Biomedical subjects

E Murdaugh

Publications and source records attributed to E Murdaugh.

3 recordsLinked to original sources

PubMed1990

The effect of blood glucose concentration on postasphyxia cerebral hemodynamics in newborn lambs.

The effect of preasphyxia blood glucose concentration on postasphyxia (PA) cerebral hemodynamics was examined in 21 newborn lambs. Glucose was unregulated in one group (n = 7), and controlled throughout the study by glucose clamp in hyperglycemic (n = 7) and hypoglycemic (n = 7) groups. Cerebral blood flow, determined using radiolabelled microspheres, and arterial and sagittal sinus O2 contents were measured at control, 5 min, 1, 2, and 4 h after resuscitation from an asphyxial insult. Preasphyxia blood glucoses were 6.48 +/- 0.55 mM (mean +/- SEM), 12.08 +/- 0.80, and 2.66 +/- 0.14 in the three study groups. In all three groups, 5 min PA cerebral blood flow was significantly increased from control. In the late period after asphyxia, the unregulated group had decreased cerebral blood flow compared with control, 53.2 +/- 3.8 mL.100 g-1.min-1, mean +/- SEM, p less than 0.01; 49.6 +/- 2.0, p less than 0.005; 53.4 +/- 3.0, p less than 0.01, at 1, 2, and 4 h PA, respectively, versus 85.7 +/- 6.9 at control, whereas both the hyper- and hypoglycemic groups did not differ significantly from control measurements. Cerebral oxygen consumption (CMRO2) was significantly decreased in all three groups 5 min PA and remained decreased in the late period after asphyxia in both the unregulated and hypoglycemic groups. In the unregulated group, CMRO2 was 191 +/- 14 microM.100 g-1.min-1, mean +/- SEM, p less than 0.05; 200 +/- 4; and 181 +/- 10, p less than 0.05 at 1, 2, and 4 h, respectively, PA versus 251 +/- 12 at control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Mitochondrial function after asphyxia in newborn lambs.

We examined mitochondrial oxidative function 5 minutes and 2 hours after a gradual asphyxial insult in newborn lambs. We subjected 16 ventilated newborn lambs to 75-90 minutes of hypoxia and hypercarbia that resulted in bradycardia and systemic hypotension over the final 15 minutes of the insult. At the end of asphyxia, the lambs were resuscitated and returned to control ventilator settings. Samples of brain were removed 5 minutes (n = 8) and 2 hours (n = 8) after asphyxia. Each group of eight lambs was subdivided into those less than 3 or greater than 3 days old to evaluate the effect of age on postasphyxia mitochondrial function. After classification into nonsynaptic and synaptic mitochondria, mitochondrial respiration (oxygen consumption) was measured using five different substrates. Data from asphyxiated lambs were compared with that from a control group of ventilated nonasphyxiated lambs (n = 8). In the lambs less than 3 days old, there was significant depression of mean +/- SEM nonsynaptic mitochondrial state 3 (adenosine diphosphate-dependent) respiration to 29.5 +/- 5.2% of control with four of the five substrates and of state 4 respiration to 33.7 +/- 0.9% of control with three of the five substrates 5 minutes after asphyxia. By 2 hours after asphyxia, mean +/- SEM nonsynaptic mitochondria state 3 respiration increased to 70.4 +/- 6.4% of control while state 4 respiration increased to 58.2 +/- 4.5% of control. In contrast, lambs greater than 3 days old exhibited no inhibition of nonsynaptic mitochondrial function after asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗

PubMed1989

The role of oxygen free radicals in postasphyxia cerebral hypoperfusion in newborn lambs.

Previous work in a neonatal lamb model has demonstrated abnormalities in cerebral blood flow (CBF) and oxygen consumption (CMRO2) after asphyxia. Immediately after resuscitation, there was a marked increase in CBF and a significant decrease in CMRO2 compared to control. During the late period after asphyxia (30 min to 4 h), both CBF and CMRO2 were significantly depressed. The same postasphyxia model (n = 16) was used to examine the hypothesis that generation of oxygen free radicals during cerebral reperfusion may be involved in the genesis of late postasphyxia hypoperfusion and depressed CMRO2. Before asphyxia, the animals were pretreated with either inactivated (n = 8) or active (n = 8) polyethylene glycol superoxide dismutase, 5000 U/kg, and polyethylene glycol catalase, 100 000 U/kg. CBF (radioactive microspheres) and arterial and venous (superior sagittal sinus) blood gases and O2 contents were measured during control, and at 5 min, 1 h, 2 h, and 4 h postasphyxia (PA). In the active enzyme group, 5 min postasphyxia CBF was significantly increased compared to control: 211.5 +/- 28.0 versus 78.6 +/- 11.4 ml.100 g-1.min-1, +/- SEM, p less than 0.005. At 1 h (82.9 +/- 17.6), 2 h (62.3 +/- 5.5), and 4 h (78.9 +/- 12.2) PA, CBF did not differ significantly from control. More importantly, CMRO2 did not differ from control at any time PA. In the inactive enzyme group, both CBF and CMRO2 were depressed at 1, 2 and 4 h PA. These findings are consistent with a conclusion that damage by oxygen free radicals during postasphyxia cerebral reperfusion is important to the genesis of late PA blood flow and O2 metabolism abnormalities. To the extent that depressions in CBF and CMRO2 result in ongoing brain injury, agents that ameliorate these abnormalities may improve neurologic outcome.

Animals↗