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Biomedical subjects

John C Drummond

Publications and source records attributed to John C Drummond.

9 recordsLinked to original sources
PubMed2006

Cerebral ischemia as an apparent complication of anterior cervical discectomy in a patient with an incomplete circle of Willis.

A 58-yr-old patient sustained a cerebral ischemic injury in the distribution of the carotid artery ipsilateral to retraction during an anterior cervical discectomy. Relative hypotension was permitted during the anesthetic. Angiography revealed an anatomic variant of the circle of Willis that resulted in minimal collateralizaton of the left internal carotid artery territory. The combination of that vascular variant with relative hypotension and some degree of carotid compression appears to have resulted in clinically significant cerebral ischemia.

Brain Ischemia↗
PubMed2006

Precordial Doppler probe placement for optimal detection of venous air embolism during craniotomy.

Verification of appropriate precordial Doppler probe position over the anterior chest wall is crucial for early detection of venous air embolism. We studied responses to normal saline (NS) and carbon dioxide (CO2) test injections at various probe locations during elective craniotomy. All patients received four IV injections (10 mL of NS and 1 mL of CO2 via central and peripheral venous catheters). Doppler sounds were simultaneously recorded with two separate probes. In Group A, probes were placed in left and right parasternal positions. In Group B, the left probe was intentionally malpositioned as far laterally over the left precordium as was compatible with an audible signal. In Group A (n = 23), a left parasternal Doppler signal was easily obtainable in 23 of 23 patients, versus 18 of 23 patients for the right parasternal probe (P < 0.05). In Group B (n = 17), central CO2 injection yielded a positive right parasternal response rate of 88% compared with 29% over the far left precordium (P < 0.015), where central NS injections yielded a 76% response rate (P < 0.015 versus central CO2 injection). Left parasternal placement is at least as sensitive to clinical venous air embolism events as right parasternal placement. Peripheral saline injection represents a viable alternative (83% response rate). Vigorous central injection of 10 mL of NS however, risks false positive verification of left lateral precordial probe placement.

Adult↗
PubMed2006

The combination of isoflurane and caspase 8 inhibition results in sustained neuroprotection in rats subject to focal cerebral ischemia.

Although isoflurane can reduce ischemic neuronal injury after short postischemic recovery intervals, data from our laboratory have demonstrated that this neuroprotection is not sustained and that delayed apoptotic neuronal death, mediated in part by activation of caspases, contributes to the gradual increase in the size of the infarction. We tested the hypothesis that the neuroprotective efficacy of isoflurane can be prolonged with the administration of z-IETD-fmk, a specific inhibitor of caspase 8. Fasted Wister rats were anesthetized with isoflurane and randomly allocated to awake-vehicle, isoflurane-vehicle, awake-IETD, or isoflurane-IETD groups (n = 25 per group). Animals were subjected to 60 min focal ischemia by filament occlusion of the middle cerebral artery (MCAO). Daily intracerebroventricular injections of z-IETD-fmk or vehicle were administered via an implanted cannula starting before ischemia and continuing until 14 days post-MCAO. Neurological assessment was performed 14 days after ischemia after which the volume of cerebral infarction and number of intact neurons in the peri-infarct cortex were determined. Total infarction volume was less in the isoflurane-IETD group than in awake-vehicle, isoflurane-vehicle, and awake-IETD groups. Infarction volume was also less in the awake-IETD group versus the awake-vehicle group. The number of intact neurons within the peri-infarct cortex was significantly less in the awake-vehicle group in comparison with the other three experimental groups. The isoflurane-IETD group had better neurologic outcomes than both vehicle-treated groups at 14 days post-MCAO. These results suggest that a combination of isoflurane and a caspase 8 inhibitor can produce neuroprotection that is evident even after a recovery period of 14 days. This combination demonstrated greater efficacy than the administration of either isoflurane or z-IETD-fmk alone. These results are consistent with the premise that continuing apoptosis contributes to the enlargement of cerebral infarction during the recovery period and that its inhibition can provide sustained neuroprotection.

Animals↗
PubMed2005

Intraoperative blood salvage: fluid replacement calculations.

Intraoperative blood salvage (IBS) devices are used as adjuncts to blood conservation in spinal surgical procedures of increasing duration, complexity, and total blood loss. We applied existing information about the performance and efficiency of IBS devices together with existing information regarding the distribution of crystalloids and colloids to provide clinicians with guidelines for the prediction of the total blood loss implications of a given volume of IBS return. We also developed guidelines for estimation of the appropriate replacement volumes for the acellular component of blood loss when replacement is undertaken with either isotonic-iso-oncotic colloid or isotonic crystalloid solutions. When average hematocrit during blood loss is between 25% and 30%, total blood loss will be 3.4-4.0 times the volume of the IBS recovery. When replacement is undertaken with colloids or crystalloids, the appropriate replacement volume will be approximately 2.5 and 8.0 (respectively) times the volume of the IBS recovery. These volumes may be larger than have been appreciated by some clinicians.

Blood Coagulation Factors↗
PubMed2005

The role of nitric oxide synthase inhibition in the adverse effects of etomidate in the setting of focal cerebral ischemia in rats.

We evaluated the effect of N(G)-nitro-L-arginine-methyl-ester (l-NAME, a nitric oxide synthase [NOS] inhibitor) and L-arginine (nitric oxide substrate) on cerebral mitochondrial dysfunction (hereafter referred to as "injury") after temporary middle cerebral artery occlusion (MCAo) during halothane or etomidate anesthesia in spontaneously hypertensive rats. Sixty minutes before MCAo, rats were randomized to 1 of 5 regimens (n = 8 per group): h/control, 1.2 minimum alveolar anesthetic concentration of halothane; h/L-NAME, 1.2 minimum alveolar anesthetic concentration of halothane and L-NAME (30 mg/kg); etomidate, an electroencephalographic (EEG) burst suppression dose of etomidate; e/L-NAME, an EEG burst suppression dose of etomidate and L-NAME (30 mg/kg); or e/L-NAME/arg, an EEG burst suppression dose of etomidate, L-NAME (30 mg/kg), and L-arginine (bolus of 300 mg/kg with an infusion at 35 mg x kg(-1) x min(-1)). After 180 min of MCAo and 120 min of reperfusion, volume of injury was determined using 2,3,5-triphenytetrazolium stain. Injury volume (mm(3), mean +/- sd) was larger in the etomidate group (153 +/- 17) than the halothane anesthetized h/control group (93 +/- 16) (P < 0.05) but did not differ between the e/L-NAME (162 +/- 17) and h/L-NAME groups (155 +/- 26). Injury volume in the e/L-NAME/arg group (88 +/- 15) was not different from the h/control group (93 +/- 16) and was less than that in either the etomidate or the e/L-NAME groups (P < 0.05). The data reproduce our previous observation that, relative to a halothane-anesthetized control state, etomidate has an adverse effect on ischemic injury in the setting of temporary focal cerebral ischemia. Prior inhibition of NOS with L-NAME resulted in no difference in the volume of injury between groups receiving etomidate or halothane (162 +/- 17 versus 155 +/- 26). Administration of a large dose of L-arginine prevented the adverse effect of etomidate. The data were obtained after only 2 h of reperfusion and therefore cannot be construed as representative of final neurologic outcome. They nonetheless suggest that etomidate produces an adverse effect on mitochondrial function early in the course of focal cerebral ischemia, in part, by inhibition of NOS.

Animals↗
PubMed2004

Combination of isoflurane and caspase inhibition reduces cerebral injury in rats subjected to focal cerebral ischemia.

BACKGROUND: Recent data indicate that the neuroprotective efficacy of isoflurane is not sustained. Delayed neuronal death, mediated in part by apoptosis, contributes to the gradual increase in the size of the infarction. These data suggest that isoflurane may not be able to inhibit delayed neuronal death. The prevention of apoptosis by a caspase inhibitor might provide neuroprotection in addition to that provided by isoflurane. The current study was conducted to determine whether isoflurane-mediated neuroprotection can be made more durable with the administration of z-VAD-fmk, a nonspecific caspase inhibitor. METHODS: Fasted Wister rats were allocated to awake-zVAD, awake-vehicle, isoflurane-zVAD, or isoflurane-vehicle groups (n = 16/group). Animals were subjected to focal ischemia for 60 min by filament occlusion of the middle cerebral artery. In the awake groups, isoflurane was discontinued after occlusion of the middle cerebral artery. In the isoflurane groups, isoflurane anesthesia was maintained at 1.5 minimum alveolar concentration during occlusion of the middle cerebral artery. Before and after ischemia, daily injections of z-VAD-fmk or vehicle were administered into the lateral cerebral ventricle for 14 days. Neurologic assessment was performed 14 days after ischemia. The volume of cerebral infarction and the number of intact neurons in the periinfarct cortex were determined by image analysis of hematoxylin and eosin-stained coronal brain sections. RESULTS: Infarction volume was less in the isoflurane-zVAD group (23 +/- 11 mm, mean +/- SD) than in isoflurane-vehicle, awake-vehicle, and awake-zVAD groups (82 +/- 31, 86 +/- 31, and 59 +/- 25 mm, respectively; P < 0.05). In comparison with the awake-vehicle and isoflurane-vehicle groups, the administration of z-VAD-fmk significantly decreased infarction volume (P < 0.05). The infarction volume between the awake-vehicle and isoflurane-vehicle groups was not different. The number of intact neurons within the periinfarct cortex was significantly less in the awake-vehicle group than in the other three groups (P < 0.05). The isoflurane-zVAD group demonstrated better neurologic function than the awake-vehicle group (P < 0.05). CONCLUSION: These findings are consistent with the premise that ongoing delayed neuronal death, in part mediated by apoptosis, contributes to the progression of cerebral infarction during the recovery period, and its inhibition can provide sustained neuroprotection.

Amino Acid Chloromethyl Ketones↗
PubMed2004

Effect of isoflurane on neuronal apoptosis in rats subjected to focal cerebral ischemia.

UNLABELLED: Although isoflurane can reduce ischemic neuronal injury after short postischemic recovery intervals, this neuroprotective efficacy is not sustained. Neuronal apoptosis can contribute to the gradual increase in infarct size after ischemia. This suggests that isoflurane, although capable of reducing early neuronal death, may not inhibit ischemia-induced apoptosis. We investigated the effects of isoflurane on markers of apoptosis in rats subjected to focal ischemia. Fasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to awake (n = 40) or isoflurane (n = 40) groups. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery for 70 min. Pericranial temperature was servo-controlled at 37 degrees C +/- 0.2 degrees C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 MAC (minimum alveolar anesthetic concentration). Animals were killed 7 h, 1 day, 4 days, or 7 days after reperfusion (n = 10/group/time point). The area of cerebral infarction was measured by image analysis in a hematoxylin and eosin stained section. In three adjacent sections, apoptotic neurons were identified by TUNEL staining and immunostaining for active caspase-9 and caspase-3. Infarct size was smaller in the isoflurane group than the awake group 7 h, 1 day, and 4 days after reperfusion (P < 0.05). However, this difference was absent 7 days after reperfusion. The number of apoptotic (TUNEL, caspase-3, and caspase-9 positive) cells 1 day after ischemia was significantly more in the awake versus isoflurane group. After a recovery period of 4 or 7 days, the number of apoptotic cells in the isoflurane group was more than in the awake group. After 7 days, the number of caspase-3 and -9 positive neurons was more in the isoflurane group (P < 0.05). The data indicate that isoflurane delays but does not prevent the development of cerebral infarction caused by ischemia. Isoflurane reduced the development of apoptosis early after ischemia but did not prevent it at later stages of postischemic recovery. IMPLICATIONS: The effect of isoflurane on neuronal apoptosis was investigated in rats subjected to focal cerebral ischemia. In isoflurane-anesthetized animals, ischemia-induced apoptosis occurred during the later stages of postischemic recovery. Isoflurane did not inhibit postischemic neuronal apoptosis.

Anesthetics, Inhalation↗