Biomedical subjects

C A Gleason

Publications and source records attributed to C A Gleason.

At least 37 records · Page 2Linked to original sources

PubMed1995

Recombinant human erythropoietin stimulates erythropoiesis and reduces erythrocyte transfusions in very low birth weight preterm infants.

DESIGN AND METHODS: We hypothesized that treatment with recombinant human erythropoietin (r-HuEPO) would stimulate erythropoiesis and would thereby reduce the need for erythrocyte transfusions in preterm infants. We treated 157 preterm infants born at 26.9 +/- 1.6 weeks of gestation who weighed 924 +/- 183 g at birth with either subcutaneous r-HuEPO (100 U/kg/d, 5 days per week) or placebo for 6 weeks in a randomized, double-blind, controlled clinical trial. All patients received oral iron and were managed according to uniform conservative transfusion guidelines. RESULTS: Treatment with r-HuEPO was associated with fewer erythrocyte transfusions (1.1 +/- 1.5 per infant in the r-HuEPO group versus 1.6 +/- 1.7 per infant in the placebo group; P = .046) and with a reduction in the volume of packed erythrocytes transfused (16.5 +/- 23.0 mL versus 23.9 +/- 25.7 mL per infant; P = .023). Overall, 43% of the infants in the r-HuEPO group and 31% of placebo-treated infants were transfusion-free during the study (P = .18). The volume of blood removed for laboratory tests and the need for respiratory support at the start of treatment had major effects on transfusion requirements independent of r-HuEPO. Reticulocyte counts were higher during treatment in the r-HuEPO group (P = .0001), and r-HuEPO-treated infants had higher hematocrit values at the end of the study (32% versus 27.3% in the placebo group; P = .0001). We found no differences in the incidence of major complications of prematurity between the treatment groups. CONCLUSION: We conclude that treatment with r-HuEPO at a weekly dose of 500 U/kg stimulates erythropoiesis, moderates the course of anemia, is associated with a reduction in erythrocyte transfusions, and appears safe in very low birth weight preterm infants who are receiving iron supplements. Conservative transfusion criteria, minimization of phlebotomy losses, and treatment with r-HuEPO are complementary strategies to reduce erythrocyte transfusions in these infants.

Anemia↗

PubMed1994

The human locus coeruleus and anxiogenesis.

Electrical stimulation of locus coeruleus (LC), via permanently implanted electrodes with confirmed localization and effectiveness, did not elicit any subjective or behavioral manifestations of anxiety. This is evidence against the hypothesis that LC is a mediator of anxiogenesis in man.

Adult↗

PubMed1994

Laparoscopically implantable nerve-stimulating electrode (LINSE): application to the cavernous nerve in acute and chronic canine models.

Using a new laparoscopic procedure, we investigated stimulation of the cavernous nerves to achieve erection in a canine model. The technique was developed during acute experiments in four dogs, following which, chronic studies (4- to 6-weeks survival after surgery) were undertaken in three dogs. A monopolar cuff electrode was inserted laparoscopically by a transperitoneal approach and placed around the cavernous nerve. The leads were brought out to the subcutaneous space, where they were attached to stimulation receivers that could be activated by an external radiofrequency transmitter. An intracavernous pressure elevation indicative of successful stimulation was obtained acutely in five of eight cavernous nerves in the four acute-study dogs and in four of six nerves in the three chronic-study dogs. The implanted equipment associated with four of six cavernous nerves failed mechanically in the chronic-study animals, such that only two receiver-electrode sites were intact at the time of sacrifice 4 to 6 weeks later. Transmitter-driven stimulation of one of these two sets produced an intracavernous pressure rise above 100 cm H2O. We present this technique as part of the continuing evolution of laparoscopy as both a research and a clinical tool. The present use of the laparoscopically implantable nerve-stimulating electrode is a new animal research tool and a potential first step in the human application of the technology.

Animals↗

PubMed1994

Cerebrovascular response to carbon dioxide in lambs receiving extracorporeal membrane oxygenation.

OBJECTIVE: To determine if the institution of extracorporeal membrane oxygenation (ECMO) alters the cerebrovascular response to changes in PaCO2. DESIGN: Prospective, randomized, controlled animal trial. SUBJECTS: Anesthetized 1- to 7-day-old lambs of mixed breed (n = 16). SETTING: University research laboratory. INTERVENTIONS: The experimental group was placed on ECMO. Both experimental and control groups (n = 8) were exposed to three concentrations of PaCO2 (hypocarbia, normocarbia, and hypercarbia) by varying mechanical ventilation and by adding carbon dioxide to the ventilator gases. MEASUREMENTS AND MAIN RESULTS: Cerebral blood flow was measured by the radiolabeled microsphere method. Arterial blood gases and sagittal sinus blood gases were drawn at the time of cerebral blood flow measurement so that cerebral metabolism, cerebral oxygen transport, and extraction could be calculated. In the control group, as PaCO2 increased from 34 +/- 2 (SD) to 53 +/- 4 torr (4.5 +/- 0.3 to 7.1 +/- 0.5 kPa), cerebral blood flow increased from 53 +/- 12 to 147 +/- 50 mL/min/100 g. This increase in cerebral blood flow was not different from that of the ECMO group, where PaCO2 increased from 33 +/- 2 to 56 +/- 3 torr (4.4 +/- 0.3 to 7.5 +/- 0.4 kPa) and cerebral blood flow increased from 48 +/- 17 to 106 +/- 38 mL/min/100 g. As PaCO2 decreased from 34 +/- 2 to 19 +/- 2 torr (4.5 +/- 0.27 to 2.5 +/- 0.27 kPa), cerebral blood flow decreased from 53 +/- 12 to 43 +/- 8 mL/min/100 g in the control group. This decrease was not different from that of the ECMO group, where cerebral blood flow decreased from 48 +/- 17 to 39 +/- 10 mL/min/100 g as PaCO2 decreased from 33 +/- 2 to 22 +/- 3 torr (4.4 +/- 0.3 to 2.9 +/- 0.4 kPa). When regional cerebral blood flow was analyzed, no regional differences in the cerebrovascular responses to PaCO2 between ECMO and control groups were found. The cerebral metabolic rate was not different between ECMO and control groups at any level of PaCO2, nor was the cerebral metabolic rate affected by changes in PaCO2. Oxygen extraction increased with hypocarbia and decreased with hypercarbia in a similar fashion in both ECMO and control groups. CONCLUSION: The cerebrovascular response to changes in PaCO2 was unaffected by ECMO.

Animals↗

PubMed1994

Cerebrovascular autoregulation during fetal development in sheep.

There are scant data regarding the development of cerebrovascular autoregulation in fetuses. We tested the hypothesis that a decrease in cerebrovascular resistance (CVR) at reduced cerebral perfusion pressure (CPP) is absent in midgestation and near-term fetal sheep. Catheters were chronically implanted for microsphere determination of cerebral blood flow (CBF) in 9 fetuses at 92 days and in 10 fetuses at 132 days gestation (full term = 145 days). CPP was reduced by ventricular infusion of artificial cerebrospinal fluid. In 92-day fetuses, CPP was reduced stepwise from 35 to 25 and 18 mmHg and CBF decreased from 52 +/- 5 to 43 +/- 4 and 27 +/- 5 (SE) ml.min-1 x 100 g-1, respectively. Half of the immature fetuses showed some reduction in CVR at moderate reduction in CPP; however, there was no significant change in CVR in the group as a whole (from 0.72 +/- 0.06 to 0.61 +/- 0.04 and 0.89 +/- 0.20 mmHg.ml-1.min.100 g). In 132-day fetuses, CPP was reduced from 45 to 33 and 28 mmHg and CBF was unchanged (from 105 +/- 7 to 97 +/- 11 and 89 +/- 8 ml.min-1 x 100 g-1). CVR decreased from 0.45 +/- 0.05 to 0.41 +/- 0.08 and 0.33 +/- 0.03 mmHg.ml-1.min.100 g. There were no significant changes in arterial blood gases at reduced CPP in either age group. We conclude that cerebrovascular autoregulation at reduced CPP is not well developed at 92 days (0.63 gestation) in fetal sheep but that autoregulatory capacity is evident near term. We speculate that poor autoregulation may place the premature fetal brain at risk for injury.

Animals↗

PubMed1994

Fetal responses to acute fetal cocaine injection in sheep.

Maternal cocaine injection causes fetal hypoxemia, hypertension, and increased cerebral blood flow (CBF) in sheep. To test the hypothesis that increased fetal CBF is not due solely to fetal hypoxemia, we injected cocaine directly into a fetal vein. A single dose of cocaine [1 (group 1; n = 7) or 2 (group 2; n = 8) mg/kg i.v.] was administered to chronically catheterized, unanesthetized, near-term fetal sheep. Fetal CBF (microspheres), arterial blood pressure (BP), O2 content, and cerebral O2 consumption (CMRo2) were measured at baseline, 30 s, and 2, 5, and 15 min after fetal cocaine injection. Fetal CBF increased 27 +/- 9% (SE) at 5 min in group 1 and returned to baseline by 15 min, whereas fetal CBF increased 57 +/- 8% at 5 min and remained elevated at 15 min in group 2. Fetal BP increased at 30 min in both groups and remained increased at 2 min in group 1 and at 5 min in group 2. Cerebrovascular resistance increased at 30 s in both groups and then decreased at 5 min only in group 2. Fetal hypoxemia was observed in group 2 5 min after cocaine injection (arterial PO2 decreased 24 +/- 5%), whereas no hypoxemia was noted in group 1. CMRO2 was unchanged in group 1 but increased in group 2 at 5 min (41 +/- 10%) and was associated with an increase in cerebral O2 extraction. Increases in myocardial and adrenal blood flows and reductions in both small and large intestinal blood flows were noted at 5 min in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Cerebral responses to single and multiple cocaine injections in newborn sheep.

Newborn infants exposed to cocaine near birth display a wide range of neurologic abnormalities, but the mechanism or mechanisms for these injuries remain unknown. We studied the cerebral effects of a single acute dose (4 mg/kg; n = 7) and multiple binge doses (4 mg/kg hourly for 5 h; n = 7) of i.v. cocaine in unanesthetized newborn (5 +/- 1 d old) sheep. We measured cerebral blood flow, mean arterial blood pressure, arterial blood gases, and cerebral O2 metabolism. Measurements were made at baseline; 30 s; and 5, 15, and 60 min after a single injection of cocaine in the acute group and at the same time intervals after the 5th dose of cocaine in the binge group. CBF increased by 98 +/- 68% (mean +/- SD) at 30 s after a single acute dose and by 97 +/- 94% at 30 s after the 5th of five hourly binge doses. Although it returned to baseline by 5 min in the acute group, cerebral blood flow remained elevated 5, 15, and 60 min after the 5th cocaine dose in the binge group. At 30 s, mean arterial blood pressure increased by 57 +/- 21% in the acute group and 46 +/- 15% in the binge group. In both groups, mean arterial blood pressure remained elevated at 5 min. Although no change occurred in cerebral O2 metabolism in the acute group, an increase in cerebral O2 consumption (7.4 +/- 1.3 mL/100 g/min versus 5.5 +/- 1.1 at baseline) was observed at 5 min in the binge group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Fetal responses to acute maternal cocaine injection in sheep.

Maternal cocaine abuse has been associated with neonatal neurological and neurobehavioral problems of unknown pathogenesis. We administered a single intravenous dose of cocaine (2 mg/kg) to 12 unanesthetized pregnant sheep; their fetuses had been catheterized in utero 2 days before the study. We measured fetal cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), mean arterial blood pressure (MAP), and blood gases before and 2, 5, 15, and 30 min after maternal cocaine injection. Fetal CBF increased by 37 +/- 33% (mean +/- SD) at 5 min and returned to baseline by 15 min. Regional brain blood flow changes paralleled CBF changes with the greatest increases occurring in cerebellum (54 +/- 43%) and brain stem (54 +/- 52%). Cerebral vascular resistance was decreased for cerebellum (22%) and brain stem (19%) but was unchanged for cerebral hemispheres and caudate. Increased CBF at 5 min was associated with a 20 +/- 9% increase in fetal MAP and a 38 +/- 13% decrease in fetal arterial O2 content. Fetal CMRO2 was unchanged. There was a decrease in fetal intestinal blood flow at 2 min, an increase in myocardial, adrenal, and renal blood flow at 5 min, and no change in placental blood flow. Maternal cocaine injection causes fetal hypoxemia, hypertension, and increased CBF. Possible mechanisms for cerebral vasodilation (in some areas) include hypoxemia, impaired autoregulatory response to increased blood pressure, and/or direct or indirect vascular effects of cocaine or its metabolites.

Animals↗

PubMed1993

An elevated hematogenous photosensitizer in the preterm neonate.

PURPOSE: Human blood contains low levels of protoporphyrin IX (PP IX), a photoactive compound that produces reactive oxygen species when exposed to light. It has been proposed that photoactivation of PP IX and subsequent generation of potentially tissue-damaging reactive oxygen may be a mechanism of retinal injury in retinopathy of prematurity (ROP). The purpose of this study is to determine an association between blood PP IX level and infant birth-weight and gestational age. METHODS: Erythrocyte PP IX levels were measured from the umbilical cord blood of 31 neonates, both full term and preterm. Birthweights and gestational ages were recorded. RESULTS: PP IX levels in infants weighing < 1000 grams (n = 7) average 200 micrograms/dl, which is significantly higher than PP IX levels in infants weighing > 1000 grams (125 micrograms/dl, n = 24; P < 0.02). CONCLUSION: Elevated PP IX levels may place preterm neonates at increased risk for photosensitizing retinal injury.

Fetal Blood↗

PubMed1992

The effect of magnetic resonance imagers on implanted neurostimulators.

This in-vitro study was designed to investigate the safety of various implanted neurostimulators in magnetic resonance (MR) imagers. The effects of the static and changing magnetic fields and the radio frequency (RF) electromagnetic field generated by 0.35 and 1.5 T MR imagers on the voltage output of four models of implantable passive neurostimulators and two models of implantable self-powered neurostimulators was studied. The neurostimulators were mounted on a support and placed in the imagers. An oscilloscope monitored the voltages at the outputs of the neurostimulators. For an Avery single-channel stimulator, located at the isocenter, the amplitude of the output pulses induced by the 0.35 T imager was 6V; from a 1.5 T imager, it was 12 V. These amplitudes can cause discomfort and possible harm to a patient if the typical therapeutic value is 1-5 V. The amplitude of the stimulator receiver's output decreased to relatively safe values beyond 40 cm from the isocenter. By contrast, there was no significant voltage output from the Medtronic SE-4 receiver. For two models of self-powered neurostimulators, the Medtronic Itrel and the Cordis MK II, the programmed stimulus parameters were not affected by the pulsed magnetic fields of the MR imagers. However, the RF fields at the isocenter heated the metal case of the stimulators. The rotational and linear forces produced by the fixed magnet on the Cordis MK II were judged to be too strong for a patient with this implant to be scanned. The study showed that patients with certain types of implanted neurostimulators can be scanned safely under certain conditions.

Electric Stimulation Therapy↗

PubMed1992

Cerebral responses to acute maternal alcohol intoxication in immature fetal sheep.

Previous studies in mature fetal sheep have shown that alcohol depresses cerebral blood flow (CBF), cerebral O2 consumption (CMRO2), and cerebral glucose consumption (CMRglu). This effect earlier in gestation might contribute to the pathogenesis of fetal alcohol syndrome. Physiologic studies of immature fetal sheep have demonstrated lower CBF, CMRO2, and CMRglu as well as a blunted vasodilatory response to hypoxia compared with mature fetal sheep. The purpose of this study was to determine whether immature fetal responses to alcohol are blunted compared with near-term fetal responses. We studied seven immature fetal sheep in utero at 92 +/- 1 d gestation (term = 147 d) 2 d after placement of vascular catheters. Pure ethanol (1 g/kg) was infused i.v. to the mother over 1 h. We measured CBF and myocardial blood flow by radioactive microspheres and calculated CMRO2 and CMRglu using arterial and sagittal sinus O2 and glucose concentrations. At a fetal ethanol concentration of 33 + 8 mmol/L (150 +/- 37 mg/dL), there were no significant changes in CBF, CMRO2, or CMRglu. There was mild hypoglycemia (glucose concentration = 1.05 +/- 0.2 versus 1.33 +/- 0.2 mM baseline) and lactic acidemia (lactate concentration = 1.29 +/- 0.3 versus 1.07 +/- 0.2 mM baseline). Cardiovascular variables were unchanged as was myocardial blood flow. The immature fetal sheep brain shows no significant cerebrovascular and metabolic response to acute alcohol intoxication compared with mature fetal sheep. Mild hypoglycemia and lactic acidemia did develop. The reason for the developmental differences in response to alcohol and their relationship to fetal alcohol syndrome remain to be elucidated.

Alcoholic Intoxication↗

PubMed1991

Control of the transition from sensory detection to sensory awareness in man by the duration of a thalamic stimulus. The cerebral 'time-on' factor.

A 'time-on' theory to explain the cerebral distinction between conscious and unconscious mental functions proposes that a substantial minimum duration ('time-on') of appropriate neuronal activations up to about 0.5 s is required to elicit conscious sensory experience, but that durations distinctly below that minimum can mediate sensory detection without awareness. A direct experimental test of this proposal is reported here. Stimuli (72 pulses/s) above and below such minimum train durations (0-750 ms) were delivered to the ventrobasal thalamus via electrodes chronically implanted for the therapeutic control of intractable pain. Detection was measured by the subject's forced choice as to stimulus delivery in one of two intervals, regardless of any presence or absence of sensory awareness. Subjects also indicated their awareness level of any stimulus-induced sensation in each and every trial. The results show (1) that detection (correct greater than 50%) occurred even with stimulus durations too brief to elicit awareness, and (2) that to move from mere detection to even an uncertain and often questionable sensory awareness required a significantly larger additional duration of pulses. Thus simply increasing duration ('time-on') of the same repetitive inputs to cerebral cortex can convert an unconscious cognitive mental function (detection without awareness) to a conscious one (detection with awareness).

Awareness↗

PubMed1990

Effect of acute hypoxemia on brain blood flow and oxygen metabolism in immature fetal sheep.

Studies of cerebral blood flow and oxygen metabolism during acute hypoxic hypoxia in fetal sheep have been confined to late gestation, a time when brain development in this species is largely complete. There is no systematic study of cerebral vascular responses to acute hypoxic hypoxia in immature fetal sheep or, indeed, in immature brains of any species. We studied 13 fetal sheep in utero at 93 +/- 1 days gestation (term = 145-150 days), 48 h after intravascular catheters were placed into the superior sagittal sinus, axillary arteries, and inferior vena cava. We measured brain blood flow by the microsphere method. Cerebral oxygen consumption was calculated with the use of blood flow to the cerebral hemispheres (cerebrum, diencephalon, mesencephalon) and arterial and sagittal sinus values for oxygen content. Fractional oxygen extraction was calculated as the ratio between oxygen consumption and oxygen transport. We altered fetal oxygenation by changing the mother's inspired oxygen concentration. As in the near-term fetus, acute hypoxic hypoxia resulted in increased blood flow to cerebral hemispheres, cerebellum, and pons-medulla; furthermore, the increase in blood flow was sufficient to sustain cerebral oxygen consumption. However, in contrast to near-term fetuses, the increase in blood flow to the cerebral hemispheres was not sufficient to maintain convective oxygen transport. Cerebral oxygen consumption was therefore sustained in part by an increase in fractional extraction. Blunted hypoxic vasodilation in immature fetuses might reflect either immature regulatory mechanisms or an inability of cerebral vessels to respond to the usual stimuli. It is also possible that hypoxic vasodilation was blunted by reflex stimulation of the sympathetic nervous system.

Acute Disease↗

PubMed1990

Effect of extracorporeal membrane oxygenation on cerebral blood flow and cerebral oxygen metabolism in newborn sheep.

Extracorporeal membrane oxygenation (ECMO) supplies respiratory support to term or near-term infants with respiratory failure. Although infants requiring this therapy may have already sustained significant hypoxia and/or ischemia predisposing them to neurologic injury, the high incidence of neuroimaging abnormalities in the ECMO population raises concerns about the additional neurologic risk associated with the ECMO procedure itself. Our study was undertaken to evaluate the effects of ECMO on the normal neonatal cerebral circulation. Thirteen newborn lambs (1-7 d of age) were placed on normothermic venoarterial ECMO using a silicone membrane oxygenator and roller occlusion pump. Regional brain blood flows, cerebral oxygen consumption, fractional oxygen extraction, and oxygen transport were determined 30 and 120 min after initiation of ECMO. Neither cerebral blood flow (baseline, 60.2 +/- 23.6; 30 min, 56.1 +/- 18.1; 120 min 56.1 +/- 12.9 mL/100 g/min) nor oxygen metabolism (cerebral oxygen consumption: baseline, 4.48 +/- 1.48; 30 min, 3.86 +/- 1.53; 120 min, 4.10 +/- 1.32 mL/100 g/min and oxygen extraction: baseline, 0.52 +/- 0.09; 30 min, 0.47 +/- 0.14; 120 min, 0.46 +/- 0.14 mL/100 g/min) changed after the initiation of ECMO. Regional and left/right blood flow differences were not noted. These findings suggest that in healthy newborn lambs, initiation of ECMO does not alter cerebral blood flow or oxygen metabolism.

Animals↗

PubMed1989

Cerebral blood flow and metabolism during and after prolonged hypocapnia in newborn lambs.

We studied the effects of prolonged (6 hours) hypocapnia and the abrupt termination thereof on cerebral blood flow and metabolism in six paralyzed, sedated (but not anesthetized) newborn lambs. Thirty minutes after institution of hyperventilation to an arterial carbon dioxide pressure of 15 +/- 2 torr, hyperventilation, cerebral blood flow had returned to baseline. Abrupt termination of hyperventilation after 6 hours resulted in a 110 +/- 71% increase in cerebral blood flow over baseline after 30 minutes of normocapnia. This cerebral hyperemia persisted for at least 90 minutes after hyperventilation was discontinued. Cerebral oxygen consumption did not change throughout the study. The posthypocapnia hyperemia noted in these animals after abrupt normalization of arterial carbon dioxide pressure may contribute to the increased risk of intracranial hemorrhage in newborn infants who are treated similarly in the management of pulmonary hypertension.

Animals↗

PubMed1989

Cerebral blood flow, oxygenation, and carbohydrate metabolism in immature fetal sheep in utero.

Studies of cerebral blood flow (CBF) and metabolism in fetal sheep have been largely confined to late gestation, a time when brain development in this species is largely complete. Few studies have been done at a time when the fetal sheep brain is in the midst of rapid differentiation and development. We studied seven fetal sheep in utero at 91 days of gestation (term = 145-150 days) 24 h after catheters were placed into the sagittal sinus, axillary artery, and inferior vena cava. We measured CBF by the microsphere method and used arteriovenous differences of O2, lactate, and glucose to calculate cerebral O2 consumption (CMRo2), fractional O2 extraction, glucose consumption, O2-glucose index (OGI), and cerebral lactate production. Compared with near-term fetal sheep, we found lower CBF (33.9 +/- 5.3 ml.100 g-1.min-1), lower glucose consumption (8.5 +/- 1.25 mumol.100 g-1.min-1), and lower CMRo2 (41.8 +/- 8.8 mumol.100 g-1.min-1). Fractional O2 extraction was 0.29 +/- 0.04, which is similar to near-term fetal sheep. There was consistent cerebral lactate production (2.45 +/- 1.58 mumol.100 g-1.min-1). The OGI was 81 +/- 16%, i.e., oxidative metabolism could account for 81% of glucose uptake. Lactate production accounts for virtually all glucose uptake exceeding that required for oxidation.

Animals↗

PubMed1989

Relationship of diaphragmatic contractility to diaphragmatic blood flow in newborn lambs.

We determined the relationship of diaphragmatic contraction rate to diaphragmatic blood flow (Qdi), metabolism, and contractility in nine open-chested mechanically ventilated newborn lambs. The diaphragm was paced for 15 min at slow (20/min) and fast (100/min) contraction rates each followed by a 30-min rest period. There was a mild reduction in transdiaphragmatic pressure (Pdi) during the slow contraction period accompanied by a shift to the right of the curve relating stimulation frequency (10-100 Hz) to Pdi. Pdi returned to control at the start of the fast contraction period, but then fell by 30% within 2 min with continued fast contraction rates. The frequency-Pdi curve was significantly shifted to the right. Qdi, O2 transport, and O2 consumption increased during slow contraction and to an even greater extent during fast contraction. Fractional O2 extraction reached an apparent maximum during slow contraction. Lactate efflux from the right phrenic vein during slow contraction remained unchanged from control. During fast contraction lactate efflux rose proportionately more than did O2 consumption. We conclude that the energy demands at fast rates of diaphragmatic contraction in newborn lambs cannot be met by aerobic metabolism alone despite increasing O2 transport to the diaphragm.

Animals↗

PubMed1989

Stimulation of locus coeruleus in man. Preliminary trials for spasticity and epilepsy.

Stimulating electrodes were chronically implanted unilaterally (in 1975-1977) in the vicinity of the locus coeruleus (LC) in three patients, one with cerebral palsy-spastic quadriplegia, two with epilepsy (one grand mal, one psychomotor). Effective excitation of efferent LC axons was indicated by measuring rises in 3-methoxy-4-hydroxyphenylethyleneglycol in the jugular and systemic venous blood following a 6-min stimulus with discontinuous bursts of pulses. There was a substantial reduction of spasticity during and after stimulation. Improvement was verified by double-blind failures of the stimulator, and the stimulus therapy is still in use after 9 years. There appeared to be a reduction in incidence and severity of both types of epileptic seizures, although this was not rigorously established. The patient with psychomotor epilepsy reported a considerable lengthening of preseizure auras (to 15-30 min), an unusual number of which terminated without a seizure.

Adolescent↗