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Biomedical subjects

K Peter

Publications and source records attributed to K Peter.

At least 199 records · Page 11Linked to original sources
PubMed1992

Systemic antibiotic treatment of nosocomial pneumonia.

Nosocomial pneumonia continues to represent a significant cause of morbidity and mortality in hospitalized patients. Bacteria are responsible for greater than 90% of the pneumonias, the most common isolates being aerobic Gram-negative bacilli and S. aureus. Cornerstones of treatment are intravenous antibiotics and supportive care. In the individual case the true etiology is usually unknown; therefore empiric broad spectrum treatment is commonly used based on the prevalence of local pathogens, their antibiotic sensitivity pattern and on host factors. Combination antibiotic regimens, including beta-lactams and aminoglycosides, are considered as standard therapy and are associated with clinical success rates of greater than 80%. Monotherapy with broad spectrum antibiotics, such as third generation cephalosporins, imipenem and fluoroquinolones, can be considered as equally effective in non-neutropenic patients and in the absence of P. aeruginosa infection. More active and less toxic antibiotics are still needed for problematic pathogens such as methicillin-resistant S. aureus strains, multiresistant Enterobacteriaceae and Pseudomonas species. Because further improvement in morbidity and mortality may be limited with antibiotics alone, new emphasis should be placed on prevention of infection and the use of immunotherapy.

Anti-Bacterial Agents↗
PubMed1992

Patient controlled analgesia for extracorporeal shock wave lithotripsy of gallstones.

Sixty patients undergoing shock wave lithotripsy of gallbladder stones (ESWL) were randomly assigned to receive alfentanil either by infusion controlled by the attending anesthesiologist (standard treatment group, n = 31) or by analgesia controlled by the patient (PCA group, n = 29). Patients using PCA were allowed to self-administer 0.25 mg of alfentanil i.v. every minute as required. Data collected during treatment included the total dose of drug required, transcutaneous pCO2 values, verbal pain and sedation scores, visual analogue scale (VAS) patient satisfaction scores, and the incidence of nausea or vomiting. PCA patients used less alfentanil than the standard treatment group (PCA group: 12.8 micrograms/kg; standard treatment group: 44.3 micrograms/kg; mean values, P = 0.0001), tolerated significantly higher pain intensities and self-administered the narcotic only to moderate levels of pain but not to pronounced analgesia. Standard treatment patients reported lower levels of pain, were more sedated (P less than 0.05) and showed significantly higher transcutaneous pCO2 values. There was a trend towards a lower incidence of nausea or vomiting in PCA patients without reaching statistical significance. No significant difference with regard to patient satisfaction with pain relief could be demonstrated. Self-administered alfentanil during ESWL of gallbladder stones provided adequate analgesia with minimal side effects and high patient satisfaction. ESWL may represent a new and useful indication for PCA.

Adult↗
PubMed1992

Continuous intra-arterial oximetry, pulse oximetry, and co-oximetry during cardiac surgery.

This study evaluated arterial catheter oximetry versus pulse oximetry in eight patients (ASA III-IV) who underwent cardiac surgery. Co-oximeter saturation values served as the standard. Arterial oxygen saturation was determined simultaneously with these three methods at 162 prospectively defined points of measurement before, during, and after cardiopulmonary bypass (CPB). At the same times before and after CPB, arterial, pulmonary arterial, and central venous pressures, and cardiac output determinations were recorded. Saturation readings were obtained in more than 99% of measurements with catheter oximetry and in only 59% to 84% of measurements with pulse oximetry. Failure of pulse oximetry correlated with low mean arterial pressures and low cardiac outputs, but not with high systemic vascular resistance. The mean saturation values determined by catheter oximetry as well as by pulse oximetry differed from the mean values obtained by co-oximetry by less than 1% (= bias). The standard deviations of the individual differences between readings of catheter or pulse oximetry and readings of co-oximetry (= precision) were +/- 0.5% to +/- 1.0% for catheter oximetry and +/- 1.0% to +/- 1.2% for pulse oximetry. In summary, catheter oximetry was superior to pulse oximetry with regard to obtaining readings and to reliability of the obtained readings. Invasiveness and high costs influence the decision as to whether to use catheter oximetry, but if reliable and precise measurements of saturation are important at any time during surgery, pulse oximetry is an insufficient method and co-oximetry is a time-consuming method of analysis, whereas catheter oximetry is quick, reliable, and precise.

Adult↗
PubMed1992

Propofol/fentanyl versus etomidate/fentanyl for the induction of anesthesia in patients with aortic insufficiency and coronary artery disease.

The purpose of this study was to gain information about the hemodynamic effects following the induction of anesthesia with fentanyl and either 1 mg/kg of propofol (P) or 0.25 mg/kg of etomidate (E) in ASA III-IV patients with aortic insufficiency (AI) or coronary artery disease (CAD). Four patient groups resulted: (1) AI and P, n = 10; (2) AI and E, n = 10; (3) CAD and P, n = 6; and (4) CAD and E, n = 8. Hemodynamics were recorded in the awake state, following induction, intubation, and 10 minutes after intubation. No complications occurred in groups 1, 2, and 4. In 2 patients of group 3, who suffered from three-vessel CAD, induction resulted in severe hypotension associated with an increase in pulmonary capillary wedge pressure. Because of this, the investigation of group 3 was prematurely terminated after the sixth patient. The following changes were observed under general anesthesia: in all four groups, arterial pressure (AP), cardiac index (CI), and left ventricular stroke work index decreased. Significantly different values between group 1 (AI and P) and 2 (AI and E) were observed for heart rate (HR) (P less than E), stroke volume (SV) (P greater than E), arterial elastance (Ea), and systemic vascular resistance (SVR) (P less than E); differences between group 3 (CAD and P) and 4 (CAD and E) were seen for AP, Ea, and SVR (P less than E each). After tracheal intubation, baseline values of AP and HR were not surpassed in any group. Signs of systolic myocardial dysfunction were present in all groups (P greater than E).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Onset and recovery of rocuronium (Org 9426) and vecuronium under enflurane anaesthesia.

We have studied the onset, duration of action and recovery index of twice the ED90 of rocuronium (Org 9426) (0.6 mg kg-1) and of vecuronium (0.08 mg kg-1) in patients during enflurane anaesthesia. Rocuronium had a significantly shorter mean onset time of 1.8 (SD 0.4) min, compared with vecuronium 3.4 (0.8) min. Clinical duration (time for the first twitch in the train-of-four to recover to 25% of control) was similar for both drugs (29 (10) min vs 31 (12) min). Spontaneous recovery times (TOF ratio 70%) did not differ significantly between rocuronium (47 (10) min) and vecuronium (44 (11) min).

Adolescent↗
PubMed1992

Effect of interpleural morphine on postoperative pain and pulmonary function after thoracotomy.

We have investigated the effect of interpleural morphine on postoperative pain and pulmonary function after thoracotomy. At the end of surgery, an interpleural catheter was inserted in 17 patients and, in a double-blind and randomized manner, either a bolus of morphine 2.5 mg interpleurally (i.p.) and normal saline i.v. (group I) or, as a control for systemic absorption, morphine 2.5 mg i.v. and i.p. saline (group II) was injected. After the initial bolus, a continuous infusion of morphine 0.5 mg h-1 i.p. and saline i.v. (group I) or morphine 0.5 mg i.v. and saline i.p. (group II) was maintained for 24 h. Postoperative pain was assessed by a visual analogue scale, a numerical rating scale and the McGill Pain Questionnaire. Pulmonary function was assessed by spirometry. Supplementary analgesics, side effects, degree of sedation, vital signs and chest tube drainage were recorded. All variables were assessed on the day before surgery and 1, 2, 3, 4, 5, 6 and 24 h and 7 days after surgery. Supplementary morphine was given upon request. There was no significant difference in any pain measure or postoperative pulmonary function variable between the groups. We conclude that, after thoracotomy, interpleural morphine does not provide superior analgesia or improve pulmonary function compared with systemic morphine.

Forced Expiratory Volume↗
PubMed1992

Coronary microcirculation during halothane, enflurane, isoflurane, and adenosine in dogs.

We investigated the effects of clinically administered volatile anesthetics and of adenosine on the microvasculature of the in situ beating canine heart. Thirteen dogs were studied during general anesthesia with an opioid (piritramide), which was infused throughout the experiments. Measurements were obtained in each animal at control (piritramide only) and during hypotension (mean arterial pressure 60 mmHg) induced by halothane, enflurane, isoflurane, and adenosine. Using epiillumination and fluorescence microscopy, 354 arterial microvessels with diameters from 20 to 450 microns were examined through all experimental periods. Hypotension by halothane, enflurane, isoflurane, and adenosine reduced coronary vascular resistance by 13%, 23%, 40%, and 85%, respectively. Coronary venous PO2 was unchanged from control with halothane (+/- 0%) and enflurane (+7%) and significantly increased with isoflurane (+16%) and adenosine (+65%). Left ventricular blood flow decreased significantly during halothane (-35%) and enflurane (-23%); was unchanged from control during isoflurane (-9%); but significantly increased during adenosine (+397%). Coronary arterial and arteriolar diameters increased with all hypotensive agents. Vasodilation was least with halothane, intermediate with enflurane and isoflurane, and most pronounced with adenosine. Diameters increased considerably more in vessels with initial diameters below 100 microns as opposed to larger vessels. Calculation of microvascular segmental resistances revealed that the maximum conductance changes during volatile anesthetics were located in the vessel segments visualized by microscopy, i.e., in vessels larger than 20 microns. However, this was not the case with adenosine. We conclude that volatile anesthetics induce coronary vasodilation by preferentially acting on vessels with diameters from 20 microns to approximately 200 microns, whereas adenosine, in addition, has a pronounced impact on the small precapillary arterioles.

Adenosine↗
PubMed1992

Effect of leukopenia on pulmonary hypertension after heparin-protamine in pigs.

Heparin neutralization by protamine after cardiac surgery and cardiopulmonary bypass may be associated with complement activation, transient leukopenia, thromboxane A2 release, and severe pulmonary hypertension. The role of leukocytes in the heparin-protamine reaction was studied in leukopenic pigs (n = 9) and a control group (n = 8). Leukopenia was induced by pretreatment with cyclophosphamide (30 mg.kg-1.day-1) for 6-7 days. During general anesthesia and after catheterization, baseline recordings of hemodynamics were performed and blood samples were withdrawn. Heparin (250 IU/kg) was injected and measurements were repeated after 10 min. Protamine sulfate (100 mg) was then infused over 2 min and measurements were performed after 2, 5, and 15 min. Prostanoid concentrations were measured by radioimmunoassays. In additional in vitro experiments, the release of thromboxane B2 from washed platelets and leukocytes after heparin-protamine stimulation was measured. Pretreatment with cyclophosphamide reduced leukocyte counts by 95.5% and the number of neutrophils by greater than 99.9%. Protamine infusion increased mean pulmonary arterial pressure by 74 and 46% and pulmonary vascular resistance by 185 and 384% in control and leukopenic animals, respectively. Thromboxane B2 concentrations increased in both groups. Stimulation by heparin, protamine, or heparin and protamine in sequence did not induce any thromboxane A2 release from washed blood cells. It is concluded that leukocytes do not contribute to pulmonary hypertension after heparin-protamine.

Animals↗
PubMed1992

No evidence for the existence of preformed antibodies against hydroxyethyl starch in man.

Using the highly sensitive ELISA technique for detecting anti-hydroxyethyl starch (HES) antibodies in man sera from 1,056 patients were analyzed. Patients of both sex, who had never had any prior contact with HES, were included in the study. In none of the cases could any titer of HES-reactive antibodies be detected. These data suggest that in man preformed HES-reactive antibodies do not exist or are extremely rare. In any case, unlike dextran-reactive antibodies, they should not have a high clinical importance. The mechanism behind the very rarely observed anaphylactoid reactions after HES application is still unknown.

Adult↗
PubMed1992

Systemic and regional hemodynamics of isoflurane and sevoflurane in rats.

The authors studied the effects of sevoflurane and isoflurane on systemic hemodynamics and regional blood flow distribution (microsphere technique) in 15 rats during general anesthesia with intravenous chloralose and controlled ventilation. Inhaled anesthetics were applied to reduce mean arterial blood pressure (MAP) to 70 mm Hg (1.66 vol% sevoflurane and 0.96 vol% isoflurane) and 50 mm Hg (MAP 50; 3.95 vol% sevoflurane and 2.43 vol% isoflurane). Control recordings were obtained with intravenous chloralose only. At a MAP of 70 mm Hg, both anesthetics reduced heart rate, cardiac output, and systemic vascular resistance to a similar degree. Isoflurane decreased systemic vascular resistance markedly at a MAP of 50 mm Hg and thereby maintained cardiac output at higher levels than sevoflurane. The left ventricular rate-pressure product decreased comparably with both anesthetics. Cerebral blood flow increased dose-dependently with both inhaled anesthetics but to a greater degree with isoflurane. Total hepatic blood flow remained unchanged from control at a MAP of 70 mm Hg but decreased at a MAP of 50 mm Hg. This was due to reductions of hepatic arterial and portal venous tributaries. Renal blood flow was reduced with only the high concentrations of the anesthetics. Myocardial blood flow was reduced at all concentrations of volatile anesthetic; however, the decrease was less with isoflurane. This would indicate a more pronounced coronary vasodilation by isoflurane as the rate-pressure product, as a measure of the actual left ventricular oxygen demand, decreased by comparable degrees with both anesthetics. Our results indicate that sevoflurane and isoflurane (each approximately 0.7 MAC) have no dissimilar systemic and regional hemodynamic effects at a MAP of 70 mm Hg in this animal model. At higher concentrations (approximately 1.7 MAC), cerebral blood flow was more with isoflurane than with sevoflurane and was associated with a more pronounced vasodilation in the myocardium.

Anesthesia, General↗
PubMed1992

Blood flow and tissue oxygen pressures of liver and pancreas in rats: effects of volatile anesthetics and of hemorrhage.

The object of this investigation was to compare the effects of volatile anesthetics and of hemorrhage at comparable arterial blood pressures on splanchnic blood flow (radioactive microspheres) and tissue oxygenation of the liver and pancreas (surface PO2 [PSO2] electrodes). In contrast to earlier studies, we did not use identical minimum alveolar anesthetic concentration multiples as a reference to compare volatile anesthetics; rather, we used the splanchnic perfusion pressure. Under general anesthesia (intravenous chloralose) and controlled ventilation, 12 Sprague-Dawley rats underwent laparotomy to allow access to abdominal organs. Mean arterial pressure was decreased from 84 +/- 3 mm Hg (mean +/- SEM) at control to 50 mm Hg by 1.0 +/- 0.1 vol% halothane, 2.2 +/- 0.2 vol% enflurane, and 2.3 +/- 0.1 vol% isoflurane in a randomized sequence. For hemorrhagic hypotension, blood was withdrawn gradually until a mean arterial pressure of 50 mm Hg was attained. Volatile anesthetics and hemorrhage reduced cardiac output, and hepatic arterial, portal venous, and total hepatic blood flows by comparable degrees. Mean hepatic PSO2 decreased significantly from 30.7 +/- 2.6 mm Hg at control to 17.4 +/- 2 and 17.5 +/- 2 mm Hg during enflurane and isoflurane (each P less than 0.05) anesthesia, respectively. The decrease to 11.5 +/- 2.5 mm Hg was more pronounced during halothane anesthesia. Hemorrhagic hypotension was associated with the lowest hepatic PSO2 (3.4 +/- 1.3 mm Hg) and the highest number of hypoxic (0-5 mm Hg 86%) and anoxic PSO2 values (0 mm Hg 46%). Pancreatic blood flow and oxygenation remained unchanged from control during halothane and enflurane administration, whereas isoflurane increased both variables. Hemorrhagic hypotension slightly reduced pancreatic flow (-8%) but significantly decreased PSO2 from 58 +/- 5 mm Hg at control to 36 +/- 3 mm Hg, with 7% of all measured values in the hypoxic range. Thus, volatile anesthetics preserved pancreatic but not hepatic blood flow and tissue oxygenation in this rat model. Despite comparable effects on perfusion, the PSO2 of the liver and pancreas was the least during hemorrhagic hypotension compared to that with the anesthetics. Because the volative anesthetic-induced hypotension has such a different effect on splanchnic tissue oxygenation compared with hemorrhagic-induced hypotension, the authors conclude that the method of inducing hypotension may have different effects on oxygenation of various tissues.

Anesthetics↗
PubMed1992

[Acute dyskinesia as the cause of jaw dislocation].

A case of an acute dyskinesia of a young, schizophrenic woman caused by neuroleptic therapy is reported. The acute dyskinesia was the reason for a complete luxation in the jaw-joint. The patient showed phenomenons (brain-atrophy, cognitive dysfunction, negative symptoms) which are discussed to be connected with acute dyskinesia. They also are a danger-signal regarding the beginning of a tardive dyskinesia.

Adult↗
PubMed1992

Context rules of rightward overlapping reading.

We have investigated the mechanism and sequence context rules governing ribosome frameshifting promoted by aminoacyl-tRNA limitation. In the case of one shifty sequence, frameshifting promoted by lysyl-tRNA limitation occurs at the sequence AAG C and is due to rightward movement of the ribosome so as to read the AGC triplet overlapping the hungry codon from the right. The frequency of this event is unaffected by sequence elements more than three bases to the left (upstream) or two bases to the right (downstream) of the hungry codon, and only slightly affected by the identity of the base two bases to the right. It is strongly affected by the base immediately to the right of the hungry codon, which becomes the wobble base of the shifted triplet; and by the third base of the hungry codon, even though the two synonyms (AAG and AAA) call for the same aminoacyl-tRNA; and by the identity of the base immediately to the left of the hungry codon. The latter result suggests that the aminoacyl-tRNA in the P site affects the maintenance of reading frame at the adjacent A site of the ribosome. However, the DNA sequence makes it seem unlikely that the P-site tRNA shifts to the right in concert with the A-site tRNA, a mechanism that can account for leftward frameshifting (in the opposite direction) in retroviral translation. The specificity of sequence determinants of leftwing versus rightwing frameshifting is discussed.

Amino Acid Sequence↗
PubMed1992

Dilation of coronary microvessels by adenosine induced hypotension in dogs.

An experimental model was established for fluorescence video microscopy of coronary microvessels. Nineteen dogs were anesthetized with a narcotic. Catheters were placed for hemodynamic monitoring and sampling of arterial and coronary venous blood. Myocardial perfusion was measured with radioactive microspheres. Following thoracotomy, movements of the myocardial surface area under investigation were restricted by a specially designed heart holder. Plasma was stained with FITC labelled dextran. Diameters were determined in arteriolar and venular microvessels greater than or equal to 20 microns. Measurements were performed during baseline conditions, i.e. only the basic anesthetic drug was applied, and during coronary vasodilation by continuous infusion of adenosine in a randomized sequence. Mean arterial pressure was reduced from 85 +/- 2 mmHg during baseline to 59 +/- 1 mmHg by infusion of 16.9 +/- 2.2 mg.kg-1.h-1 adenosine. Adenosine increased left ventricular blood flow by 253%, left ventricular oxygen demand remained unchanged. A total of 495 arteriolar and 170 venular diameters were measured during baseline condition and during adenosine infusion. Arteriolar diameters increased in all vessel segments between 20 and 600 microns, however, arterioles below a critical size of 100 microns had a greater dilating capacity than larger arterioles. Maximal decrease of segmental resistance occurred in 20-40 microns arterioles and amounted to 74%, which is less than the 82% decrease of total coronary resistance. Venular diameter changes, too, were more pronounced in smaller vessels.

Adenosine↗