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Biomedical subjects

R A Girton

Publications and source records attributed to R A Girton.

6 recordsLinked to original sources
PubMed1994

15-HETE: selective incorporation into inositol phospholipids of MDCK cells.

The interaction of 15-hydroxyeicosatetraenoic acid (15-HETE) and cultured MDCK renal tubular epithelial cells was investigated to determine whether incorporation of this lipoxygenase product will affect polyphosphoinositide formation. MDCK cells were incubated with 1 microM [3H]-15-HETE for 15 to 120 minutes. Maximum uptake occurred between 15 and 30 minutes, and after 60 minutes, 70% of the incorporated 15-HETE was present in the phosphatidylinositol (PI) fraction. Some 15-HETE was also incorporated into phosphatidylinositol-4-monophosphate (PIP) and phosphatidylinositol-4,5-bisphosphate (PIP2). However, even though more 15-HETE than arachidonic acid was incorporated into PI, the fractional amount of 15-HETE present in the polyphosphoinositides was smaller than arachidonic acid. Therefore, although 15-HETE is selectively channeled into PI, conversion of PI species containing 15-HETE to PIP and PIP2 is relatively impaired. This suggests that either PI containing 15-HETE is a less effective substrate for phosphorylation, or PI containing arachidonic acid is a preferred substrate. MDCK cells converted 15-HETE to polar metabolites that were released into the extracellular fluid. This process may constitute a renal tubular mechanism for the clearance of 15-HETE and related lipoxygenase products.

Animals↗
PubMed1989

Nicardipine after spinal cord compression in the lamb.

To study the effects of the calcium channel blocker nicardipine on spinal cord blood flow and spinal evoked potentials, the following study was undertaken. After cord compression, which was productive of paraparesis, nicardipine was administered intravenously in 10 anesthetized lambs. Ten control animals were subjected to compression but received saline instead. Nicardipine produced a significant decrease in mean arterial pressure when compared to the control group. Thirty minutes after compression, spinal cord blood flow also was lower in the nicardipine group compared with controls. Spinal evoked potentials did not recover after compression in either group.

Animals↗
PubMed1989

Methylprednisolone in spinal cord compression.

In acute nonsurvival studies, eight anesthetized lambs were subjected to cord compression at T13 by means of an epidural balloon distended to a pressure of 200 mm Hg for 40 minutes. Subsequent to withdrawal of the balloon, each animal received 30 mg/kg of methylprednisolone succinate in an intravenous bolus followed by a continuous infusion of 10 mg/kg/hr for the duration of the experiment. Spinal cord blood flow (SCBF) and spinal evoked potential (SEP) determinations were obtained sequentially prior to, during, and at 1/2, 1 1/2, and 2 1/2 hours following compression. In spite of the absence of ischemia following compression, SEPs failed to recover. Methylprednisolone had no apparent effect on blood flow or on the recovery of SEPs when compared with results in ten control animals that received saline alone.

Animals↗
PubMed1989

Effect of hetastarch, mannitol, and phenylephrine on spinal cord blood flow following experimental spinal injury.

Anesthetized lambs were subjected to epidural cord compression at T13 by means of an epidural balloon distended to 200 mmHg for 80 minutes. Determinations of spinal cord blood flow (SCBF) were made by labelled microspheres prior to and during compression, and then 1/2, 1 1/2, and 2 1/2 hours after compression. Twelve control animals received saline (80 ml/h). Nine animals received hetastarch (a 20 ml/kg bolus followed by an 80 ml/h infusion) and 8 animals received mannitol (a 1 g/kg bolus followed by 1 g/kg/hr). An additional 10 animals received phenylephrine to raise mean arterial pressure by 20 to 40%. Somatosensory evoked potentials (SEPs) were recorded following each determination of SCBF. Animals were killed following determination of the 2 1/2 hour postcompressive flow. The animals treated with either hetastarch or phenylephrine had a postcompressive mean arterial pressure that was significantly greater than that of the controls (P less than 0.01). During treatment, cardiac output in the hetastarch and mannitol animals was significantly greater and hematocrit significantly less than in the controls (P less than 0.05). In spite of these changes, postcompressive SCBF was significantly increased only in those animals treated with phenylephrine (P less than 0.05). Statistical analysis of the relationship between mean arterial pressure and postcompressive SCBF revealed that autoregulation is indeed lost with this experimental model of spinal cord injury. Histological examination of the injured site failed to demonstrate any difference in the area of hemorrhagic necrosis among the four groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effect of hemorrhagic shock upon spinal cord blood flow and evoked potentials.

Although somatosensory evoked potentials are being used in the evaluation of spinal cord injury and the monitoring of cord function during surgical procedures, their limitations in the face of fluctuations in blood pressure await further clarification. To study the effect of hypotension upon spinal cord blood flow (SCBF) and spinal evoked potentials (SEPs), we subjected five anesthetized lambs to graded hypotension to a mean arterial pressure (MAP) of 80, 60, 40, and less than or equal to 30 mm Hg. Five animals served as controls. Maximal hypotension was associated with a significant decrease in renal and sciatic nerve blood flow of 83% and 77%, respectively. SCBF, on the other hand, showed no decrease with hypotension down to a MAP of 40 mm Hg. As hypotension progressed, a gradual but significant slowing in nerve conduction velocity was noted without alteration in the cord conduction velocity from L7 to L1. Control animals demonstrated a decline in sciatic nerve blood flow of 48%, without any change in latency or amplitude of nerve action potentials. These findings suggest that, in hypotension, the peripheral nerve (lacking autoregulation) becomes ischemic, resulting in slowing of nerve conduction velocity with an increase in latency and decrease in amplitude of SEPs. Cord conduction velocity, on the other hand, remains unchanged. Caution is advised in relying upon SEPs generated by peripheral nerve stimulation to monitor cord function in situations where profound hypotension is anticipated. Variations in SEPs may reflect alterations in the peripheral nerve and not the spinal cord.

Action Potentials↗