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Biomedical subjects

K Peter

Publications and source records attributed to K Peter.

At least 235 records · Page 13Linked to original sources
PubMed1990

Ifosfamide plus etoposide combined with regional hyperthermia in patients with locally advanced sarcomas: a phase II study.

From July 1986 to July 1989, 40 patients (92% pretreated) with deep-seated, advanced soft tissue sarcomas (STS, 25 patients), Ewing's sarcomas (ES, eight patients), osteosarcomas (OS, three patients) and chondrosarcomas (ChS, four patients) were treated at the University of Munich in a protocol involving regional hyperthermia (RHT) combined with ifosfamide plus etoposide. A total of 265 RHT treatments (mean, 6.6 RHT per patient) were applied including 33 pelvic, four extremity, and three abdominal sites. The mean tumor volume was 537 cc (range, 50 to 2,980 cc). For systemic chemotherapy, all patients received ifosfamide (1.5 g/m2, days 1 to 5), etoposide (100 mg/m2, days 1, 3, and 5), and mesna (300 mg/m2 x 4, days 1 to 5) with RHT given only on days 1 and 5 in repeated cycles every 4 weeks. Acute toxicity consisted primarily of pain (57%) combined with local discomfort within the annular phased array applicator (AA) of the BSD hyperthermia system (BSD Medical Corp, Salt Lake City, UT). The average maximum systemic temperature was 37.4 +/- 0.5 degrees C, and there was no indication of enhanced bone marrow toxicity due to the addition of RHT to the systemic chemotherapy. Detailed thermal mapping by invasive thermometry was performed in all patients. In 38 assessable patients, the overall objective response rate was 37%: six complete responses (CRs), four partial responses (PRs), and four favorable histologic responses (FHRs) (95% confidence limits, 22% to 54%). Complete responders are alive and disease-free at 40, 35, 23, 19, 19, and 8 months. Of patients with PR and FHR, two died from metastatic disease after 4 and 17 months and one died from other disease after 27 months. The remaining five patients are stable at 37, 25, 21, 13, and 8 months. Eleven patients showed no change (NC), and 13 patients showed local tumor progression (PD). The mean observation time for all patients was 11.6 months. The time-averaged temperatures (Ts) of all RHT treatments calculated as 20% (T20), 50% (T50), or 90% (T90) of measured tumor sites differed significantly between responders and nonresponders (T20, P = .003; T50, P = .006; and T90, P = .004; respectively). These data support activity for ifosfamide-etoposide combined with RHT in pretreated patients with advanced sarcomas.

Adolescent↗
PubMed1990

Pulmonary hypertension after heparin-protamine: roles of left-sided infusion, histamine, and platelet-activating factor.

Severe pulmonary hypertension after protamine neutralization of heparin is an infrequent but life-threatening event following cardiopulmonary bypass. The effect of left ventricular infusion of protamine on pulmonary hypertension as well as a possible role of platelet-activating factor (PAF) or histamine in the heparin-protamine reaction was investigated in 30 pigs in four different groups during general anesthesia. Group 1 animals received 250 IU/kg heparin, followed by 100 mg protamine intravenously after 15 min. In group 2 protamine was infused into the left ventricle. Group 3 animals received the histamine H1- and H2-antagonists clemastine and ranitidine 5 min before protamine infusion. In group 4 the PAF receptor blocker WEB 2086 was given 5 min before protamine. Platelet-activating factor was measured by a bioassay in serum samples of group 1 and group 4 animals. In all four groups protamine caused severe pulmonary hypertension, thromboxane A2 release, and a transient decrease in leukocyte counts. No PAF release was detected after protamine infusion. Neither left ventricular infusion of protamine nor histamine or PAF antagonists prevented or attenuated the reactions after protamine infusion. The authors conclude that left ventricular infusion of protamine provides no protection from pulmonary hypertension, and that histamine and PAF are not involved in the acute pulmonary vasoconstriction after protamine neutralization of heparin.

Animals↗
PubMed1990

[Hypovolemic-hemorrhagic shock. Pathophysiology and therapy].

The common features of all different kinds of circulatory shock are a disturbance of the microcirculation and an imbalance between cellular oxygen demand and supply. The pathophysiology is discussed by the example of hypovolemic-hemorrhagic shock, including macrocirculation, humoral regulatory mechanisms, the role of vascular endothelium, and cellular dysfunction. The first aim of therapeutic efforts is the rapid restitution of a normal circulatory volume as a basic requirement for the normalisation of the microcirculation. Actual concepts of volume substitution and transfusion therapy are presented.

Blood Transfusion↗
PubMed1990

Induction of beta-lactamases: in vitro phenomena and clinical relevance.

An in vitro model was used to stimulate the plasma concentration-time curves for cefotaxime and cefoxitin as they would appear during treatment of patients with infections due to Enterobacter cloacae and Proteus vulgaris. The data showed that the induction of the chromosomally mediated beta-lactamase took place in both bacteria but that it had little or no effect on the bacterial kill. It is concluded that treatment failures in these settings were due to the selection of resistant mutants.

Cefotaxime↗
PubMed1989

Myocardial contractility, blood flow, and oxygen consumption in healthy dogs during anesthesia with isoflurane or enflurane.

Left ventricular contractility (Vmax), myocardial blood flow (MBF), and oxygen consumption (O2C) were determined together with systemic hemodynamic parameters in a total of 21 mongrel dogs. Baseline recordings were obtained under basal anesthetic conditions with a narcotic (piritramid, IV). In the control group (n = 7), recordings were obtained during a three-hour observation period with infusion of piritramid. In experimental groups measurements were repeated with equi-anesthetic concentrations of isoflurane (0.7 and 1.4 vol%; n = 8) and enflurane (1.1 and 2.2 vol%; n = 6). Dose-dependent reductions of arterial pressure, cardiac output (CO) and peripheral vascular resistance were observed with isoflurane and enflurane. CO at the higher anesthetic level was depressed significantly more with enflurane. This difference was obviously due to a more severe depression of myocardial contractility with enflurane; Vmax was decreased by 18% and 26% with enflurane, but only by 10% and 17% with isoflurane (P less than 0.01). MBF and the fraction of CO received by the heart were increased above their baseline values with both concentrations of isoflurane. In contrast, the fraction of CO remained constant with enflurane while MBF decreased. O2C was reduced due to decreases of afterload and left ventricular contractility. The reduction was greater with enflurane than with isoflurane. All parameters remained unchanged in the control group. The results of this study indicate that the most striking difference in the actions of isoflurane and enflurane on cardiac parameters is on myocardial vascular resistance; MBF is increased with isoflurane, but is decreased with enflurane although myocardial perfusion pressure is reduced by almost identical amounts.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1989

Myocardial surface PO2--an indicator of myocardial tissue oxygenation?

The validity of myocardial surface tissue PO2 (PtO2) as a reliable indicator of transmural myocardial tissue oxygenation was studied in six anaesthetised, open chest pigs. Epicardial surface PtO2 was correlated with other variables of myocardial tissue oxygenation such as regional blood flow, coronary venous PO2, O2 saturation, PCO2 and regional myocardial lactate extraction. The study design was based on an experimental model in which the effects of a pacing induced tachycardia on tissue oxygenation of ischaemic and normally supplied myocardium were measured. Two platinum multiwire surface electrodes were placed on the epicardium, on the areas supplied by the left anterior descending coronary artery (LAD) and the left circumflex coronary artery (CX). The LAD was constricted to reduce mean surface PtO2 in the LAD area to about 50% of its baseline value. This did not affect surface PtO2 in the CX area. The reduction of surface PtO2 in the LAD area was associated with decreases in coronary venous PO2 and O2 saturation and with increases in coronary venous lactate and PCO2. Subendocardial regional blood flow and the subendocardial to subepicardial flow ratio were significantly lower than in the CX area. Increasing the heart rate by pacing (+45 beats.min-1) led to an increased degree of ischaemia as shown by fall in surface PtO2 in the LAD area to values around zero kPa, by marked increase in coronary venous lactate and PCO2, by reduction in total (-10%) and subendocardial (-40%) LAD flow and by deterioration of the subendocardial to subepicardial flow ratio. The increased degree of ischaemia was not accompanied by an increase in O2 extraction. The marked decrease in surface PtO2 occurred in spite of a slight increase in the subepicardial regional blood flow (+10%); thus the increase in O2 delivery was not sufficient to meet the increase in O2 demand. Total flow was increased by 27% in the CX area without changes in the subendocardial to subepicardial flow ratio and in the surface PtO2 values. When pacing was stopped, surface values of PtO2 in the LAD area returned to prepacing values, as did lactate extraction and coronary venous PCO2. Clear and close relationships with surface PtO2 were found for regional lactate extraction, coronary venous PCO2 and the normalised subendocardial RBF. Poor or no correlations were found for the normalised subepicardial regional blood flow, the coronary venous O2 saturation and the absolute values of subendocardial and subepicardial regional blood flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Regional blood flow and tissue oxygen pressures of the collateral-dependent myocardium during isoflurane anesthesia in dogs.

The authors investigated the effects of isoflurane on blood flow and tissue oxygen pressures of a collateral-dependent myocardium. Seventeen dogs divided into two groups were studied 3-4 weeks after implantation of ameroid coronary artery constrictors to completely occlude the proximal part of the left anterior descending artery. Experiments were performed during anesthesia with an opiate that was infused intravenously throughout the experiments. In Group 1 (n = 9), measurements were obtained during control and during isoflurane- (1.6-2.2 vol%) induced hypotension (mean arterial pressure, 60 mmHg). In Group 2 (n = 8), the identical protocol was applied, but norepinephrine was infused to maintain normotension. Dipyridamole effects were studied in five animals of Group 2 after a second control period at least 1 h after discontinuation of isoflurane. Isoflurane-induced hypotension caused reductions of blood flow and surface tissue oxygen pressures in the collateral flow-dependent area. Vasodilation in the normal left ventricular areas was demonstrated by an unchanged blood flow despite a reduced oxygen consumption and by a significantly increased coronary sinus hemoglobin oxygen saturation. When arterial pressure was maintained at its control level by norepinephrine, tissue oxygen pressures remained constant and collateral as well as normal area flow increased significantly during isoflurane. Coronary vascular resistance was lower during administration of isoflurane and norepinephrine compared with that during isoflurane induced hypotension, suggesting a significant contribution of tissue oxygen demand in regulation of coronary vascular resistance. At comparable levels of arterial pressure and left ventricular oxygen consumption, normal zone blood flow was significantly higher during dipyridamole than during isoflurane and norepinephrine. Thus, isoflurane-induced hypotension decreased blood flow and tissue oxygen pressures of collateral flow-dependent myocardial areas. However, neither isoflurane nor dipyridamole caused such alterations when arterial pressure was normal.

Anesthesia, Intravenous↗
PubMed1989

Peripheral opioid receptors mediating antinociception in inflammation. Evidence for involvement of mu, delta and kappa receptors.

This study examined a possible peripheral site of action of opioids in the modulation of the response to noxious pressure on inflamed tissue. Rats developed a unilateral localized inflammation upon injection of Freund's complete adjuvant into one hindpaw. 4-6 days after inoculation, intraplantar administration of mu, delta and kappa selective agonists [D-Ala2,N-methyl-Phe4,Gly-ol5]-en-kephalin (1 micrograms), [D-Pen2,5]-enkephalin (40 micrograms) and U-50, 488H (50 micrograms) produced marked antinociceptive effects in inflamed but not noninflamed paws. Equivalent doses applied systemically (s.c. and i.v.) were without effect. Dose dependency and stereospecificity of these effects were demonstrated using (-)- and (+)-morphine and (-)- and (+)-tifluadom. Furthermore, by use of (-)- and (+)-naloxone, dose-dependent and stereospecific antagonism was shown. Lastly, reversal of effects of [D-Ala2,N-methyl-Phe4,Gly-Ol5]-enkephalin, [D-Pen2,5]-enkephalin and U-50,488H by mu, delta and kappa selective antagonists D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2, ICI 174,864 and nor-BNI, respectively, indicated that these agents interact with discriminable populations of receptors. These observations suggest that several selective opioid agonists can modulate responses to noxious pressure through a peripheral opioid receptor-specific site of action in inflammation and that these receptors possess distinguishable pharmacological characteristics resembling those of mu, delta and kappa receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1989

[Opioid analgesia during extracorporeal shockwave lithotripsy of gallstones].

Gallstone lithotripsy is a new and noninvasive therapeutic option for approximately 20% of patients who harbor cholesterol gallstones. Technologically advanced second-generation lithotripters such as the Dornier MPL 9000 device have greatly simplified biliary lithotripsy with a consecutive reduction in anesthetic requirements. Despite these technical improvements, patients still can experience considerable pain and discomfort during biliary ESWL. Due to its relatively predictable pharmacokinetic profile and its short duration of action, alfentanil appeared to be a suitable drug for pain relief during stone fragmentation. In order to analyze the degree and distribution of pain during gallstone lithotripsy and to evaluate pain control by alfentanil, 44 consecutive patients (ASA I-II) with no previous ESWL therapy were studied. Pain intensity and degree of opioid-induced sedation during shock wave application were evaluated according to 5-point verbal scales that ranged from 0 = no pain to 4 = unbearable pain and 0 = patient awake to 4 = patient asleep. All patients were treated while in the prone position and received oxygen at 6 l/min. After stone focusing, an alfentanil infusion at an initial rate of 2.5 micrograms/kg min was started. Single shock waves were released as test shocks after approximately 2 min. If they were well tolerated, stone fragmentation was begun. If not, more alfentanil was allowed to accumulate until continuous treatment was tolerated. Further in- or decreases of the infusion rate were titrated according to patient response. Registered variables included the required alfentanil loading dose, maintenance and total doses, and the applied shock wave energy approximated by multiplication of shock wave number and voltage squared.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Pulmonary complications within the scope of multiple organ failure].

The adult respiratory distress syndrome (ARDS) is the pulmonary manifestation of multiple organ failure. Respiratory distress, alveolar consolidation and hypoxemia refractory to oxygen are the result of uniform and unspecific morphological reactions of the alveolo capillary membrane. The development of ARDS is most commonly associated with risk factors such as sepsis, trauma, shock or pneumonia. A causal therapy for ARDS is not known. Treatment of the underlying disease, maintenance of arterial oxygenation and prevention of secondary complications are the most important therapeutic measures.

Combined Modality Therapy↗