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Biomedical subjects

M S Scheller

Publications and source records attributed to M S Scheller.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effect of a hypertonic lactated Ringer's solution on intracranial pressure and cerebral water content in a model of traumatic brain injury.

There has recently been an increased interest in the use of hypertonic solutions for fluid resuscitation of trauma victims. In this study, we examined the acute cerebral effects of a hypertonic lactated Ringer's solution (measured osmolality = 469 mOsm/kg) in an animal model of traumatic brain injury. Following the production of a cerebral cryogenic lesion, eight New Zealand white rabbits were randomized to undergo hemodilution with either lactated Ringer's (measured osmolality = 254 mOsm/kg) or hypertonic lactated Ringer's. Over the course of the experiment the lactated Ringer's group required significantly more fluid than the hypertonic group to maintain stable central venous and mean arterial pressure (245 +/- 5 ml vs. 132 +/- 20 ml; p less than 0.0001). Osmolality increased in the hypertonic group by 13.5 +/- 3.3 mOsm/kg whereas it decreased in the lactated Ringer's group by 5.5 +/- 2.6 mOsm/kg. Intracranial pressure increased in both groups over the course of the experiment but the increase in pressure was greater in the lactated Ringer's group than the hypertonic group (9.5 +/- 2.4 mm Hg vs. 1.7 +/- 1.5 mm Hg; p less than 0.001). Brain water content was significantly increased in the region of the lesion as assayed by both the wet/dry weight method and cortical specific gravity determinations, but there was no difference between the two treatment groups. Water content of the nonlesioned hemisphere was significantly less in the hypertonic group. This study suggests that hypertonic saline solutions may be useful for the resuscitation of hypovolemic patients with localized brain injury.

Animals↗
PubMed1989

Nimodipine does not improve neurologic outcome after 14 minutes of cardiac arrest in cats.

We tested the effects of nimodipine upon neurologic outcome in 31 cats subjected to 14 minutes of cardiac arrest followed by resuscitation. With the dose schedule used, nimodipine had no effect upon neurologic outcome or upon the percentage of ischemic neurons in frontal, hippocampal, occipital, or cerebellar brain sections. The electroencephalographic recovery pattern did not correlate with neurologic or pathologic findings.

Animals↗
PubMed1988

MAC of sevoflurane in humans and the New Zealand white rabbit.

The minimum alveolar concentration of sevoflurane necessary to prevent movement in 50 per cent of patients (MAC) was determined to be 2.05 per cent in 20 adult surgical patients. Because this value was higher than the only other experimentally determined human MAC value for sevoflurane (1.71 per cent), MAC was also determined in New Zealand white rabbits. Comparisons of the MAC ratios of sevoflurane to other volatile anaesthetics in both the human and the rabbit suggest that the human MAC value we obtained for sevoflurane is consistent with experimental determinations of MAC of other volatile anaesthetics in humans.

Adult↗
PubMed1988

The effects of sevoflurane on cerebral blood flow, cerebral metabolic rate for oxygen, intracranial pressure, and the electroencephalogram are similar to those of isoflurane in the rabbit.

The effects of 0.5 and 1.0 MAC end-tidal concentrations of sevoflurane on intracranial pressure, cerebral metabolic rate for oxygen, cerebral blood flow, and the electroencephalogram were compared to those of equi-MAC concentrations of isoflurane in rabbits anesthetized with morphine-nitrous oxide. At 1.0 MAC end-tidal level, both sevoflurane and isoflurane caused a significant reduction in cerebral metabolic rate for oxygen of about 50%. Neither anesthetic caused a significant change in global cerebral blood flow or cortical cerebral blood flow during either 0.5 or 1.0 MAC administration. However, both sevoflurane and isoflurane caused small but significant increases in intracranial pressure during 0.5 MAC and 1.0 MAC administration. The electroencephalogram of animals anesthetized with 1.0 MAC of either anesthetic demonstrated a burst suppression pattern with no evidence of spike or seizure activity. The data suggest that the effects of sevoflurane on cerebral blood flow, cerebral metabolic rate for oxygen, intracranial pressure, and the electroencephalogram are indistinguishable from those of equivalent concentrations of isoflurane in the rabbit.

Animals↗
PubMed1988

Acute cerebral effects of isotonic crystalloid and colloid solutions following cryogenic brain injury in the rabbit.

Despite the numerous studies examining the relative merits of crystalloids versus colloids for expansion of intravascular volume, little attention has been directed to the cerebral effects of these solutions. In particular, the effect of changes in plasma oncotic pressure on brain water content are poorly understood. The authors recently examined the acute effects of changes in plasma osmolality and colloid oncotic pressure in normal animals, and found that a 65% reduction in oncotic pressure had no detectable effect on brain water content or intracranial pressure. In an effort to extend these studies to a more clinically relevant situation, the authors have now compared the acute effects of 0.9% saline, 6% hetastarch, and 5% albumin on regional cerebral water content and intracranial pressure in an animal model of brain injury produced by focal cortical freezing. Under general anesthesia and following the production of the cryogenic brain lesion, rabbits underwent a 45-min period of isovolemic hemodilution to a hematocrit of 20-25% with one of the three selected fluids. The saline group required approximately twice as much fluid (207 +/- 17 ml) to maintain a stable mean arterial pressure and central venous pressure as did the hetastarch (105 +/- 14 ml) or albumin (103 +/- 29 ml) groups. As intended, the oncotic pressure decreased by a mean of 9.6 +/- 2.4 mmHg in the saline group, while remaining stable in the hetastarch and albumin groups. There were no significant changes in osmolality in any group during the hemodilution period.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1987

The intracranial pressure effects of isoflurane and halothane administered following cryogenic brain injury in rabbits.

The intracranial pressure (ICP) responses to administration of either halothane or isoflurane were compared in New Zealand white rabbits following a standardized cryogenic brain injury. Animals were tracheally intubated and paralyzed, and background anesthesia was maintained with morphine sulfate and nitrous oxide. Following injury and attainment of an elevated and stable ICP, animals were divided into four groups. Animals in groups I and III were maintained normocapnic throughout the experiment and administered 1 MAC halothane or isoflurane, respectively. Group II and IV animals were made hypocapnic (PaCO2 = 20 mmHg) prior to the administration of either 1 MAC halothane or isoflurane, respectively. Monitored variables were mean arterial blood pressure, ICP (ventriculostomy), end-tidal (ET) CO2, ET volatile anesthetic, the electroencephalogram, temperature, and arterial blood gases. Prior to producing the lesion, ICP was approximately 5 mmHg in all animals with no differences among groups. Sixty to ninety minutes after injury, ICP increased significantly to approximately 20 mmHg in all animals. Introduction of either halothane or isoflurane was associated with significant increases in ICP in all groups to approximately 30 mmHg. These data suggest that further significant increases in ICP may occur following introduction of either halothane or isoflurane in the presence of acute brain injury and elevated ICP. Furthermore, these ICP increases may not be altered by the prior establishment of hypocapnia.

Animals↗
PubMed1987

The effect of nitrous oxide on cortical cerebral blood flow during anesthesia with halothane and isoflurane, with and without morphine, in the rabbit.

The effect of nitrous oxide on cortical cerebral blood flow (CBF) was examined during a varying background anesthetic state in the New Zealand White rabbit. Seventy percent nitrous oxide resulted in significant and similar increases in CBF during anesthesia with both 0.5 MAC of halothane (44 +/- 14 to 63 +/- 17 ml.100 g-1.min-1) (mean +/- SD) and anesthesia with isoflurane (34 +/- 9 to 41 +/- 11 ml.100 g-1.min-1). During anesthesia with 1.0 MAC halothane or isoflurane, N2O also increased CBF, but the increments (halothane, 73 +/- 34 to 111 +/- 54 ml.100 g-1 min-1; isoflurane 34 +/- 13 to 69 +/- 34 ml.100 g-1.min-1) were significantly greater than those observed at 0.5 MAC. When 0.5 MAC halothane or isoflurane was supplemented with morphine (10 mg/kg followed by an infusion of 2 mg.kg-1.min-1), the CBF effect of N2O was not significantly different from that observed with 0.5 MAC alone. It was concluded that, in the rabbit, the effects of N2O on cortical CBF vary with the background anesthetic state and that the increase in CBF caused by N2O becomes greater as the end-tidal concentration of halothane or isoflurane increases from 0.5 to 1.0 MAC. Morphine, when added to 0.5 MAC of halothane or isoflurane, does not alter the effect of 70% N2O on cortical CBF.

Animals↗
PubMed1986

Isoflurane, halothane, and regional cerebral blood flow at various levels of PaCO2 in rabbits.

The effects of halothane and isoflurane on regional cerebral blood flow (CBF) were studied in 18 New Zealand White rabbits anesthetized with nitrous oxide (N2O) and morphine sulfate (MS) at three different levels of PaCO2. CBF was measured using the hydrogen clearance technique. Monitored variables were intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, electroencephalogram, arterial blood gases, end-tidal (ET) volatile anesthetic, and ET CO2. Addition of 1 MAC halothane to the N2O/MS background anesthetic caused flow to increase significantly in all three regions studied (cortex, dorsal hippocampus, white matter) at all three levels of PaCO2 (low: 20-25 mmHg; normal: 35-40 mmHg; high: 50-55 mmHg). Addition of 1 MAC isoflurane to the background anesthetic caused CBF to decrease significantly in all regions during hypocapnia. During normocapnia, CBF was unchanged with the addition of 1 MAC isoflurane in all regions and during hypercapnia, CBF increased significantly only in the dorsal hippocampus following addition of 1 MAC isoflurane to the MS/N2O background anesthetic. Volatile anesthetic administration was associated with significant, although small, increases in ICP at all PaCO2 levels. We conclude that 1 MAC concentrations of halothane and isoflurane have opposite effects on CBF when added to a N2O/MS anesthetic during hypocapnia and that the effects of isoflurane on regional CBF are dependent on PaCO2 in rabbits under the anesthetic conditions of this experiment.

Anesthesia↗
PubMed1986

A comparison of the direct cerebral vasodilating potencies of halothane and isoflurane in the New Zealand white rabbit.

Halothane is commonly viewed as a more potent cerebral vasodilator than isoflurane. It was speculated that the lesser vasodilation caused by isoflurane might be the result of the greater reduction in cerebral metabolic rate (CMR) that it causes, and that the relative vasodilating potencies of halothane and isoflurane would be similar if the two agents were administered in a situation that precluded volatile-agent-induced depression of CMR. To test this hypothesis, cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) were measured in two groups of rabbits before and after the administration of 0.75 MAC halothane or isoflurane. One group received a background anesthetic of morphine and N2O, which resulted in an initial CMRO2 of 3.21 +/- 0.17 (SEM) ml X 100 g-1 X min-1; second group received a background anesthetic of high-dose pentobarbital, which resulted in an initial CMRO2 of 1.76 +/- 0.16 ml X 100 g-1 X min-1. In rabbits receiving a background of morphine sulfate/N2O, halothane resulted in a significantly greater CBF (65 +/- 10 ml X 100 g-1 X min-1) than did isoflurane (40 +/- 5 ml X 100 g-1 X min-1). Both agents caused a reduction in CMRO2, but CMRO2 was significantly less during isoflurane administration. By contrast, with a background of pentobarbital anesthesia, CBF increased by significant and similar amounts with both halothane and isoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1985

The relationship of beta-endorphin and ACTH in the cerebrospinal fluid and plasma of adult surgical patients.

Cerebrospinal fluid and plasma beta-endorphin/beta-lipotropin immunoreactivity and adrenocorticotropin hormone were determined in simultaneously obtained samples from 25 healthy, adult surgical patients about to undergo spinal anesthesia using radioimmunoassay techniques. Cerebrospinal fluid adrenocorticotropin concentrations were significantly higher than those in plasma (25.76 +/- 2.11 fm/ml vs. 8.83 +/- 0.84 fm/ml), whereas beta-endorphin/beta-lipotropin concentrations in cerebrospinal fluid were significantly lower than those in plasma (6.60 +/- 0.43 fm/ml vs. 3.35 +/- 0.30 fm/ml). In cerebrospinal fluid, a significant positive correlation was found between beta-endorphin/beta-lipotropin and adrenocorticotropin (r = 0.64, p less than 0.01), whereas no such relationship could be demonstrated in plasma. This suggests that beta-endorphin/beta-lipotropin and adrenocorticotropin might enter the cerebrospinal fluid via a mechanism unrelated to their entry into plasma. This may have implications for the pharmacologic manipulation of these peptides within the central nervous system.

Adrenocorticotropic Hormone↗
PubMed1985

A comparison of the sensitivity of pulmonary artery pressure, end-tidal carbon dioxide, and end-tidal nitrogen in the detection of venous air embolism in the dog.

The authors sought to define the relative sensitivities of endtidal carbon dioxide analysis (ETCO2), end-tidal nitrogen analysis (ETN2), and pulmonary artery pressure (PAP) monitoring in the detection of venous air embolism (VAE). Serial injections of air (0.25, 0.5, 0.75, 1.0, and 1.5 ml/kg) were performed in six mongrel dogs. The frequency with which positive responses (PAP increase greater than 2 mm Hg; ETCO2 decrease greater than 0.2%; ETN2 increase greater than 0.04%) were observed following VAE was not different for the three methods. The response time (time to maximum change following VAE) was significantly more rapid for PAP and ETN2 than for ETCO2; although the range for the three methods was narrow, e.g., for 1.5 ml/kg--PAP, 0.92 +/- 0.7 (SD) min; ETN2, 1.20 +/- 0.5 min; ETCO2, 1.85 +/- 0.7 min. The time from injection of air to return to baseline levels was significantly more rapid for ETN2 than for ETCO2 which was in turn significantly faster than PAP, e.g., for 1.5 ml/kg--ETN2, 8.0 +/- 4.3 min; ETCO2, 19.4 +/- 6.0 min; PAP, 23.8 +/- 6.1 min. The results indicate that, where the capacity to identify increases in expired nitrogen on the order of 0.04% can be achieved, ETN2 monitoring will identify VAE events with a sensitivity similar to that of PAP and ETCO2. However, the difficulties inherent in achieving this level of nitrogen detection sensitivity probably represent a current major limitation in the application of this method. Furthermore, the data indicate that, after VAE, ETN2 will return to preinjection levels although PAP and ETCO2 remain abnormal. This observation suggests that ETN2 may not be a reliable indicator of recovery from the physiologic impact of VAE, and may therefore not be the optimum method to base decisions regarding resumption of the head-up posture and continuation of surgery during procedures in which VAE has occurred.

Animals↗