischemia (20 min) on cerebral cortical prostanoid synthesis and microvascular responses to hypercapnia and topical acetylcholine were examined in anesthetized newborn pigs. Pial arteriolar dilation in response to hypercapnia (10% CO2 ventilation, 10 min) was absent 2 h after ischemia and reversed toward constriction by 24 h postischemia. In sham control piglets, hypercapnia increased cortical periarachnoid fluid prostanoid concentrations. After ischemia, hypercapnia did not affect prostanoid concentrations on the brain surface. Acetylcholine (10(-3) M)-induced pial arteriolar constriction was reversed toward dilation 24 h after cerebral ischemia. Further, acetylcholine-induced prostanoid synthesis was markedly attenuated after ischemia. We conclude that cerebral ischemia-reperfusion alters cerebral prostanoid synthesis and microvascular control in newborn pigs. These abnormalities persist for at least 24 h.

6-Ketoprostaglandin F1 alpha↗

PubMed1989

Influence of intraarterial norepinephrine on cerebral hemodynamics of newborn pigs.

Effects of intraarterial norepinephrine on cerebral hemodynamics were investigated in conscious newborn pigs. Intracarotid infusion of norepinephrine (100 ng/min) increased cerebral blood flow from 72 +/- 5 to 82 +/- 8 ml/100 g.min. The norepinephrine-induced increase in cerebral blood flow was accompanied by an increase in cerebral oxygen consumption from 2.75 +/- 0.17 to 3.11 +/- 0.29 ml O2/100 g.min. Both the increase in cerebral oxygen consumption and the increase in cerebral blood flow were blocked by propranolol and unchanged by combined prazosin and yohimbine treatment. These data show that intraarterial norepinephrine increases cerebral blood flow and cerebral oxygen consumption in newborn pigs. beta-Adrenergic stimulation increases cerebral oxygen consumption. This increase may produce the increase in cerebral blood flow caused by the norepinephrine.

Animals↗

PubMed1989

Permissive role of prostanoids in acetylcholine-induced cerebral vasoconstriction.

The present study was designed to test the hypothesis that prostanoids play a permissive role in acetylcholine-induced cerebral constriction. Pial arterioles of newborn pigs were observed using a closed cranial window. Pial arteriolar constriction induced by topical acetylcholine (10(-5) M) was blocked by indomethacin (5 mg/kg i.v.), but was restored when acetylcholine was coadministered with topical prostaglandin (PG) F2 alpha (1 ng/ml), U46619 (1 ng/ml) or PGH2 (100 ng/ml). The restored acetylcholine response was blocked by topical pirenzepine (10(-3) M), a muscarinic-1 antagonist. Constriction and ability of all three prostanoids to restore acetylcholine-induced constriction was blocked by SQ 29,548 (10(-4) M), a purported thromboxane A2/PGH2 receptor antagonist. Subthreshold concentrations of U46619 and PGF2 alpha (0.1 ng/ml) restored acetylcholine-induced constriction, whereas threshold and subthreshold concentrations of PGE2, platelet-activating factor and norepinephrine had no effect. Therefore, activation of the thromboxane A2/PGH2 receptor appears to be necessary for acetylcholine-induced constriction to occur. Thus, prostanoids appear to play a permissive role in acetylcholine-induced pial arteriolar constriction in newborn pigs.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1989

Low-dose aspirin in pregnancy.

In a prospective study, we evaluated the effects of low-dose aspirin on maternal and neonatal plasma 6-keto-prostaglandin (PG) F1 alpha concentration, platelet aggregation, platelet thromboxane production, and neonatal transitional circulation. Forty women, at a mean (+/- SD) of 37 +/- 2 weeks' gestation, were randomized to receive (N = 10 each) placebo or 20, 60, or 80 mg of aspirin per day until delivery. Maternal serum 6-keto-PGF1 alpha levels were not affected by these doses of aspirin, whereas thromboxane B2 generated during clotting of maternal blood was decreased significantly by 60 and 80 mg of aspirin by 1 week of therapy. Maternal platelet thromboxane B2 production in response to adenosine diphosphate or collagen was reduced 98% by the 80-mg dose after 1 week of aspirin therapy. The 60-mg dose reduced maternal platelet thromboxane B2 production in response to adenosine diphosphate (50% decrease) or collagen (60% decrease) after 1 week of treatment, a nonsignificant difference. After 2 weeks of treatment with 60 mg of aspirin, platelet thromboxane B2 production induced by both collagen and adenosine diphosphate was inhibited significantly (P less than .01). Neonatal serum levels of 6-keto-PGF1 alpha and thromboxane B2 were not affected by any doses of aspirin. Further, neonatal platelet aggregation in response to platelet stimulation by collagen and adenosine diphosphate was not inhibited. All neonates had echocardiographic evidence of a patent ductus arteriosus, and noninvasive estimates of pulmonary arterial pressure were similar among the groups of infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗

PubMed1988

Effect of 15-HETE on cerebral arterioles of newborn pigs.

Effects of topical application of 15-HETE on pial arteriolar diameter and cortical periarachnoid cerebrospinal fluid (CSF) prostanoid concentrations were investigated in chloralose-anesthetized newborn pigs. Pial arteriolar diameters were measured using a closed cranial window, and CSF samples from under the window were collected for prostanoid analysis after applying artificial CSF without drug and CSF containing 15-HETE (1, 10, 100, 10000 ng/ml). 15-HETE caused significant dose-related constriction from 162 +/- 17.0 microns (control diameter) to 136 +/- 14.5 and 129 +/- 18.7 microns (100 and 1000 ng/ml, respectively). The concentration of PGE2 (but not of PGF2 alpha or 6-keto-PGF1 alpha) increased in CSF at 100 and 1000 ng/ml of 15-HETE. Pial arteriolar responses to 15-HETE were determined before and after indomethacin treatment (5 mg/kg, i.v.). 15-HETE (100 ng/ml) constricted pial arterioles before indomethacin (diameter change, -15 +/- 10%); after indomethacin, constriction was potentiated in response to the same dose (diameter change, -26 +/- 7%). These data support the hypothesis that, in newborn piglets, 15-HETE exerts a vasoconstrictor effect on pial arterioles, which appears to be attenuated by 15-HETE-induced stimulation of dilator prostanoids.

Animals↗

PubMed1988

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

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.

Animals↗

PubMed1988

Histamine dilates pial arterioles of newborn pigs through prostanoid production.

To test the hypothesis that histamine would dilate pial arterioles via a prostanoid mechanism, histamine was placed on the brain surface of anesthetized newborn pigs via a closed cranial window. Pial arteriolar diameters were measured after topical application of 10(-7), 10(-6), 10(-5), 10(-4), and 10(-3) M histamine. In addition, cortical cerebrospinal fluid (CSF) was collected for radioimmunoassay of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), thromboxane B2 (TxB2), prostaglandin D2 (PGD2), prostaglandin E2 (PGE2), and prostaglandin F2 alpha (PGF2 alpha). The animals were then randomized to receive either indomethacin trihydrate (5 mg/kg, iv) or an equal volume of saline (vehicle). The protocol then was repeated. Histamine (before indomethacin or vehicle infusion) caused concentration-dependent vasodilation. This vasodilation was accompanied by a significant increase in cortical CSF 6-keto-PGF1 alpha and PGE2. Concentrations of TxB2, PGD2, and PGF2 alpha were not altered significantly by histamine application. Pretreatment with indomethacin blocked the histamine-induced cerebral vasodilation, but vasodilation after vehicle was intact. These data imply that histamine dilates the pial arterioles of newborn pigs by stimulating the synthesis of vasodilator prostanoids.

Animals↗

PubMed1988

Postischemic generation of superoxide anion by newborn pig brain.

Cerebral superoxide anion generation during reperfusion after total cerebral ischemia was measured in newborn pigs. Superoxide dismutase (SOD)-inhibitable nitroblue tetrazolium (NBT) reduction was determined using two closed cranial windows inserted over the parietal cortices. Twenty minutes of total cerebral ischemia was produced by increasing intracranial pressure, and SOD-inhibitable NBT reduction was determined during 20 min of reperfusion. SOD-inhibitable NBT reduction (8.7 +/- 1.5 pmol.mm-2.20 min-1) was greater in piglets subjected to cerebral ischemia followed by reperfusion than in control piglets not exposed to ischemia (1.6 +/- 1.3 pmol.mm-2.20 min-1). Pretreatment with indomethacin (5 mg/kg iv) markedly reduced postischemia SOD-inhibitable NBT reduction (2.8 +/- 1.1 pmol.mm-2.20 min-1). We conclude that superoxide anion radical is produced by newborn pig brain during postischemic reperfusion. Furthermore, cyclooxygenase metabolism of arachidonic acid appears to be a major source of this activated oxygen during reperfusion of ischemic piglet brain.

Animals↗

PubMed1988

Platelet activating factor: a potent constrictor of cerebral arterioles in newborn pigs.

This study characterized the nature of the response to platelet activating factor (PAF) in the cerebral microcirculation of the newborn pig. Pial arterioles were observed directly using a closed cranial window in chloralose-anesthetized piglets. Topical application of 10-100 ng/ml PAF produced dose-dependent decreases in pial arteriolar diameter; diameters were 193 +/- 27 microns for control, 167 +/- 25 microns at 10 ng/ml, and 129 +/- 21 microns at 100 ng/ml. Topical application of 30-300 ng/ml norepinephrine and 3-30 ng/ml U46619, a purported thromboxane A2 receptor agonist, also produced dose-dependent decreases in pial arteriolar diameter. After topical administration of U66985 (1 microgram/ml), a putative PAF antagonist, responses to PAF were attenuated significantly, but responses to norepinephrine and U46619 were unchanged. Moreover, intravenously administered U66985 (0.1 mg/kg) antagonized PAF responses as well. Responses to PAF were unchanged after cyclooxygenase and leukotriene receptor inhibition. Further, PAF did not increase cortical subarachnoid cerebrospinal fluid prostaglandin or leukotriene levels. These data indicate that PAF is a potent constrictor of cerebral arterioles in newborn pigs and that its mechanism of action is independent of formation of cyclooxygenase and lipoxygenase products of arachidonic acid metabolism. These data also suggest that U66985 may be a selective PAF antagonist that crosses the blood-brain barrier. Since PAF is an endogenous lipid released from a variety of tissues and may be an important mediator of inflammation and allergic reaction, PAF could be involved in the pathophysiology of the cerebral circulation in the perinatal period.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1988

Indomethacin restricts cerebral blood flow during pressure ventilation of newborn pigs.

Unanesthetized newborn pigs were studied to evaluate the immediate (10 min) and delayed (45 min) effects of increased ventilation pressure coupled with cyclooxygenase inhibition. Cardiac output and cerebral blood flow were measured at a low (5 cm H2O) and high (30 cm H2O) mean airway pressure (Paw) before and 45 min after 5 mg/kg of indomethacin. In a second group, these parameters were also measured 10 min after indomethacin was given during ventilation at a Paw of 30 cm H2O. Before treatment with indomethacin, increasing Paw decreased cardiac output without affecting cerebral blood flow. Baseline (Paw = 5 cm H2O) cerebral blood flow decreased 40% 45 min after indomethacin treatment. Adding the stress of a ventilation-induced drop in cardiac output did not further depress cerebral blood flow. When indomethacin was administered during high Paw, cerebral blood flow decreased markedly within 10 min. Cerebral oxygen consumption was maintained by increasing oxygen extraction. Therefore, indomethacin decreases cerebral blood flow at a high Paw. The fall in cerebral blood flow decreases brain oxygen delivery. However, cerebral oxygen consumption is maintained by an increase in oxygen extraction.

Animals↗

PubMed1988

Acetylcholine produces cerebrovascular constriction through activation of muscarinic-1 receptors in the newborn pig.

This study was designed to characterize the nature of responses to selective muscarinic (M)-1 and M-2 agonists and to determine the receptor subtype which mediates the vascular response to acetylcholine in the cerebral circulation of the newborn pig. Pial arterioles of anesthetized newborn pigs were observed using the closed cranial window method. Topical McN-A-343 (10(-7), 10(-4) M), an M-1 agonist, produced pial arteriolar constriction (diameters were 140 +/- 8, 127 +/- 9 and 111 +/- 8 microns for control, 10(-7) and 10(-4) M McN-A-343) that was blocked by topical pirenzepine (10(-3) M), an M-1 antagonist. Topical bethanachol (10(-7), 10(-4) M), an M-2 agonist, produced pial arteriolar dilation (diameters were 148 +/- 8, 169 +/- 10 and 181 +/- 10 microns for control, 10(-7) and 10(-4) M bethanachol) that was blocked by 4-DAMP 4-diphenylacetoxy-N'-methylpiperidine methiodide (10(-3) M), an M-2 antagonist. Responses to McN-A-343 were unchanged after 4-DAMP, and responses to bethanachol were unchanged after pirenzepine. Topical McN-A-343 and bethanachol elicited modest increases in cortical periarachnoid cerebrospinal fluid levels of 6-keto-prostaglandin F1 alpha, prostaglandin E2, thromboxane B2 and prostaglandin F2 alpha. Topical acetylcholine (10(-7), 10(-4) M) elicited pial arteriolar constriction and large increases in cerebrospinal fluid prostanoid levels which were blocked by atropine (0.5 mg/kg i.v.) and topical pirenzepine (10(-3) M), but not by topical 4-DAMP. These data demonstrate the existence of M-1 and M-2 receptors in the cerebral circulation of the newborn pig and indicate that acetylcholine elicits cerebrovascular constriction and increased cerebrospinal fluid prostanoid synthesis via activation of M-1 receptors.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed1988

The role of prostanoids in the mediation of responses to KC-404, a novel cerebrovasodilator.

The purpose of this study was to characterize the nature of the response to KC-404 in the cerebral microcirculation of the newborn pig. Pial arterioles were observed directly using a closed cranial window in chloralose-anesthetized piglets. Topical application of 100, 300, 1000, 3000 and 10,000 ng/ml of KC-404 produced concentration-dependent increases in pial arteriolar diameter. Diameters were 168 +/- 18, 190 +/- 19 and 238 +/- 21 mu for control, 100 ng/ml and 10,000 ng/ml of KC-404, respectively. Responses to KC-404 (3-isobutyryl-2-isopropylpyrazolo-[1,5a]-pyridine) were blocked by indomethacin (5 mg/kg i.v.). Moreover, KC-404, topically applied to the cerebral cortex, produced small but significant increases in cortical subarachnoid cerebrospinal fluid levels of 6-keto-prostaglandin (PG) F1 alpha and PGE2, whereas thromboxane B2 levels were unchanged. Similar to topical application, i.v. KC-404 (0.5 mg/kg) produced pial arteriolar dilation without significantly altering arterial blood pressure. Intravenous KC-404 also increased cerebrospinal fluid levels of 6-keto-PGF1 alpha and PGE2, whereas thromboxane levels were unchanged. Further, topically applied KC-404 (1 microgram/ml) potentiated dilator responses to PGE2 and PGI2, whereas responses to isoproterenol were unchanged. These data indicate that KC-404 is a potent dilator of cerebral arterioles in newborn pigs. These data also suggest that KC-404 produces cerebral vasodilation predominantly by potentiating prostanoid-mediated dilation.

Animals↗

PubMed1987

Perinatal anterior cerebral artery Doppler flow indexes: methods and preliminary results.

Using a standard 5 MHz continuous-wave Doppler system, we were able to record velocities from the anterior cerebral arteries of 20 infants both in utero (at 6 to 10 cm cervical dilatation) and after delivery. In utero tracings were of the same quality as neonatal tracings. Difficulties encountered in the course of the study included abnormal lie, small fontanelle, and excessive caput. Despite these problems our success rate in obtaining good tracings was 80%. Results showed that indexes of cerebral vascular resistance were increased during labor and decreased after birth. However, Doppler indexes of blood flow remained constant throughout the perinatal period. This preliminary report describes the methodology of this new technique. In addition our results demonstrate that in utero intracranial tracings are obtainable and may provide valuable information about cerebral hemodynamics during labor.

Asphyxia Neonatorum↗