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K Peter

Publications and source records attributed to K Peter.

At least 217 records · Page 12Linked to original sources
PubMed1992

[The determination of plasma volume using indocyanine green in man].

The importance of circulating blood (BV) and plasma volume (PV) in critically ill patients and physiological research is unchallenged. Recently, Evans blue (EB) [8, 25] and radioactively labelled serum albumin (RIHSA) [20] have mostly been used as tracers for PV determination. However, the disadvantages of radioactive contamination (RIHSA) and dye accumulation (EB), especially in repeated measurements, are obvious. In addition, recent reports show a possible carcinogenic potential for EB [15, 21]. This has prompted us to examine the feasibility of indocyanine green (ICG), a tricarbocyanine dye currently used for cardiac output and liver blood flow measurements, for the determination of PV. The volume of distribution of ICG has been reported to represent PV [5, 26]. METHODS. In 23 healthy volunteers (19 men and 4 women), PV was determined in duplicate (PV1, PV2) with an interval of 30 min. Before injection a tourniquet was put around the arm and a pressure above the systolic arterial pressure was applied for 2 min. During recirculation, ICG (2.5 mg/ml) was administered in a dose of 0.25 mg/kg as a bolus injection over 5 s via an antecubital vein. Blood was drawn from an antecubital vein of the contralateral arm at 1 min intervals. After centrifugation, the optical density (corrected for blank) was read in a densitometer. Third- to ninth-minute plasma samples were used to calculate monoexponential plasma decay curves. The ICG concentration at injection time was achieved by extrapolation. A calibration curve was generated using 5 different known ICG concentrations. PV was calculated from injected ICG dose divided by ICG concentration at injection time. BV and red cell volumes (EV) were derived from measured PV and hematocrit (hct). RESULTS. Between minutes 3 and 9, tracer decay was monoexponential in all but 1 subject. From minute 10 on the plasma decay of ICG represented another, slower compartment (Fig. 1). The plasma half-life of ICG was 3.2 +/- 0.6 min (mean +/- SD). Mean PVs per body weight and body surface area (BSA) were 44 +/- 5 ml/kg and 1662 +/- 176 ml/m2, respectively. Linear regression revealed PV2 = 0.92.PV1 + 226 (r = 0.92) (Fig. 2). The mean percentage of difference (D) was -0.6%, the methodologic error (SD) +/- 5.7% [27]. Linear regression of PV and BSA revealed PV = 1885.BSA -416 (r = 0.71, P less than 0.0001) (Fig. 3). BV and EV estimates (Table 2) obtained from PV and hct showed reproducibility in the range of the PV determination because of excellent reproducibility of hct measurements. DISCUSSION. ICG plasma half-life times in our experiments were comparable to those reported by other authors [18, 19, 24]. Reproducibility of PV determination was good and was well within the limits of other tracer methods (EB, RIHSA) [17, 27]. Using exclusively peripheral veins for ICG injection and blood withdrawal did not seem to affect the accuracy of PV determination. PV estimates obtained by the ICG method showed good agreement with those known from the literature [7, 10, 25]. Our results correspond especially well with the data reported by Hurley [14] obtained from 481 healthy men using different methods (Evans blue, RIHSA, or labelled red cells).

Adult↗
PubMed1991

Analgesic effect of intraarticular morphine after arthroscopic knee surgery.

BACKGROUND: Opioids can produce potent antinociceptive effects by interacting with local opioid receptors in inflamed peripheral tissue. In this study we examined the analgesic effects of the intraarticular, as compared with intravenous, administration of morphine after arthroscopic knee surgery. METHODS: In a double-blind, randomized trial, we studied 52 patients who had received one of four injections at the end of surgery. The patients in group 1 (n = 18) received 1 mg of morphine intraarticularly and saline intravenously; those in group 2 (n = 15), saline intraarticularly and 1 mg of morphine intravenously; those in group 3 (n = 10), 0.5 mg of morphine intraarticularly and saline intravenously; and those in group 4 (n = 9), 1 mg of morphine and 0.1 mg of naloxone intraarticularly and saline intravenously. The volume of the intraarticular injections was 40 ml, and that of the intravenous injections was 1 ml. After 1, 2, 3, 4, 6, and 24 hours, postoperative pain was assessed with a visual-analogue scale, a numerical-rating scale, and the McGill pain questionnaire. The need for supplemental analgesic agents, the patients' vital signs, and the occurrence of side effects were monitored. RESULTS: All pain scores were lower in group 1 than in group 2 at all times. The differences were significant (P less than 0.05) at three, four, and six hours (mean [+/- SD] visual-analogue score at six hours, 9 +/- 13 mm vs. 37 +/- 31 mm). The mean (+/- SD) consumption of supplemental analgesic medication per 24 hours was significantly lower in group 1 (36 +/- 51 mg of diclofenac and 1.2 +/- 3.4 mg of meperidine) than in group 2 (75 +/- 42 mg of diclofenac and 14 +/- 18 mg of meperidine, P less than 0.05). The visual-analogue scores in group 3 were slightly but not significantly higher than those in group 1 at all times except 6 and 24 hours after injection. The visual-analogue scores were significantly higher in group 4 than in group 1 one to four hours after injection (P less than 0.05), indicating that the analgesic effect of intraarticular morphine was reversible by naloxone. CONCLUSIONS: Low doses of intraarticular morphine can significantly reduce pain after knee surgery through an action specific to local opioid receptors that reaches its maximal effect three to six hours after injection.

Adult↗
PubMed1991

Pentoxifylline does not act via adenosine receptors in the inhibition of the superoxide anion production of human polymorphonuclear leukocytes.

The inhibitory effect of adenosine (ADO) and pentoxifylline (POF) was studied alone and in combination on the N-formyl-methionyl-leucyl-phenylalanine (FMLP) stimulated superoxide anion production of human polymorphonuclear leukocytes (PMNL). The pharmacological analysis of the results of these experiments demonstrated greater than additive and independent interaction of the drugs, representing potentiation. These results reflect differences between the sites of action of ADO and POF. Accordingly, the ADO receptor antagonist 8-phenyltheophylline only diminished the inhibition mediated by ADO, but totally failed to affect POF. Therefore, we hypothesize that POF acts as a phosphodiesterase inhibitor, potentiating the increase in cyclic AMP induced by ADO due to the stimulation of the adenylate-cyclase of human PMNL.

Adenosine↗
PubMed1991

[Pathophysiologic and therapeutic aspects of the adult respiratory distress syndrome (ARDS)].

Since the first characterization of the adult respiratory distress syndrome (ARDS), knowledge of its aetiology and pathogenesis has grown considerably. In spite of this, mortality remains up to 50 to 90%, particularly if multiple organ failure is present. Because no causative clinical therapy is available up to now, significant attention is given to preventive measures like early operative stabilisation of long bone fractures, or prophylaxis of nosocomial infections. After clinical manifestation of ARDS, treatment focuses on functional disturbances of the cardiopulmonary system and on the underlying disease. The aim of this symptomatic therapy is to ensure oxygen supply according to the organisms demand. It is still unknown, however, whether the mortality of patients with ARDS can be reduced by optimising the oxygen supply. In general, oxygen supply can be enhanced by improving pulmonary gas exchange, cardiac output and blood oxygen transport capacity. For practical use the therapy often ends up with a therapeutical dilemma: On one hand, the improvement of the pulmonary gas exchange by application of PEEP can be associated with a critical decline in cardiac output, particularly if the afterload of the right ventricle is elevated. On the other hand, to increase cardiac output, both volume replacement and vasodilators can severely affect pulmonary gas exchange if the alveolo-capillary permeability is increased and pulmonary hypoxic vasoconstriction is disturbed. Thus, oxygen supply can be optimised only via invasive monitoring of the cardiorespiratory system. Although still experimental, the most promising approaches seem to be pharmacological interventions directed at suppressing the formation and effects of various humoral and cellular mediators. An improved understanding of the inflammatory processes might provide new insights in the pathophysiology of ARDS and the related therapeutic interventions.

Humans↗
PubMed1991

Left ventricular surface tissue oxygen pressures determined by oxygen sensitive multiwire electrodes in pigs.

STUDY OBJECTIVE: Polarographic oxygen sensitive electrodes can be used to measure tissue oxygen pressures on the surface of the beating heart. The purpose of the study was to clarify the significance of these PO2 determinations. DESIGN: Changes in left ventricular surface oxygen pressures, subendocardial or subepicardial wall functions (ultrasonic dimension technique), and blood flow (radioactive microsphere technique) were correlated during different degrees of acute coronary artery stenoses in pigs. EXPERIMENTAL MATERIAL: 19 anaesthetised open chest pigs, 28-40 kg body weight, were studied during different degrees of constriction of the left anterior descending artery which did not influence overall left ventricular function or irreversibly damage the myocardium. MEASUREMENTS AND MAIN RESULTS: Highly significant (p less than 0.001) correlations (each % delta) were obtained for surface tissue oxygen pressures (y) with subepicardial (y = 0.002 e 0.10x; r = 0.89) and subendocardial (y = 1.44 e 0.04x; r = 0.98) blood flow values, as well as with subendocardial function (y = 82.4 + 0.22x; r = 0.89); a significant correlation was also obtained for subendocardial function (y) with subendocardial blood flow (y = 66.0 + 0.28x; r = 0.69). However, no significant correlation was obtained for polarographic tissue PO2 with subepicardial segment function, indicating that regional function was maintained when tissue PO2 recordings were not much above 0 kPa and when blood flow was reduced by 25 to 30%. CONCLUSIONS: Oxygen pressures of the superficial layers of the left ventricle are relatively high at normal values of oxygen consumption but decrease rapidly if blood supply is reduced. Regional wall function is preserved at low oxygen pressures. Polarographic surface PO2 electrodes hence can be used to study influences of experimental interventions on oxygenation of the normally perfused and of the moderately ischaemic myocardium.

Animals↗
PubMed1991

Heparin reversal by protamine in humans--complement, prostaglandins, blood cells, and hemodynamics.

Fourteen noncardiac surgical patients received heparin (10,000 IU), which was neutralized by 100 mg protamine injected within 2 min during steady-state anesthesia. After protamine application, plasma complement C3a, thromboxane B2 (TxB2), prostaglandin F2 alpha (PGF2 alpha) and KH2PGF2 alpha increased significantly, whereas prostacyclin (6-keto-PGF2 alpha) levels did not change. This mediator response was associated with transient leukopenia and thrombocytopenia. Arterial pressure, pulmonary arterial pressure, and transpulmonary pressure gradient increased significantly. Heart rate, cardiac output, pulmonary capillary wedge pressure, and arterial PO2 remained constant. Positive correlations of plasma C3a were observed with pulmonary leukosequestration and plasma TxB2. Inverse correlations of C3a were noted with the counts of leukocytes and of platelets. A positive correlation was found between TxB2 and pulmonary arterial pressure. Our results indicate that marked activation of the complement system and the cyclooxygenase pathway is common after heparin reversal by protamine in anesthetized patients. This is in contrast to previous human studies performed after cardiopulmonary bypass but agrees well with results obtained in animal experiments. The mediator response in our patients, however, was not accompanied by hemodynamic instability, suggesting appropriate compensatory mechanisms.

Aged↗
PubMed1991

[The neuromuscular blocking effects of ORG 9426].

ORG 9426 is a new non-depolarizing steroidal muscle relaxant with a short onset time and intermediate duration of action. Its ED90 ist estimated to be between 0.25 and 0.36 mg/kg. The present study investigated the onset time, duration of action and time to spontaneous recovery after 0.3 and 0.9 mg/kg ORG 9426, respectively (i.e. about single or triple ED90). METHODS. Following the consent of the ethics committee and informed patient consent, two groups of 18 patients (ASA I or II) were formed, each scheduled for general or ORL surgery. After premedication with lormetazepam, anesthesia was induced with midazolam (0.07 mg/kg) and etomidate (0.3 mg/kg) and maintained with N2O/O2 at a 65:35 ratio, enflurane (0.8-1.5%) and supplements of fentanyl as needed. The ulnar nerve was stimulated with supramaximal 2 Hz Train-of-four (TOF) every 20 s. Neuromuscular twitch response was registered with EMG. Muscle relaxation was achieved by administration of ORG 9426 0.3 (group 1) and 0.9 mg/kg (group 2), respectively. The following parameters were measured: onset time (time interval from injection to maximal or total block), T125/75 (time for T1 to reach 25% or 75% of control), TOF70 (time for TOF ratio to reach 70% of control), heart rate and blood pressure. RESULTS. (mean +/- SD). At a dosage of 0.3 mg/kg, the onset time was 3.1 +/- 0.8 min and the maximum blockade was 87 +/- 9%. A dosage of 0.9 mg/kg led to complete paralysis (100%) in all patients within 1.2 +/- 0.3 min. The time for recovery of T1 to 25 and 75% of baseline was 18 +/- 7 and 26 +/- 8 min in group 1, in group 2 46 +/- 11 and 53 +/- 17 min, respectively. TOF70 (i.e., time to adequate spontaneous recovery of neuromuscular function) was achieved after 30 +/- 10 and 63 +/- 14 min, respectively. CONCLUSIONS. At a dosage of 0.3 mg/kg, ORG 9426 has an onset time of about 3 min and a duration of activity of nearly half an hour. Its neuromuscular effects are similar to a single ED90 dose of vecuronium. In contrast to a previous study, we observed a much shorter onset time of 70 s following the administration of 0.9 mg/kg. The clinical duration of action and spontaneous recovery of neuromuscular function, however, were significantly prolonged to more than 1 h. The hemodynamic parameters showed only slight alterations.

Adult↗
PubMed1991

[Conscious and unconscious acoustic perception during general anesthesia].

The possibility of processing sensory information during general anesthesia and the ability to recall it postoperatively is of major ethical, medical and even theoretical importance. Auditory stimuli especially are perceived intraoperatively and remembered postoperatively. Neuropsychological experiments indicate that sensory information can be processed and recalled both at a conscious and at an unconscious level. Therefore, we have to distinguish between explicit and implicit memory. Explicit memory is characterized by an active and conscious recall of space- and time-related events, i.e., episodes in a person's life. In contrast, implicit memory recalls passively and unconsciously without being related to space and time, i.e., language and general knowledge. Experimental results from amnesic patients indicate that these two memory systems work independently from each other. Even when explicit memory is grossly impaired the function of the implicit memory may still be completely preserved. Various studies on intraoperative awareness show that explicit memory is widely eliminated during general anesthesia. The incidence of conscious awareness that can be actively recalled postoperatively is reported to be 1-3%. In contrast, the implicit memory function can be partially preserved. When implicit memory tasks or hypnosis are employed, traces of unconscious memory of intraoperative auditory information can be shown in 20-30% of the patients. These observations are of important clinical relevance, because the unconsciously recalled information about the intraoperative procedure may have a negative influence on the patient's postoperative recovery and well-being. So far it is still not known which anesthetics most reliably suppress auditory perception and conscious and unconscious memory during the intraoperative period. Therefore, future studies should focus on several different points. The anesthetic state should be defined exactly and the functional state of the auditory modality should be monitored when auditory information is presented to the patients. The recollection of intraoperative events should be investigated using implicit memory tests, because these are regarded as more sensitive than explicit memory tests.

Anesthesia, General↗
PubMed1991

[Complications caused by protamine. 1: Pharmacology and pathophysiology].

Protamine is a strongly alkaline polypeptide with a molecular weight of about 4500. Protamine solutions contain paraben compounds as antimicrobial agents. Rapid neutralization of heparin by protamine may cause an anaphylactoid reaction characterized by a non-immunogenic histamine release and by unknown mediators mechanisms. This response is associated with systemic peripheral vasodilation resulting in slight to moderate hypotension. Weak negative inotropic effects by mechanisms different from the reduction of ionized calcium concentrations may also contribute to systemic hypotension. Apart from these mostly slight reactions, severe reactions may occur with life-threatening systemic hypotension, bronchospasm and, in rare cases, death. They are caused by anaphylactic/anaphylactoid reactions resulting in catastrophic pulmonary vasoconstriction which induces right and eventually global ventricular failure. Sensitization to protamine (anaphylactic) and anaphylactoid reactions are the underlying mechanisms. The majority of anaphylactic/anaphylactoid reactions are associated with complement activation and the release of anaphylatoxins C3a and C5a. These activate the cyclo-oxygenase pathway of the arachidonic acid metabolism in yet unidentified cells, probably within the lung. As a result, thromboxane and prostaglandins are released. Thromboxane is the pivotal mediator responsible for the pulmonary vasoconstriction and, presumably, also for the bronchospasm during protamine reactions. The pronounced activation of polymorphonuclear leukocytes and the decrease in platelet counts may reflect a mere epiphenomenon. The degree of right ventricular afterload increase at which systemic hypotension requiring immediate therapy would occur depends mainly on the contractile state of the heart. Potential risk patients for severe protamine reactions are depot insulin-dependent diabetics and patients with prior exposure to protamine.

Anaphylaxis↗
PubMed1991

[Complications caused by protamine. 2. Therapy and prevention].

Treatment of reactions. The treatment of reactions to protamine is still symptomatic. Hypotension resulting from systemic vasodilation (anaphylactoid reaction) is treated by volume infusion, and alpha-stimulating catecholamines may be necessary. The combination of increased right ventricular afterload and systemic hypotension (anaphylactic/anaphylactoid reaction) requires primarily the improvement of coronary perfusion pressure and, thus, of O2 delivery to the right ventricular myocardium. To this end, catecholamines with alpha-stimulating action should be administered. Nitroglycerin is indicated when pulmonary hypertension persists in the presence of essentially normal systemic pressure. In the acute situation, steroids and antihistamines have no beneficial effect. Prevention of protamine reactions. For prevention of systemic hypotension by vasodilatation, protamine should be infused very slowly and not during hypovolemia. General prophylaxis using H1/H2 antagonists is not justified. Reliable preoperative identification of patients who would suffer an anaphylactic/anaphylactoid reaction to protamine, for example by skin tests or by measuring specific anti-protamine IgE or IgG antibodies, is not possible. This prevents individual prophylaxis in risk patients. In view of the low incidence of severe protamine reactions and the lack of better alternatives to the heparin/protamine regimen, general prevention is not indicated. For patients who are potentially at risk (insulin-dependent diabetics, prior protamine exposure), the side-effects of preventive measures must be weighed against their benefits. Only known sensitivity to protamine justifies certain preventive actions. In vascular surgery prostacyclin can be used instead of heparin/protamine or can be withheld (fading out of heparin action). Administration of steroids and/or antihistamines should be avoided. In cardiac surgery the use of hexadimethrine (if available) or total avoidance of protamine is paramount. Corticosteroids may be considered. Aortic administration of protamine and anticoagulation with ancrod are not recommended. The most promising compounds for rpharmacologic prevention of anaphylactic/anaphylactoid reactions in the future are thromboxane receptor antagonists.

Anaphylaxis↗
PubMed1991

[A life-threatening arrhythmia (ventricular tachycardia) triggered by a Swan-Ganz catheter in a patient with the WPW syndrome].

The induction of dysrhythmias during or after pulmonary artery catheterization is a serious complication in critically ill patients. The following case presentation reports the incidence of life-threatening ventricular tachycardia after catheterisation in a patient known to have Wolff-Parkinson-White (WPW)-Syndrome. The dysrhythmia began during repositioning of the patient 10 h after placement of the catheter. Attempted inversion by administration of Ajmalin was unsuccessful. Removal of the catheter resulted in prompt cessation of the dysrhythmia.

Adult↗
PubMed1990

Epicardial oxygen tensions during changes in arterial PO2 in pigs.

Arterial hypoxemia decreased epicardial tissue PO2, measured by means of a multiwire surface electrode, as well as coronary venous PO2 and myocardial lactate extraction. Left ventricular blood flow increased, O2 delivery, O2 demand and O2 consumption of the left ventricle remained unchanged. Thus, epicardial and coronary venous PO2 indicated decreased capillary and interstitial PO2 rather than cellular hypoxia. A linear relation between mean epicardial PO2 and coronary venous PO2 proves both parameters equally effective in reflecting changes in myocardial tissue oxygenation. However, PO2 distribution curves provide additional information and epicardial PO2 is superior in models with regional changes of myocardial oxygenation.

Animals↗
PubMed1990

Opioids from immunocytes interact with receptors on sensory nerves to inhibit nociception in inflammation.

Exogenous opioids can produce localized opioid receptor-mediated antinociception in peripheral inflamed tissue. Previous studies show that activation of endogenous opioids by a cold water swim in rats with hind paw inflammation results in a similar local antinociceptive effect but suggest that pituitary-adrenal opioid pools are not directly involved in producing this effect. Here we show increased amounts of opioid peptides in immune cells infiltrating the inflamed tissue. Furthermore, we demonstrate immunoreactive opioid receptors on peripheral terminals of sensory neurons. The local administration of antibodies against opioid peptides or receptors or systemic pretreatment with the immunosuppressant cyclosporine blocks cold water swim-induced antinociception. These findings suggest that antinociception in inflammation can be brought about by endogenous opioids from immune cells interacting with opioid receptors on peripheral sensory nerves.

Animals↗