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Biomedical subjects

C Werner

Publications and source records attributed to C Werner.

At least 127 records · Page 7Linked to original sources
PubMed1997

[Mild and moderate hypothermia as a new therapy concept in treatment of cerebral ischemia and craniocerebral trauma. Pathophysiologic principles].

Hypothermia protects the brain and other vital organs during periods of ischaemia. We differentiate between mild (36-34 degrees C), moderate (33-29 degrees C), deep (28-17 degrees C) and profund (16-4 degrees C) hypothermia. During hypothermia, cerebral metabolic rate and cerebral blood flow decrease dependent on temperature. The relation between temperature and cerebral metabolism is expressed by the temperature coeffizient Q10, which is the ratio between two metabolic rates separated by 10 degrees C. The following factors contribute to decreases in cerebral blood flow seen during hypothermia: cerebral metabolic depression, decreases in cardiac output, and decreases in arterial blood pressure with pH-stat management, increases in hematocrit and in blood viscosity. Mild or moderate hypothermia reduces histopathological damage and neurological deficits if started before and during cerebral ischaemia. Hypothermia may also improve neurologic outcome if initiated following focal cerebral ischaemia, but is less effective after global ischaemic insults. Mild hypothermia appears to be safer and more effective compared to moderate hypothermia. In most instances, deep hypothermia renders neurologic outcome worse, which is most likely related to the generation of toxic metabolites and inadequate myocardial function during rewarming. The neuroprotective effects of hypothermia are related to several mechanisms along the ischaemic cascade: prevention of postischaemic hypoperfusion, reduction of functional and basal metabolism, decreased accumulation of lactic acid and oedema formation, inhibition of excitatory neurotransmitter release, prevention of Ca(++)- and Na(+)-influx, inhibition of lipid peroxidase activity, and free radical formation, stimulation of regenerative immediate early genes. The side effects of hypothermia include myocardial ischaemia, cardiac arrhythmias, decreased left ventricular contractility, coagulation abnormalities, and suppression of metabolic and immunological processes.

Brain↗
PubMed1997

[Effect of S-(+)-ketamine on autoregulation of cerebral blood flow].

PURPOSE: The present study investigates the effects of S-(+)-ketamine on cerebral blood flow (CBF) autoregulation in rats. METHODS: Following IRB approval, 24 nonfasted male Sprague-Dawley rats were anesthetised with isoflurane, intubated and mechanically ventilated. Catheters were inserted into the right femoral artery, both femoral veins, and into the right jugular vein for drug administration, measurement of mean arterial blood pressure (MAP), and blood sampling. Cortical cerebral blood flow was measured using laser-Doppler-flowmetry (PF 403, Perimed). At the end of surgery isoflurane was discontinued and all animals were randomly assigned to one of the following anaesthetic treatments. In group 1 (n = 8, control), anaesthesia was maintained using fentanyl (10 micrograms/kg i.v. bolus, followed by 25 micrograms/kg/h i.v.) and N2O/O2 (FiO2: 0.3). In group 2 (n = 8) and group 3 (n = 8) animals received 0.5 mg/kg/min S-(+)-ketamine i.v. or 1.0 mg/kg/min S-(+)-ketamine i.v. and O2/air (FiO2: 0.3), respectively. CBF was tested by graded haemorrhage. Arterial blood gases, arterial pH, and pericranial temperature were controlled over time. RESULTS: CBF autoregulation was maintained under low and high doses of S-(+)-ketamine compared to fentanyl/N2O-anaesthetised controls. However, low-dose S-(+)-ketamine shifted the autoregulatory curve towards higher MAP values. CONCLUSIONS: The present study indicates that autoregulatory cerebrovascular dilation is preserved with low and high doses of S-(+)-ketamine. Differences in the lower limit of CBF autoregulation may be consistent with an increased sympathetic tone induced by low doses of S-(+)-ketamine.

Anesthetics, Dissociative↗
PubMed1997

Inhaled nitric oxide increases survival rates in newborn rats with congenital diaphragmatic hernia.

The high mortality of newborn infants with congenital diaphragmatic hernia (CDH) can be partly attributed to pulmonary hypertension causing extrapulmonary right-to-left shunting with subsequent severe hypoxemia. Inhaled nitric oxide (NO) may reduce elevated pulmonary artery pressure and has been successfully improve arterial oxygenation in some newborns with CDH. However, it is not clear whether inhaled NO will actually improve survival of newborns with CDH. We therefore investigated the effect of inhaled NO on the survival rate of newborn rats with CDH following intrauterine exposure to nitrofen. A total of 151 newborn rats (9 litters) were exposed to nitrofen on day 11 of pregnancy, After spontaneous delivery, 63 newborn rats (4 litters) were allowed to spontaneously breathe air containing NO (80 parts per million), while 88 newborn rats (5 litters) were given air without NO. Survival was checked 15 min after birth and then hourly until the animals were sacrificed at 24 h of age to verify the absence or presence of CDH. The 2 groups of newborn rats breathing air with or without NO did not differ significantly with respect to the presence or size of CDH. Twenty-four of 63 (38%) newborn rats breathing air with NO survived for 24 h, compared to 12 of 88 (14%) rats breathing air alone (p < 0.01). Of newborn rats that were actually found to have CDH (n = 113), 8 of 42 (19%) animals breathing air with NO survived for 24 h, compared to 2 of 71 (2.8%) animals breathing air alone (p < 0.01). In animals with CDH confirmed by autopsy, the median survival time was significantly longer with NO (p < 0.001) ( 2 h, interquartile range 2h-15h), than those breathing or without NO (median/interquartile range 15 min). We conclude that in the nitrofen rat CDH model, significantly improved survival rates occur with inhaled NO as a sole intervention. The combined impact of inhaled NO and mechanical ventilation remains to be determined.

Administration, Inhalation↗
PubMed1997

Late intraoperative clonidine administration prevents postanesthetic shivering after total intravenous or volatile anesthesia.

Postoperative administration of clonidine is an effective treatment for shivering. However, the ability of this drug to stop postanesthetic shivering when administered intraoperatively remains controversial. Furthermore, the relative efficacy of clonidine during isoflurane and propofol anesthesia remains unknown. We therefore evaluated the incidence of postanesthetic shivering in patients given clonidine during nitrous oxide/isoflurane or propofol anesthesia. Because clonidine is an analgesic, we also evaluated postoperative pain and analgesic requirements. We studied 60 patients undergoing elective ear or nose surgery. General anesthesia was induced with 2.0 mg/kg propofol, 1.5 micrograms/kg fentanyl, and 0.1 mg/kg vecuronium. General anesthesia was maintained with isoflurane and 70% nitrous oxide in one group of patients; in the other, a continuous infusion of propofol (8 mg.kg-1.h-1) was administered (without nitrous oxide). Five minutes before tracheal extubation, patients in each group were randomly assigned to receive saline, placebo, or 3 micrograms/kg clonidine intravenously. Postanesthetic shivering was evaluated by a blind investigator. Postoperative pain was assessed using a visual analog scale. Postoperative shivering was observed in 53% of the patients given isoflurane without clonidine and in 13% of the patients given propofol without clonidine. No patient given clonidine shivered. Clonidine administration significantly reduced postoperative pain. The incidence of postanesthetic shivering was significantly less after propofol anesthesia than after isoflurane/nitrous oxide anesthesia. However, a late intraoperative bolus administration of 3 micrograms/kg clonidine prevents postoperative shivering in patients given either type of anesthesia.

Adult↗
PubMed1997

Jugular bulb oxygen saturation and middle cerebral blood flow velocity during cardiopulmonary bypass.

This study investigates changes of jugular bulb oxygen saturation (SjO2) measured by fiberoptic jugular bulb oximetry and changes of intracranial hemodynamics using transcranial Doppler sonography (TCD) during cardiopulmonary bypass (CPB) for coronary artery bypass graft (CABG) in 17 ASA III patients. Anesthesia was maintained with fentanyl, midazolam, and continuous infusion of etomidate. Hypothermic CPB (27 degrees C) was managed according to alpha-stat conditions. SjO2 (%) was measured by a fiberoptic catheter (Opticath F 5.5; Abbott Critical Care Systems) placed in the right jugular bulb via the right internal jugular vein. Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a bidirectional 2-MHz TCD system (Transpect, Medasonics). Data were recorded continuously from the beginning to the end of the CPB. During cooling and hypothermia (27 degrees C); SjO2 and Vmean did not change compared with values at the start of CPB. However, with the beginning of rewarming, Vmean was increased 65% compared with stable hypothermia (27 degrees C). This increase in Vmean was associated with a 25% decrease in SjO2. Maximum desaturation occurred at a 36 degrees C jugular bulb temperature. During cooling and stable hypothermia, global oxygen balance and intracerebral perfusion seemed to be maintained. However, a major alteration in the balance of the cerebral oxygen supply and demand may occur in response to rewarming despite increases in Vmean. Findings suggest inadequate increases in CBF to meet cerebral metabolic demand. Further investigations need to validate these findings with biochemical techniques and neuropsychological tests.

Anesthesia, General↗
PubMed1997

The effects of fentanyl and sufentanil on cerebral hemodynamics.

Our study investigated the effects of moderate doses of fentanyl and sufentanil versus high-dose sufentanil on cerebral hemodynamics by using transcranial Doppler ultrasonography (TCD). Thirty American Society of Anesthesiologists (ASA) II and III patients scheduled for elective coronary artery bypass graft (CABG) were studied after Institutional Review Board (IRB) approval and informed consent. The evening before surgery, all patients received oral flurazepam (1 mg/kg), Atropine (0.4 mg/70 kg s.c.) and a combination of droperidol (70 micrograms/kg s.c.) plus fentanyl (1.5 micrograms/kg s.c.) were given as preanesthetic medication 1 h before induction of anesthesia. Anesthesia was induced with either 25 micrograms/kg fentanyl i.v. (group 1, n = 10), 3 micrograms/kg sufentanil i.v. (group 2, n = 10) or 6 micrograms/kg sufentanil i.v. (group 3, n = 10). All patients received 100 micrograms/kg pancuronium i.v. With the induction of respiratory depression, assisted ventilation was performed followed by controlled ventilation to maintain normoxia and normocapnia (FiO2, 1.0). Cerebral blood flow velocity (CBFV, cm/s) was measured continuously in the middle cerebral artery by using a bidirectional 2-MHz TCD system. Monitoring included heart rate (HR, beats/min), direct mean arterial blood pressure (MAP, mm Hg), and PaCO2. Physiologic variables including arterial blood gases were measured at baseline, 5 min, and 10 min after infusion of fentanyl or sufentanil. In all patients, HR, MAP, end-tidal carbon dioxide tension (PetCO2), and PaCO2 were constant over time and did not differ between groups. CBFV did not change with moderate doses of fentanyl (group 1) or sufentanil (group 2). In contrast, infusion of high-dose sufentanil (group 3) was associated with 27 to 30% decreases in CBFV (p < 0.05). Our results suggest that sufentanil decreases CBFV in a dose-related fashion with a threshold effect. Increases in CBFV and CBF seen in previous studies may be related to an increasing PaCO2 when maintenance of normocarbia is based on only real-time capnography with a constant PetCo2 rather than additional arterial blood gas monitoring.

Analgesics, Opioid↗
PubMed1996

[Effect of arterial blood pressure on cerebral vein oxygen saturation in the rewarming phase of extracorporeal circulation].

UNLABELLED: This study concerns the effects of elevated mean arterial blood pressure (MAP) on decreases in jugular bulb oxygen saturation (SjO2) using fiberoptic jugular bulb oximetry and on cerebral blood flow velocity measured by transcranial Doppler sonography (TCD) during cardiopulmonary bypass (CPB) for coronary artery bypass graft (CABG). METHODS: 27 ASA III patients undergoing CABG were studied. Anaesthesia was maintained with fentanyl, midazolam and continuous infusion of etomidate. CPB was managed according to alpha-stat conditions under moderate hypothermia (27 degrees C). SjO2 (%) and jugular bulb temperature were measured using a fiberoptic catheter placed in the right jugular bulb via the right internal jugular vein. TCD recordings of middle cerebral artery mean blood flow velocity (Vmean, cm/s) were taken during the investigation period. Data were recorded continuously before and for 40 min following start of rewarming. In group 1 (n = 17) MAP was kept between 55 and 65 mmHg, in group 2 (n = 10) MAP was maintained above 70 mmHg using norepinephrine infusion during rewarming of CPB. RESULTS: Following rewarming MAP was statistically significant elevated in group 2 compared to group 1. In groups 1 and 2, Vmean was increased and SjO2 was decreased to a similar extent during rewarming of CPB. Decreases in SjO2 below 50% were seen in both groups. CONCLUSION: The present data show decreases in Sjo2 during rewarming regardless to the level of arterial blood pressure (range 55-80 mmHg). This suggests that desaturation during rewarming of CPB is not a function of decreases in MAP since CBF autoregulation appears to be maintained within this pressure range.

Adult↗
PubMed1996

The effects of surgical stimulation on intracranial hemodynamics.

This study investigates the effects of surgical stimulation on cerebral blood flow velocity using transcranial Doppler sonography (TCD) in 1 and 2 maximum alveolar concentration (MAC) isoflurane anesthetized patients. Sixty ASA I and II patients undergoing breast surgery were studied. Anesthesia was maintained with 0.6% isoflurane (groups 1 and 2) or 1.2% isoflurane (groups 3 and 4) and nitrous oxide in oxygen (FIO2, 0.33). TCD recordings of middle cerebral artery mean blood flow velocity (Vmean, cm/s) were taken before each respective treatment and for the 15-min investigation period. In groups 1 and 3 (each n = 20), the patients were exposed to surgical stimulation (skin incision). In groups 2 and 4 (each n = 10), norepinephrine infusion (0.1 microgram.kg-1.min-1) was used to increase mean arterial blood pressure (MAP) to levels similar to those seen with surgical stimulation (groups 1 or 3). Body temperature and PETCO2 remained constant over time and did not vary between treatment groups. In groups 1 and 3, MAP increased 22 and 16% after surgical stimulation. In groups 2 and 4, MAP increased 28 and 36% after norepinephrine infusion. Vmean was increased 23 and 17% after surgical stimulation during 1 and 2 MAC isoflurane but did not change with norepinephrine infusion. These data show that cerebral blood flow velocity increases with surgical stimulation in 1 and 2 MAC isoflurane-anesthetized patients. This is not a function of changes in MAP. These data suggest that surgical stimulation increases cerebral blood flow, possibly because of arousal.

Adult↗
PubMed1995

Cumulative birth rates following cryopreservation of all embryos in stimulated in vitro fertilization (IVF) cycles.

OBJECTIVE: To cryopreserve all good-quality embryos available after IVF is one way to avoid an impending hyperstimulation and a more attractive alternative to a couple than cancellation of the cycle. At Sahlgrenska University Hospital this method has been practiced since 1991. The aim of this study was to assess the success rate (defined as childbirth per couple) after IVF treatment including one stimulated cycle, resulting in cryopreservation of all good-quality embryos available, followed by replacement of frozen/thawed embryos in one or more natural cycles. DESIGN: A cohort of 32 women undergoing one stimulation for IVF between January 1991 and December 1993 where all good-quality embryos were cryopreserved and transferred in a later spontaneous cycle were studied retrospectively. The cumulative childbirth rate per couple was calculated. RESULTS: A total of 28 women underwent a total of 45 transfers with frozen-thawed embryos. In 4 women no transfer has taken place so far. The clinical pregnancy rate per embryo transfer was 33% (15/45) and per patient 54% (15/28). Three spontaneous abortions occurred giving a cumulative childbirth rate per patient of 39% (11/28). In addition, 6 out of the 28 women still have embryos left in the freezer. CONCLUSION: Cryopreservation of all good-quality embryos available after IVF is a highly effective alternative to cancellation of a cycle when there is impending hyperstimulation. The use of this approach results in a cumulative childbirth rate per couple of at least 39%. Since only one stimulation was performed, it also seems to be cost effective.

Abortion, Spontaneous↗
PubMed1995

[Propofol-alfentanil reduced cerebrovascular CO2 reactivity in comparison with isoflurane].

The present study compared the effects of propofol/alfentanil versus isoflurane anaesthesia on cerebral vascular reactivity to changes in carbon dioxide (CO2) using transcranial Doppler sonography (TCD). METHODS. Seventeen ASA class I patients undergoing minor elective surgery were studied following IRB approval and informed consent. In group 1 (n = 10), anaesthesia was induced with thiopental 4 mg/kg and alfentanil 15 micrograms/kg. Endotracheal intubation was facilitated by vecuronium 0.1 mg/kg. Anaesthesia was maintained with 1% end-tidal isoflurane and nitrous oxide (N2O) in oxygen O2 (6 l/min; FiO2 0.3). In group 2 (n = 7), anaesthesia was induced with propofol 2 mg/kg, alfentanil 15 micrograms/kg, and vecuronium 0.1 mg/kg for endotracheal intubation and maintained by infusion of propofol, alfentanil, and N2O-O2 (6 l/min; FiO2 0.3) according to the following protocol: propofol: 10, 8, and 6 mg/kg.h for 10 min each followed by 4 mg/kg.h; alfentanil: 55 micrograms/kg.h. Monitoring included measurement of mean arterial blood pressure (MAP, mm Hg), heart rate (HR), body temperature (T), end-tidal CO2 (PetCO2, mm Hg), isoflurane concentrations, and arterial O2 saturation (SaO2, %). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a bidirectional 2-MHz TCD system (TranspectT, Medasonics). Mechanical ventilation was adjusted to achieve PetCO2 levels of 40-50-40-30 and 40 mm Hg. Ten minutes of equilibration were allowed at each PetCO2 level. The CO2 reactivity index was calculated as delta Vmean/delta PetCO2 (cm/s.mm Hg). RESULTS. MAP, HR, T, and SaO2 were constant over time and were not different between groups. The CO2 reactivity index over the CO2 range of 30-50 mm Hg was higher in isoflurane (2.32 +/- 1.51 delta cm/s.mm Hg) compared to propofol/alfentanil patients (1.15 +/- 0.77 delta cm/s.mm Hg) (mean +/- SD, P < 0.05). CONCLUSIONS. The data show that although CO2 reactivity is maintained during both isoflurane and propofol/alfentanil anaesthesia, the cerebral vascular response to CO2 was lower in propofol/alfentanil compared to isoflurane patients. This is likely due to propofol/alfentanil-induced cerebral vasoconstriction. These data suggest that CO2 reactivity is a function of the pre-existing cerebral vascular tone induced by the anaesthetic.

Adult↗
PubMed1995

[Cerebral monitoring with trancranial doppler-sonography and cerebrovenous oximetry during resuscitation].

This case report describes cerebral monitoring of intracranial haemodynamics using transcranial Doppler sonography (TCD) and jugular bulb oxygen saturation (SjO2) by fiberoptic jugular bulb oximetry during cardiac arrest following cardiac surgery involving cardiopulmonary bypass (CPB). CPB for aortic valve replacement and coronary artery bypass grafting was performed in a 63-year-old patient previously operated upon for heart disease. Mean blood flow velocity was measured in the middle cerebral artery using a bidirectional 2 MHz TCD system. SjO2 was measured using a fiberoptic thermodilution catheter placed in the right jugular bulb via the right internal jugular vein under radiographic control. At the end of the operation, low cardiac output syndrome and cardiac arrest occurred, which required reopening of the thorax and cardiopulmonary resuscitation (CPR) until CPB could be resumed. Following extrathoracic cardiac resuscitation, systolic "spikes", loss of the diastolic flow profile, and no increase in SjO2 were recorded by the monitors, indicating cerebral circulatory arrest. However, a normal flow profile with increasing diastolic portions and an increase in SjO2 to 52% were seen following optimisation of the open thorax cardiac resuscitation. This monitoring may be able to give information to optimise therapy during CPR to avoid ischaemic cerebral injury.

Anesthesia↗
PubMed1995

Sevoflurane improves neurological outcome after incomplete cerebral ischaemia in rats.

We have studied the effects of sevoflurane on neurological outcome in a rat model of incomplete cerebral ischaemia. After institutional approval, 30 non-fasted male Sprague-Dawley rats (455-555 g) were anaesthetized, the trachea intubated and the lungs ventilated mechanically with isoflurane and 30% oxygen in air. Catheters were inserted into the right femoral artery, both femoral veins and into the right jugular vein for measurement of arterial pressure, drug administration and blood sampling. At completion of surgery, isoflurane was discontinued and the rats were allowed an equilibration period of 30 min according to the following regimens: group 1 (n = 10) received 70% nitrous oxide in oxygen and fentanyl (bolus 10 micrograms kg-1 i.v.; infusion 25 micrograms kg-1 h-1); group 2 (n = 10) received 1.98 vol% sevoflurane in oxygen and air (FIO2 0.3); group 3 (n = 10) received 1.98 vol% sevoflurane in oxygen and air (FIO2 0.3) and 40% glucose (6 ml kg-1 i.p.) 30 min before ischaemia. Ischaemia was produced by combined unilateral common carotid artery ligation and haemorrhagic hypotension to 35 mm Hg for 30 min. Temperature, arterial blood-gas variables and arterial pH were maintained within the physiological range. Plasma glucose concentration was measured before, during and after ischaemia. Neurological deficit was evaluated for 3 days after ischaemia. Neurological outcome was better in sevoflurane anaesthetized animals, regardless of the plasma glucose concentration, compared with nitrous oxide-fentanyl controls. This indicates that differences in plasma glucose concentrations do not account for the cerebral protection seen with sevoflurane.

Anesthetics↗
PubMed1995

Transcranial Doppler sonography indicates critical brain perfusion during hemorrhagic hypotension in dogs.

This study investigated the effects of hemorrhagic hypotension on cerebral blood flow velocity and brain electrical activity (by electroencephalogram [EEG]). Eleven mongrel dogs were anesthetized with isoflurane (1 minimum alveolar anesthetic concentration [MAC]) and catheters were placed into both femoral arteries and veins for mean arterial blood pressure (MAP) measurement, blood withdrawal, and drug administration. Brain temperature, arterial blood gases, and pH were maintained constant. EEG was recorded from temporoparietal recording sites versus a frontal reference. A pulsed transcranial Doppler (TCD) probe (2 MHz, Transpect, Medasonics) was placed on the dura via a temporal bone window to measure mean (Vmean, cm/s) and diastolic blood flow velocity (Vdiast, cm/s) in the middle cerebral artery. At the end of the surgical preparation, isoflurane was discontinued and all animals received fentanyl (bolus, 25 micrograms/kg intravenously (IV); infusion, 50 micrograms.kg-1.h-1 IV) plus 50% N2O/O2 during 30 min of equilibration. After recordings of baseline data, the dogs were hemorrhaged at a rate of 80-100 mL/min. The observation interval was 14 min. EEG spectral edge frequency (SEF 95%) and Vmean did not change when MAP was decreased from 109 +/- 10 to 63 +/- 7 mm Hg. This indicates preserved neuronal function and intact autoregulation of cerebral blood flow. Below MAP of 49 +/- 9 mm Hg, a shift of the EEG to lower frequencies was associated with decreases in Vmean and Vdiast. EEG burst suppression occurred at a MAP of 31 +/- 7 mm Hg, paralleled by a loss of the diastolic flow velocity pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗