Biomedical subjects

L Bennet

Publications and source records attributed to L Bennet.

58 records · Page 4Linked to original sources

PubMed1988

Perinatal cerebral asphyxia: pharmacological intervention.

Perinatal asphyxia is associated with an increased risk of cerebral palsy and significant mortality. We investigated the use of flunarizine, a calcium antagonist and MK-801, an excitatory amino acid antagonist, in preventing the sequelae of severe hypoxic/ischemic insults. Flunarizine was neuroprotective in the infant rat subjected to unilateral carotid ligation and 2 h of hypoxia. Preliminary analysis of experiments in a novel model of cerebral ischemia in the fetal sheep suggests that prophylactic treatment with flunarizine greatly modified the outcome after 30 min of total ischemia. Treatment with MK-801 prevented post-ischemic seizures. The background to these developments is outlined and future prospects considered.

Animals↗

PubMed1988

The central effects of thyrotropin-releasing hormone on the breathing movements and electrocortical activity of the fetal sheep.

The fetal respiratory and electrocortical effects of thyrotropin-releasing hormone (TRH) administered into the lateral cerebral ventricles, have been investigated in chronically catheterized unanesthetized fetal sheep at 125-140 days of gestation. Stimulatory effects on fetal breathing movements were seen at doses as low as a lug bolus. TRH given as a 5-micrograms bolus followed by a 10 micrograms/h infusion for 2 h induced a rapid switch to significantly faster, deeper, and continuous fetal breathing movements, while the electrocorticogram remained episodic. Fetal breathing movements did not stop during hypoxia. TRH given as a 2-micrograms bolus followed by a 4 micrograms/h infusion or as a 5-micrograms bolus followed by a 5 micrograms/h infusion induced the same stimulation of FBMs, but breathing essentially remained episodic, state related and inhibited by hypoxia. As hypothermia presumably induces a surge in TRH secretion at birth it is possible that TRH has some role in the switch from fetal to postnatal breathing patterns.

Animals↗

PubMed1988

Precocial neural function in the growth-retarded fetal lamb.

Clinical studies suggest that growth-retarded prematurely delivered infants are neurologically precocious. We investigated this paradoxical observation in the fetal lamb. Somatosensory and brainstem auditory-evoked potentials were studied in chronically instrumented fetal lambs in late gestation with varying degrees of growth retardation induced by preconception uterine carunclectomy. The components of the brainstem auditory-evoked response appeared earlier (p less than 0.05) in fetuses at least 2 SD less than the mean weight for gestational age (n = 5) compared to normal controls (n = 8) or carunclectomized fetuses of normal size (n = 7). Several waveforms of both the somatosensory (N20, P/N 30, and P200) and the brainstem auditory-evoked response (I, III, IV, and V) demonstrated shorter (p less than 0.05) latencies in growth-retarded fetuses relative to normal-sized fetuses. The ability to follow increasing stimulus rates for both stimuli also demonstrated precocial maturation (p less than 0.05) in growth-retarded as compared to normal-sized fetuses. Growth retardation is thus associated with precocial neurologic maturation in utero.

Animals↗

PubMed1986

The central effects of morphine on fetal breathing movements in the fetal sheep.

The fetal respiratory and electrocortical effects of 0.6 microgram to 600 micrograms of morphine, administered into the lateral cerebral ventricle, have been studied in chronically catheterised, unanaesthetized fetal sheep at 115-135 days gestation. Morphine at 0.6 microgram had no effect on breathing movements or electrocorticographic activity, and at 6 micrograms induced a period of apnoea (43-122 min) but had no effect on electrocortical activity. Intravenous naloxone (2 mg bolus and infusion of 2 mg/kg/h for 2 h) to the fetus had no effect on this apnoea. Morphine at 60 micrograms induced an initial period of apnoea (30-65 min) followed by episodic but significantly deep breathing movements with no effect on electrocortical activity and at 600 micrograms induced an initial period of apnoea (22-95 min) which was followed by deep, irregular and continuous (126-302 min) breathing movements. During the apnoea electrocortical activity initially remained cyclic, but as apnoea progressed there was a gradual reduction in the voltage of the electrocorticogram to a low voltage state. Intravenous naloxone (2 mg bolus and infusion of 2 mg/kg/h for 2 h) reversed both the respiratory and electrocortical effects. The hyperventilation was also inhibited by hypoxia. Naloxone alone had no effect on fetal breathing activity.

Animals↗