Control of laser high-harmonic generation with counterpropagating light.

Relatively weak counterpropagating light is shown to disrupt the emission of laser high-harmonic generation. Harmonic orders ranging from the teens to the low thirties produced by a 30-femtosecond pulse in a narrow argon jet are "shut down" with a contrast as high as 2 orders of magnitude by a chirped 1-picosecond counterpropagating laser pulse (60 times less intense). Alternatively, under poor phase-matching conditions, the counterpropagating light boosts harmonic production by similar contrast through quasiphase matching where out-of-phase emission is suppressed.

Tonic endogenous opioid inhibition of visceral noxious information in rabbits.

BACKGROUND & AIMS: A tonic intrinsic spinal inhibitory system on spinal motor reflexes in rabbits has been shown earlier. The aim of this study was to examine the effects of different opioid antagonists against visceral noxious stimulation in awake rabbits. METHODS: The opioid receptor antagonists examined were naloxone (nonselective), MR2266 (kappa), and naltrindole (delta). The effects on the visceromotor response thresholds induced by colorectal distention in rabbits were determined after intrathecal and intramuscular administration of the antagonists. RESULTS: Intrathecal naloxone resulted in a dose-dependent decrease of visceromotor response thresholds. The selective antagonists MR2266 and naltrindole had no significant effects. In the presence of MR2266, intrathecal naloxone reduced thresholds to the same degree as when given alone. Analysis of the data from all rabbits showed a statistically significant reduction in visceromotor response thresholds after intrathecal naloxone compared with intramuscular administration. CONCLUSIONS: In rabbits, tonic active intrinsic spinal and supraspinal endogenous opioids modulate visceral noxious information. This inhibition is exerted at the mu opioid receptor.

[The effect of suxamethonium on intracranial pressure]. / Suxamethons virkning på det intrakraniale tryk.

The literature concerning the effect of suxamethonium on intracranial pressure in animals and in humans is presented. The studies have not provided firm indications that suxamethonium per se increases the intracranial pressure. Patients with increased intracranial pressure who are to receive suxamethonium should first be deeply anaesthetized and given a defasciculating dose of a non-depolarizing blocker.

The effect of intrathecal opioid-receptor agonists on visceral noxious stimulation in rabbits.

BACKGROUND & AIMS: Conflicting results have been published concerning the effects of different opioid-receptor agonists against visceral noxious stimulation. The introduction of colorectal distention facilitates research in this field. The aim of this study was to examine intrathecally administered opioid agonists against colorectal distention in conscious rabbits. METHODS: Rabbits were equipped with a subcutaneous intrathecal injection system. Colorectal distention was induced by inflation of a balloon inserted into the descending colon. The test parameter was the pressure eliciting a characteristic visceromotor response. Examinations were performed before and after administration of the following drugs: morphine, U50488H, [D-Pen2, D-Pen5]enkephalin (DPDPE), naloxone, MR2266, naltrindole, saline, and acidified saline. RESULTS: The visceromotor response to colorectal distention was inhibited in a dose-dependent fashion by intrathecal opioids acting as agonists at all three types of opioid receptors. Morphine was antagonized more effectively by intrathecal than intramuscular naloxone. U50488H and DPDPE were equally antagonized by the specific antagonists MR2266 and naltrindole. Electrical thresholds in the lumbar region were increased, although they remained unaltered in the cervical region after administration of all three agonists. CONCLUSIONS: Intrathecal administration of different opioid agonists produces a dose-dependent spinal effect. The rank order of potencies in this model is DPDPE > U50488H > morphine > saline = 0.

Direct spinal effect of intrathecal and extradural midazolam on visceral noxious stimulation in rabbits.

We measured alterations in a noxious visceromotor reflex in rabbits subjected to intestinal distension, after i.m., extradural or intrathecal injection of midazolam or saline. Spinal catheters were inserted and tunnelled surgically and the animals allowed to recover for 2 weeks. A balloon catheter was placed in the distal part of the descending colon, in the awake rabbit. Intraluminal pressures were increased continuously by water instillation until a sudden withdrawal of the pelvis was observed. Pressure values at withdrawal threshold were recorded immediately before the injection and after 5, 15 and 30 min. Pain thresholds were unaltered after saline. Extradural midazolam 12.5-250 micrograms kg-1 produced a dose-dependent increase in the percent maximum possible effect ranging from 7% after the smallest dose to 80%. Similar dose-dependent effects were observed after intrathecal injection of midazolam 25-62.5 micrograms kg-1. Extradural and intrathecal, but not i.v. injection of flumazenil 25 micrograms kg-1 (a benzodiazepine receptor antagonist) reduced the antinociceptive effect of extradural and intrathecal midazolam to pretreatment levels. A segmental effect of intrathecal midazolam was demonstrated using transcutaneous electrical stimulation in the areas of the neck and the lower back. The effect of intrathecal midazolam 62.5 microrgrams kg-1 was restricted to the lumbar region, demonstrating a selective action on the spinal cord. Thus extradural and intrathecal midazolam produced a dose-dependent effect on the reflex response to visceral distension in rabbits. This effect is caused by a direct spinal action on benzodiazepine receptors in the spinal cord.

Chronic catheterization of the epidural space in rabbits: a model for behavioural and histopathological studies. Examination of meptazinol neurotoxicity.

A technique of epidural catheterization in rabbits is described. Twelve albino rabbits received a totally implanted epidural catheter system. The system was implanted surgically, and the functioning of the system tested for a period of 3 months. X-ray examinations following epidural contrast injections showed a distribution up to Th4 following 1.5 ml and Th8-9 following 1.0 and 1.25 ml. Epidural injection of lidocaine throughout the study period proved the system to be functioning for all 3 months. Another 12 rabbits were included for the neurotoxicological examinations following epidural catheterization, without any injections (three rabbits), epidural injections of saline (four rabbits) and meptazinol (five rabbits) once a day for 14 days. Histopathological examinations showed a fibrous cocoon, at the tip of the catheter, in all rabbits. In the group of rabbits which did not receive any injections, the cocoon was slightly infiltrated with leukocytes and local depression of the spinal cord was observed in one rabbit. In the saline-injected group this infiltration was more pronounced and in one rabbit it extended into the meninges. Three rabbits showed local depression of the spinal cord and local myelopathy of the white matter in the area adjacent to the cocoon. In the group of rabbits receiving meptazinol, three out of five had local depression and myelopathy of the white matter. In this group these findings were more pronounced. In two rabbits the myelopathy extended transversely through the white matter into the grey matter of the spinal cord. The number of pathological changes in the group receiving meptazinol was significantly higher compared to the control and placebo groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of cerebral blood flow (CBF) with the Kety and Schmidt technique during craniotomy.

In this study cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice during craniotomy for supratentorial cerebral tumors by the Kety and Schmidt technique. The anaesthetic procedures included halothane, enflurane isoflurane and continuous infusion with midazolam, etomidate, althesin and neurolept anaesthesia (dehydrobenzpyridol). Moderate hypocapnia was used and the anaesthesia was supplemented with nitrous oxide and fentanyl. In general, both CBF and CMRO2 were decreased. However, with inhalation anaesthetics an increase in concentration resulted in an increase in CBF (halothane) or unchanged CBF (isoflurane and enflurane) and a decrease in CMRO2. With the hypnotic agents a dose related decrease in CMRO2 was observed, while CBF either was unchanged (midazolam) or decreased (Althesin and etomidate).

Intestinal distension test, a method for evaluating intermittent visceral pain in the rabbit.

Behavioural response to intestinal distension was studied in 12 female New Zealand albino rabbits under various conditions. On increasing intraluminal pressures, the rabbits elicited uniform behavioural responses within discrete pressure ranges, notably a sudden pelvic withdrawal at 30-50 mmHg. The pressure provoking pelvic withdrawal was chosen as the test parameter and proved to be individually reproducible, irrespective of fasting/non-fasting or the time of day and with no signs of adaptation in six days consecutive measurements. Morphine modified the pressure response in a dose-dependent manner, whereas isotonic saline or pentobarbital had no effect. In conclusion, the intestinal distension test is reproducible and mimicks intermittent visceral pain in the rabbit. This allows for paired observations in small animal populations with a minimum of discomfort to the animals, which offers a major advantage when comparing with the existing visceral pain tests.

Cerebral blood flow and metabolism during isoflurane-induced hypotension in patients subjected to surgery for cerebral aneurysms.

Cerebral blood flow and cerebral metabolic rate for oxygen were measured during isoflurane-induced hypotension in 10 patients subjected to craniotomy for clipping of a cerebral aneurysm. Flow and metabolism were measured 5-13 days after the subarachnoid haemorrhage by a modification of the classical Kety-Schmidt technique using xenon-133 i.v. Anaesthesia was maintained with an inspired isoflurane concentration of 0.75% (plus 67% nitrous oxide in oxygen), during which CBF and CMRO2 were 34.3 +/- 2.1 ml/100 g min-1 and 2.32 +/- 0.16 ml/100 g min-1 at PaCO2 4.1 +/- 0.1 kPa (mean +/- SEM). Controlled hypotension to an average MAP of 50-55 mm Hg was induced by increasing the dose of isoflurane, and maintained at an inspired concentration of 2.2 +/- 0.2%. This resulted in a significant decrease in CMRO2 (to 1.73 +/- 0.16 ml/100 g min-1), while CBF was unchanged. After the clipping of the aneurysm the isoflurane concentration was reduced to 0.75%. There was a significant increase in CBF, although CMRO2 was unchanged, compared with pre-hypotensive values. These changes might offer protection to brain tissue during periods of induced hypotension.

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2-reactivity during craniotomy for supratentorial cerebral tumours in halothane anaesthesia. A dose-response study.

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anaesthesia was induced with thiopental 4-6 mg kg-1, fentanyl and pancuronium, and maintained with an inspiratory halothane concentration of 0.45% in nitrous oxide 67% at a moderate hypocapnic level. In one group of patients (n = 7) the inspiratory halothane concentration was maintained at 0.45% throughout anaesthesia. About 1 h after induction of anaesthesia CBF and CMRO2 averaged 35 +/- 2 ml 100 g-1 min-1 and 2.7 +/- 0.3 ml O2 100 g-1 min-1 (mean +/- s.c. mean), respectively. During repeat studies 1 h later CBF and CMRO2 did not change. In another group of patients (n = 7) an increase in halothane concentration from 0.45% to 0.90% was associated with a significant decrease in CMRO2 from 2.3 +/- 0.1 to 2.0 +/- 0.1 ml O2 100 g-1 min-1. The CO2-reactivity measured after the second flow measurement was preserved. It is concluded that halothane in this study induces a dose-dependent decrease in cerebral metabolism, an increase in CBF while CO2-reactivity is maintained.

The effect of isoflurane on cerebral blood flow and metabolism in humans during craniotomy for small supratentorial cerebral tumors.

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumors. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anesthesia was induced with thiopental 5-7 mg X kg-1, fentanyl 0.2 mg, and pancuronium, and maintained with 0.75% inspired isoflurane concentration in 67% nitrous oxide, and moderate hypocapnia. In one group of patients (n = 7), the inspired isoflurane concentration was maintained at 0.75% throughout anesthesia. One hour after induction of anesthesia, CBF and CMRO2 averaged 31 +/- 3 ml X 100 g-1 X min-1 and 2.1 +/- 0.2 ml O2 X 100 g-1 X min-1 (X +/- SEM), respectively. During repeat studies 1 h later, CBF and CMRO2 were unchanged. In a second group of patients (n = 7), an increase in the inspired isoflurane concentration from 0.75% to 1.5% was associated with a significant decrease in CMRO2 from 2.4 +/- 0.1 to 1.9 +/- 0.1 ml O2 X 100 g-1 X min-1, and no change in CBF. It is concluded that this anesthetic regimen is safe to use in patients with small supratentorial tumors in whom only a small midline shift has occurred.

CBF and CMRO2 during craniotomy for small supratentorial cerebral tumours in enflurane anaesthesia. A dose-response study.

In 14 patients with supratentorial cerebral tumours with midline shift less than or equal to 10 mm, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice on the contralateral side of the craniotomy, using a modification of the Kety & Schmidt method. For induction of anaesthesia, thiopental, fentanyl and pancuronium were used. The anaesthesia was maintained with enflurane 1% in nitrous oxide 67%. Moderate hypocapnia to a level averaging 4.3 kPa was achieved. The patients were divided into two groups. In Group 1 (n = 7), 1% enflurane was used throughout the anaesthesia, and CBF and CMRO2 measured about 70 min after induction averaged 30.1 ml 100 g-1 min-1 and 1.98 ml O2 100 g-1 min-1, respectively. During the second CBF study 1 h later, CBF and CMRO2 were unchanged (P greater than 0.05). In Group 2 (n = 7), the inspiratory enflurane concentration was increased from 1 to 2% after the first CBF measurement. In this group a significant decrease in CMRO2 was observed, while CBF was unchanged. In six patients EEG was recorded simultaneously with the CBF measurements. In patients subjected to increasing enflurane concentration (Group 2), a suppression in the EEG activity was observed without spike waves. It is concluded that enflurane induces a dose-related decrease in CMRO2 and suppression in the EEG activity, whereas CBF was unchanged.

CBF and CMRO2 during continuous etomidate infusion supplemented with N2O and fentanyl in patients with supratentorial cerebral tumour. A dose-response study.

In 14 patients with supratentorial cerebral tumours with midline shift below 10 mm, CBF and CMRO2 were measured (Kety & Schmidt) during craniotomy. The anaesthesia was continuous etomidate infusion supplemented with nitrous oxide and fentanyl. The patients were divided into two groups. In Group 1 etomidate infusion of 30 micrograms kg-1 min-1 was used throughout the anaesthesia, and CBF and CMRO2 were measured twice. In this group CMRO2 (means +/- s.d.) averaged 2.31 +/- 0.43 ml O2 100 g-1 min-1 70 min after induction and 2.21 +/- 0.38 ml O2 100 g-1 min-1 130 min after induction. In Group 2 the etomidate infusion was increased from 30 to 60 micrograms kg-1 min-1 after the first study and a significant fall in CMRO2 from 2.52 +/- 0.56 to 1.76 +/- 0.40 ml O2 100 g-1 min-1 was found. Simultaneously, a significant fall in CBF was observed. The CO2 reactivity was preserved during anaesthesia.

Use of a continuous infusion of althesin in neuroanaesthesia. Changes in cerebral blood flow, cerebral metabolism, the EEG and plasma alphaxalone concentration.

Ten patients with small supratentorial tumours were studied during craniotomy. Cerebral blood flow (CBF) was measured in the contralateral hemisphere by a modification of the Kety and Schmidt technique using xenon-133 i.v. With an Althesin infusion rate of 0.2 ml kg-1 h-1, CBF was 24.4 +/- 5.4 ml min-1/100 g and CMRO2 1.87 +/- 0.44 ml min-1/100 g at PaCO2 4.1 +/- 0.7 kPa (mean +/- SD). During constant infusion rates of Althesin, steady values of CMRO2 were obtained, while an increase in infusion rate of 150% was associated with an increase in plasma alphaxalone concentration, a decrease in CMRO2 and a tendency of further EEG suppression. However, great inter- and intraindividual variations were present, and correlations between CMRO2, EEG activity and plasma alphaxalone concentration were weak.

Respiratory depression after epidural morphine in the postoperative period. Influence of posture.

Twelve females scheduled for elective lower abdominal surgery received 4 mg of morphine by lumbar epidural injection for postoperative pain relief. The patients were divided into two groups nursed postoperatively in a supine or 45 degree elevated position, respectively. Mouth occlusion pressure during CO2 stimulation was used for the determination of respiratory depression, following epidural morphine. No significant difference in occlusion pressure was found between the two groups. Within the groups a significant reduction of the occlusion pressure was found when compared with the value obtained immediately before the administration of epidural morphine. However, compared with the value obtained the day before surgery, no significant reduction of the occlusion pressure was observed. It is concluded that the 45 degree elevated position does not protect against the occurrence of respiratory depression following epidural morphine.