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Biomedical subjects

R E Hertzog

Publications and source records attributed to R E Hertzog.

4 recordsLinked to original sources
PubMed1990

Effect of calcium entry blocker nitrendipine on renal function after renal vascular occlusion.

The ability of the Ca entry blocker nitrendipine to improve postischemic renal function was studied in nine groups (n = 70) of rats. After anesthesia, nitrendipine was administered for 15 min through the femoral vein. The dose administered depended on the group. Group 1 (n = 7), the control, received only 0.9% NaCl, group 2 (n = 12) 0.25 mg/kg; group 3 (n = 10) 0.50 mg/kg; group 4 (n = 8) 0.75 mg/kg; group 5 (n = 6) 1.00 mg/kg; group 6 (n = 7) 1.50 mg/kg; group 7 (n = 7) 2.00 mg/kg; group 8 (n = 6) 2.50 mg/kg; and group 9 (n = 7) 3.00 mg/kg. After the administration of nitrendipine, the kidneys were rendered ischemic for one hour by cross-clamping the renal vessels. Comparison of 24-h creatinine clearances for 72 h after reversal of ischemia demonstrated that nitrendipine was capable of providing a degree of protection against renal ischemia and the protective effect was dose dependent (p less than .05).

Acute Kidney Injury↗
PubMed1989

The effect of fentanyl anesthesia and intrathecal naloxone on neurologic outcome following spinal cord injury in the rat.

Whereas opiate receptor agonists have resulted in spinal cord damage; opiate receptor antagonists have demonstrated protection against spinal cord injury. Because opioids are used in clinical anesthesia, the effect of an opiate antagonist was evaluated on neurologic outcome in a rat model of spinal cord injury occurring during opioid anesthesia. One day prior to spinal cord injury, a catheter was inserted into the spinal subarachnoid space with the tip at T8. On the day of spinal cord injury a balloon tipped catheter was inserted in the epidural space with the tip at the thoracolumbar junction. Spinal cord injury was produced by balloon inflation during one of the following states: 1) group 1 (A/S), injury was produced in awake rats and saline was administered in the subarachnoid space immediately following injury; 2) group 2 (F/S), injury was produced during a fentanyl/nitrous oxide (N2O) anesthetic, and subarachnoid saline administered; and 3) group 3 (F/Nx), injury was produced during a fentanyl/N2O anesthetic, and subarachnoid naloxone (1 mg/kg) was administered immediately following injury. Dose-response curves describing the relationship between the duration of balloon inflation and the percentage of animals with a persistent neurologic deficit were constructed and compared for differences by use of a group t test. The duration of balloon inflation required to produce a neurologic deficit was greater in both the F/S and F/Nx groups than in the A/S group (P less than 0.05). There was no difference between the F/S and F/Nx groups. In summary, in rats receiving a fentanyl/N2O anesthetic, neurologic outcome was improved compared with the awake state.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia Recovery Period↗
PubMed1989

The effect of hypervolemic hemodilution with and without hypertension on cerebral blood flow following middle cerebral artery occlusion in rats anesthetized with isoflurane.

The effect of hypervolemic hemodilution or hypervolemic hemodilution with dopamine-induced hypertension on cerebral blood flow (CBF) was investigated during 1.2 MAC isoflurane anesthesia in rats (n = 24) subjected to middle cerebral artery occlusion (MCAO). Prior to MCAO each animal was randomized to one of the following groups: 1) control, mean arterial pressure (89 +/- 10 mmHg [mean +/- SD]), blood volume, and hematocrit (46 +/- 1) were not manipulated; 2) hypervolemic hemodilution (HH), 30 min before MCAO, 5% albumin was administered to reduce the hematocrit to 29-32%; or 3) hypervolemic hemodilution/dopamine hypertension (HH/Dop), hemodilution was accomplished and dopamine (10 micrograms.kg-1.min-1) was infused during the ischemic period to achieve a mean arterial pressure of 111 +/- 10 mmHg (mean +/- SD). Ten minutes after occlusion of the left middle cerebral artery, CBF was determined using 14C-iodoantipyrine. Five coronal brain sections were analyzed to determine the area within each brain section with CBF ranges of 0-15 ml.100 g-1.min-1 and 15-23 ml.100 g-1.min-1. The area of 0-15 ml.100 g-1.min-1 CBF was less in both the HH and HH/Dop groups compared with control (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗