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Biomedical subjects

J T Parer

Publications and source records attributed to J T Parer.

At least 37 records · Page 2Linked to original sources
PubMed1995

Cardiovascular responses to graded degrees of hypoxaemia in the llama fetus.

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.

Animals↗
PubMed1994

Regional blood flow and metabolism in ovine fetuses during severe cord occlusion.

OBJECTIVE: Our purpose was to compare the ovine fetal response to severe, damaging asphyxia resulting from umbilical cord occlusion with that seen in uterine artery occlusion. STUDY DESIGN: Six ovine fetuses were exposed to severe asphyxia produced by partial umbilical cord occlusion for 90 minutes. Fetal blood pressure and heart rate, blood gases, acid base status, electrocorticogram, and electromyogram were recorded. Regional blood flow (radioactive microspheres) measurements were performed at control and 30, 60, and 90 minutes of occlusion and 30 minutes after release. RESULTS: During the period of occlusion pH fell from 7.37 +/- 0.01 (mean +/- SEM) to 6.82 +/- 0.03 at 90 minutes, base excess from 5 +/- 1 to -22 +/- 2 mEq.L-1 and oxygen content from 3.3 +/- 0.4 mmol.L-1 to a nadir of 1.6 +/- 0.4 mmol.L-1 (p < 0.05). There was no significant long-term change in fetal heart rate or blood pressures. The fetal electrocorticogram was profoundly suppressed during asphyxia, and seizure activity was documented after release of occlusion in all surviving animals. Umbilical blood flow fell to 21% +/- 5% of control by 60 minutes of occlusion and remained depressed until release. Brain and adrenal blood flows increased during asphyxia. Heart and intestinal blood flows did not change significantly from control values. Combined ventricular output and spleen, kidney, and carcass blood flow fell during the insult. Oxygen uptake by the cerebral cortex remained stable during occlusion. Oxygen uptake by the lower carcass fell to 15% +/- 7% of control. CONCLUSION: Umbilical cord occlusion produces similar levels of asphyxia and evidence of encephalopathy (seizures), compared with previous experiments with uterine artery occlusion. The fetal response with respect to blood flow redistribution and organ oxygen uptake, however, differs. These differences may signify that with uterine artery occlusion the brain may be more vulnerable, whereas with umbilical cord occlusion the heart may be at greater risk.

Animals↗
PubMed1994

Intrahepatic cholestasis of pregnancy: a retrospective case-control study of perinatal outcome.

OBJECTIVES: Intrahepatic cholestasis of pregnancy has been related to a high frequency of abnormal intrapartum fetal heart rate, amniotic fluid meconium, prematurity, and perinatal mortality. To determine whether these adverse perinatal outcomes could be improved with active intervention, we evaluated our results. STUDY DESIGN: We report a retrospective case-control study of 320 consecutive patients with intrahepatic cholestasis of pregnancy management with antepartum testing and active intervention over a 2-year period. RESULTS: Our results indicate a higher incidence of meconium staining in amniotic fluid at delivery (25% vs 16%, p < 0.05) and spontaneous preterm delivery (12.1% vs 3.9%, p < 0.05), without an increase in the frequency of abnormal intrapartum fetal heart rate (12% vs 11%, not significant), 5-minute Apgar score < 7 (2.0% vs 1.0%, not significant), or perinatal mortality (18/1000 vs 13/1000, not significant). CONCLUSION: Antenatal testing and timed intervention of patients with intrahepatic cholestasis of pregnancy is associated with a reduction of the previously reported adverse perinatal outcomes.

Adult↗
PubMed1994

Regional blood flow in asphyxiated fetuses with seizures.

OBJECTIVE: Our purpose was to determine ovine fetal regional blood flow changes during asphyxia of such severity that it results in seizures. STUDY DESIGN: Six ovine fetuses were exposed to severe asphyxia produced by maternal uterine artery occlusion for up to 90 minutes. Fetal blood pressure and heart rate, blood gases, acid base status, electrocorticogram, electromyogram and regional blood flow (radioactive microspheres) measurements were recorded. RESULTS: During the asphyxial insult pH fell from 7.39 +/- 0.01 (mean +/- SEM) to 6.99 +/- 0.01 at 60 minutes, base excess from 4 +/- 1 to -16 +/- 1 mEq/L, and oxygen content from 3.5 +/- 0.4 to 0.5 +/- 0.1 mmol/L (p < 0.05). There was no significant change in fetal heart rate or blood pressure. The fetal electrocorticogram was profoundly suppressed during asphyxia, and seizure activity began 50 +/- 19 minutes after the release of occlusion in all surviving animals. Blood flow increased to the heart and adrenals during asphyxia and decreased to spleen, gut, kidneys, and carcass (p < 0.05). There was no change in combined ventricular output and umbilical blood flow. There was no significant increase in total cerebral perfusion. CONCLUSION: When the ovine fetus is exposed to asphyxia of sufficient severity to produce neurologic damage (seizures), the pattern of redistribution of blood flow is comparable to the response to lesser asphyxia, except that a significant increase in total brain blood flow does not occur. This finding may have an important association with the development of long-term neurologic damage.

Adrenal Glands↗
PubMed1993

Effects of propofol and thiopental on maternal and fetal cardiovascular and acid-base variables in the pregnant ewe.

BACKGROUND: The effects of propofol on uterine blood flow are not understood well. This is a relatively new agent that is finding increased use for nonobstetric surgical procedures during pregnancy and induction of anesthesia for cesarean section. METHODS: The effects of induction and maintenance of anesthesia with propofol were studied on maternal and fetal cardiovascular and acid-base variables in a chronically instrumented pregnant sheep model. Anesthesia was induced with a 2 mg/kg bolus of propofol and maintained with of one of three continuous infusions: 150, 300, and 450 micrograms.kg-1 x min-1. The control group received thiopental for induction, and anesthesia was maintained with isoflurane. RESULTS: The use of propofol did not adversely affect maternal or fetal mean arterial pressure, heart rate, or base excess, fetal heart rate variability, or uterine blood flow. Uterine blood flow transiently decreased during induction and intubation with thiopental but remained stable during induction with propofol. However, administration of succinylcholine for intubation in the presence of propofol resulted in a transient, but severe, maternal bradycardia. Continuous infusion of 300 micrograms.kg-1.min-1 of propofol appeared to provide satisfactory anesthesia in the ewe. CONCLUSIONS: Assuming the applicability of ovine data to humans, these findings suggest that induction and maintenance of anesthesia with propofol and 50% nitrous oxide in oxygen has no adverse fetal effects but warrants caution because of the potential risk of severe maternal bradycardia during induction of anesthesia using the combination of propofol and succinylcholine.

Acid-Base Equilibrium↗
PubMed1992

The physiologic mechanisms of variable decelerations.

OBJECTIVES: The purpose of this study was to determine the cause and physiologic consequences of variable decelerations. STUDY DESIGN: Previous studies of heart rate changes in human and experimental animals were critically reviewed with respect to the autonomic nervous system component, the cause of the increased vagal activity, and the role of cord compression or other stimuli in these heart rate changes. RESULTS: There is abundant evidence from experimental and human studies that variable decelerations can be reproduced by either cord compression or head compression. The vagal reflex produced is probably caused by a combination of chemoreflex (earlier in the deceleration) and baroreflex (later). The variable deceleration is accompanied by an acidosis, primarily respiratory, and probably hypoxemia. Cord compression results in decreased umbilical blood flow. CONCLUSIONS: Recent Doppler velocimetry studies suggest that even though the variable decelerations may be similar in duration and depth, the reduction of umbilical blood flow may be greater when the prime cause is cord compression than when the prime cause is vagal reflex from another source.

Amniotic Fluid↗
PubMed1992

Hydralazine does not restore uterine blood flow during cocaine-induced hypertension in the pregnant ewe.

Cocaine abuse is widespread, and its use by the parturient has potential significant adverse effects in both the mother and the newborn. This study was undertaken in gravid ewes to determine the effects of treatment of cocaine-induced hypertension with hydralazine (Apresoline) on the maternal and fetal cardiovascular systems, catecholamine response, blood gas and acid-base status, and uterine blood flow (UBF). Twenty-one experiments were performed in 15 chronically instrumented ewes near term gestation. After a 30-min control period, cocaine was given intravenously to all ewes for 55 min to induce and maintain increased maternal mean arterial pressure (MMAP) and reduced UBF. The sheep were randomly assigned to receive either cocaine alone (n = 11, control group) or hydralazine (n = 10, treatment group), starting 15 min after the cocaine administration. Both drugs were discontinued 55 min after the start of the cocaine administration, followed by a 35-min recovery period. In the control group, cocaine administration resulted in a 31 +/- 13% (SD) increase in MMAP (P less than 0.05) and a 26 +/- 21% reduction in UBF (P less than 0.05). In the treatment group, the initial cocaine administration resulted in a similar increase in MMAP and decrease in UBF. Hydralazine therapy restored MMAP toward baseline after 20 min of administration, but UBF remained reduced (37 +/- 17%) throughout therapy (P less than 0.05) and recovery (18 +/- 13%) (P less than 0.05). The maternal heart rate increased maximally by 121 +/- 33% (P less than 0.05) after the administration of hydralazine, compared with a 14 +/- 21% increase (P less than 0.05) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Cerebral histologic and electrocorticographic changes after asphyxia in fetal sheep.

Asphyxia can cause neurologic damage in the fetus, but there are few data relating severity or duration of asphyxia to the degree of cerebral damage. We report cerebral histologic and electrophysiologic changes after asphyxia in chronically instrumented late-gestation fetal sheep. We reduced uterine blood flow to produce an ascending aortic blood oxygen content less than 1.5 mM for either 30 or 60 min (n = 13). In a subsequent protocol (n = 6), if full occlusion of the common uterine artery for 15 min did not reduce the EEG voltage to less than 20% of baseline, supplementary maternal hypoxia was added for a maximum of 120 min. Histologic outcome was assessed 3 d postinsult. Uterine artery occlusion resulted in severe hypoxemia, hypercarbia, acidosis, and an initial hypertension and bradycardia. Eight of 14 surviving fetuses showed neuronal damage, with greatest loss in the parasagittal cortex, striatum, and the CA1/2 region of the hippocampus. Neuronal damage was strongly associated with the percentage of decrease in blood pressure during the insult (r = 0.75, p less than 0.005) but not with the degree of hypoxia. No other factor was independently predictive, but, when considered separately, pH (r = 0.54; p less than 0.05) and loss of intensity of the EEG (r = 0.61, p less than 0.02) at the end of asphyxia were also correlated with outcome. The pH fell to less than 7.0 in six of eight fetuses with damage, whereas it remained greater than 7.0 in five of six without damage (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1991

Fetal heart rate variability and cerebral oxygen consumption in fetal sheep during asphyxia.

This study was designed to examine the relationship between fetal heart rate variability and fetal cerebral oxygen uptake. Fetal sheep were chronically prepared with catheters and electrodes to determine cerebral blood flow (microsphere method), cerebral arteriovenous oxygen difference, and the electrocardiogram. An adjustable occluder was placed on the maternal common internal iliac artery to induce fetal asphyxia by reducing uterine blood flow. Fetal heart rate variability tended to decrease in the first 11 min of asphyxia, when cerebral oxygen consumption was approximately 53% of control. Despite stable cerebral oxygen consumption and worsening metabolic acidosis, however, fetal heart rate variability progressively returned towards normal by 36 min. There was no relationship between the depression of FHR variability and the degree of reduction of cerebral oxygen consumption. Nor was there any relationship between an alteration in regional cerebral blood flow or myocardial blood flow and the return of FHR variability with increasing duration of asphyxia. We conclude that there is an association between loss of fetal heart rate variability and reduced cerebral oxygen consumption, but the reduced variability does not persist with time at this degree of reduced cerebral metabolism in fetal sheep. This appears to be at variance with human clinical experience. Among the explanations for this may be insufficiently severe asphyxia, a species difference, removal of an inhibitor to FHR variability, or progressive use of other substrates for metabolism.

Animals↗
PubMed1991

The effect of the inhibition of prostaglandin synthesis on renal blood flow in fetal sheep.

Treatment with prostaglandin synthesis inhibitors has been associated with oligohydramnios in the fetus. The presumed mechanism is a reduction in fetal renal blood flow. We examined the effect of meclofenamate administration on renal blood flow in chronically catheterized fetal sheep during normoxia and during moderate and severe hypoxia. Ten fetal sheep were made hypoxic twice at least 4 days after surgery: once in the presence and once in the absence of meclofenamate infusion. Renal blood flow and combined ventricular output were measured with radioactive microspheres. Prostaglandin synthesis blockade with meclofenamate caused no significant change in blood pressure, combined ventricular output, renal blood flow, or renal vascular resistance in either the normoxic or hypoxic animals. These data challenge the contention that prostaglandin activity protects the renal vascular bed of the fetus from vasoconstriction during hypoxia and they also do not support the hypothesis that prostaglandin synthesis inhibition causes oligohydramnios through reduction of fetal renal blood flow.

Animals↗
PubMed1991

Mechanisms of asphyxial brain damage, and possible pharmacologic interventions, in the fetus.

An examination of the cellular and molecular mechanisms of neuronal cell damage may lead to the design of pharmacologic interventions during presumed or actual fetal asphyxia. Hypoxia-ischemia in its severest form results in insufficient adenosine 5'-triphosphate production. The most important effect of this is failure of adenosine 5'-triphosphate-dependent membrane functions, which maintain ionic homeostasis, that is, ionic pumping. There is K+ efflux and Na+ influx across the cell membrane, depolarization of the cell membrane, opening of the voltage-dependent calcium channels, and entrance of Ca++ into the cell. Cytosolic Ca++ is also increased by Ca++ efflux from the mitochondria and the sarcoplasmic reticulum. Ca++ is a toxin in high cytosolic concentrations; it activates phospholipases A and C, which cause membrane breakdown and release of free fatty acids, including arachidonic acid. The membrane is damaged, lysis occurs, and the neuron dies. High cytosolic Ca++ also causes release of excitatory amino acids (especially glutamate), which overwhelm the suppressant neurotransmitters, causing seizures, increased metabolism, and aggravation of the insufficient adenosine 5'-triphosphate availability. Thromboxane A2 is generated from arachidonic acid, increasing smooth muscle tone and thereby worsening the ischemia. Cyclooxygenase activity also results in formation of oxygen-free radicals that contribute to cell membrane damage, lysis, and death. Possibilities for pharmacologic interventions include (1) calcium channel blockers and antagonists, (2) excitatory neurotransmitter blockers, (3) oxygen-free radical scavengers (e.g., superoxide dismutase), (4) cyclooxygenase or prostaglandin synthesis inhibitors, and (5) seizure suppressants (e.g., phenobarbital). Some of these treatments have been shown experimentally to limit neuronal death in the adult and fetus, and after more investigative work they may be applicable to clinical practice.

Adenosine Triphosphate↗
PubMed1991

Comparison of mathematical indices of fetal heart rate variability with visual assessment in the human and sheep.

Mathematical indices for quantitation of fetal heart rate variability have been proposed by numerous authors, but there have only been infrequent attempts to determine which such indices correspond to the semi-subjective evaluation of variability observed by clinicians. We have previously examined most of the published indices by using them for calculation of the variability of sets of computer-generated numbers, and seeing if they fulfill certain criteria of validity. Two sets of indices (each measuring short-term and long-term variability) were selected as acceptable. Segments of fetal heart rate records from both humans and sheep, with a wide range of subjective variability, were used to compare the mathematically derived indices with the semi-subjective evaluation of three observers. The results show that the mathematical indices of short-term variability compare closely to its subjective evaluation of being present or absent. The long-term variability of indices also increase progressively with the observers' evaluations of increasing variability. The agreement among observers, measured by Cohen's kappa test, is generally "substantial", although for some indices the agreement was "moderate" to "almost perfect". We conclude that the two sets of indices examined do quantitate what is clinically regarded as fetal heart rate variability.

Animals↗
PubMed1991

Two decades of advancement in the assessment of fetal health.

Over the past twenty years there has been a substantial refining and extension of the tests available for the assessment of fetal health. This has particularly been related to the developed of reasonably-priced real-time ultrasound and an improved understanding of the relationship between aspects of fetal behaviour and state and fetal health. The impact of these developments is briefly reviewed.

Behavior↗
PubMed1991

Effects of severe reduction in maternal placental blood flow on blood flow distribution in the sheep fetus.

To test the hypothesis that fetal lambs are able to maintain oxygen delivery to myocardial, brain and adrenal tissues during reduction in uterine blood flow to 25% of control, we performed experiments on five ewes and their fetuses. A snare occluder was placed around the maternal common hypogastric artery and catheters were placed for measurement of blood pressures, flows, blood gas tensions, pH and oxygen content. After a five day recovery period, control measurements were made. The snare occluder was then closed until the artery was fully occluded. The arterial occlusion caused uteroplacental blood flow to fall to 32 +/- 4% and maternal placental blood flow to fall to 25 +/- 3% of control values. This level of asphyxia was maintained for 19 +/- 3 minutes, when maternal and fetal blood flows were measured again. In response to occlusion, fetal ascending aortic PO2 fell from 21 +/- 2 (SEM) to 13 +/- 2 mmHg (P less than or equal to 0.01), oxygen content from 4.3 +/- 0.3 to 1.4 +/- 0.2 mM (P less than or equal to 0.01) and pH from 7.37 +/- 0.01 to 7.21 +/- 0.05 (P less than or equal to 0.01). PCO2 rose from 48 +/- 1 to 62 +/- 3 mmHg (P less than or equal to 0.01). Fetal arterial blood pressure increased from 51 +/- 3 to 61 +/- 3 mmHg (P less than or equal to 0.001) and heart rate decreased from 172 +/- 10 to 104 +/- 4 beats.min-1 (P less than or equal to 0.01). The heart, brain and adrenals showed vasodilation in response to the asphyxic stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1990

What is fetal distress?

Fetal distress is a widely used but poorly defined term. This confusion of definition compounds the difficulty of making an accurate diagnosis and initiating appropriate treatment. The fetus reacts at the onset of asphyxia with a remarkable series of responses, primarily a complexly regulated redistribution of blood flow that serves to limit the deleterious effects of oxygen limitation in vital organs. This enables the fetus to survive asphyxia intact unless the insult is profound or prolonged. The most common asphyxial stresses imposed on the fetus during labor are insufficiency of uterine blood flow, or insufficiency of umbilical blood flow, and occasionally decrease in uterine arterial oxygenation. Each of these stresses produces characteristic fetal heart rate patterns: late decelerations, variable decelerations, or prolonged bradycardia. There is strong evidence that the presence of normal fetal heart rate variability represents normal central nervous system integrity, including adequate oxygenation. A decrease or loss of variability in the presence of these patterns is a sign that the physiologic compensations are overwhelmed as a result of the severity of asphyxia. Knowledge of the fetal responses to asphyxia, together with the known evolution of fetal heart rate patterns during asphyxia, should allow a more accurate definition of the onset of unacceptable asphyxia, and more rational management and timing of intervention.

Asphyxia↗
PubMed1990

Cervical incompetence: preliminary evaluation with MR imaging.

The ability of magnetic resonance (MR) imaging to demonstrate cervical incompetence in nonpregnant women was investigated in a prospective study of 41 volunteers referred in random order. These included 20 patients with normal cervices, 11 with cervical incompetence of traumatic or congenital origin, and 10 with clinically small cervices due to in utero diethylstilbestrol (DES) exposure. On MR images of the normal patients, cervical length was 33.0 mm +/- 1.0 (mean +/- standard error of the mean) and the width of the internal cervical os was 3.3 mm +/- 0.1. In patients with cervical incompetence, the cervical length did not significantly differ from those in the normal group. However, the internal cervical os was significantly wider (4.5 mm +/- 0.3, P less than .001), and localized irregularity of the endocervical canal was demonstrated in two patients. The MR appearance of the cervical stroma varied from normal, uniformly low signal intensity (n = 4) to uniformly (n = 3) or partially (n = 4) medium-to-high signal intensity on T2-weighted images. In the patients with in utero DES exposure, the mean length of the cervical canal (22.9 mm +/- 1.7) was significantly shorter than that of the normal group. The width of the internal cervical os and the MR signal intensity of the cervical stroma were normal. In summary, MR findings of a cervical length shorter than 3.1 mm (95% confidence limit), an internal cervical os wider than 4.2 mm (95% confidence limit), or abnormal signal intensity in the cervical stroma are highly suggestive of incompetent cervix and should assist in planning further therapeutic decisions.

Cervix Uteri↗
PubMed1990

Cerebral oxygen consumption during asphyxia in fetal sheep.

Cerebral blood flow and cerebral arteriovenous oxygen content difference were measured in 17 fetal sheep, and cerebral oxygen uptake was calculated. The measurements were made under control conditions and after profound fetal asphyxia induced of uterine blood flow for up to 90 min. In 14 of the fetal sheep, sequential measurements were made to examine hemodynamic changes and cerebral oxygen consumption at comparable intervals up to 36 min of asphyxia. These fetuses initially had elevated blood pressure and lowered heart rate became hypoxemic, hypercarbic, and acidotic. There was an initial decrease in cerebral oxygen consumption. Sequential measurements, however, showed a relative stability in this decreased oxygenation during 4 to 36 min of asphyxia despite a progressive metabolic acidosis. The cerebral fractional oxygen extraction remained unchanged despite a mean pH of 6.98 at 36 min. The calculated cerebral oxygen uptake during asphyxia in all 17 sheep was grouped according to whether the ascending aortic oxygen content was greater or less than 1.0 mmol/l. In the first group with mean ascending aortic oxygen content of 1.3 mmol/l, blood flow to the brain was increased and cerebral oxygen consumption was 85% of control. In the second group with mean arterial blood oxygen content of 0.8 mmol/l, there was a narrowing of the arteriovenous oxygen content difference, but no further increase in cerebral blood flow. Cerebral oxygen consumption was only 48% of control in this more asphyxiated group. We conclude that the degree of hypoxemia in the second group represents a point where physiologic mechanisms cannot compensate, and may be associated with neuronal damage.

Adrenal Glands↗