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Biomedical subjects

K Peter

Publications and source records attributed to K Peter.

At least 253 records · Page 14Linked to original sources
PubMed1989

[Effect of inhalation anesthetics on the myocardium].

A review of the myocardial effects of the volatile anesthetics halothane (HAL), enflurane (ENF) and isoflurane (ISO) is presented. In the first part the effects on cardiac rhythm, myocardial contractility and oxygen supply are discussed. In the second part the pathophysiology of myocardial ischemia during anesthesia and surgery is summarized. Finally the role of inhalation anesthetics in inducing or preventing myocardial ischemia is considered, with special regard to the "coronary steal" phenomenon.

Anesthesia, Inhalation↗
PubMed1989

[Initial experiences with cognitive therapy of schizophrenic patients].

Based on earlier experiences of various groups of authors, we developed and modified a programme of cognitive therapy for schizophrenic patients. The aim of the application of the therapeutic programme to subacute patients was to decrease subjectively perceptible basic disorders and to improve the functions of performance. The present results and experiences with 4 groups consisting of a total of 31 patients encourage us to continue applying cognitive procedures of therapy. Problems of the ascertainment of measuring values and fundamental questions of therapeutic efficacy are discussed.

Adult↗
PubMed1989

Thromboxane mediation of pulmonary hemodynamic responses after neutralization of heparin by protamine in pigs.

Protamine neutralization of heparin is often associated with severe hemodynamic side-effects, including pulmonary hypertension and systemic hypotension. Because prostanoids may be involved, the authors studied the role of arachidonic acid metabolites, especially thromboxane A2, in this process. During anesthesia with enflurane and fentanyl, four groups of pigs were studied: Group 1 (n = 10) received heparin (250 IU/kg), followed by protamine (100 mg) after 15 minutes to neutralize the heparin. The same protocol was used in group 2 (n = 11), except that the thromboxane A2 receptor antagonist BM 13.177 (10 mg/kg) was infused 5 minutes before the protamine. The protocol for group 1 was also used for group 3 (n = 7) except that these animals were pretreated with indomethacin (10 mg/kg). Animals in group 4 (n = 10) were given protamine only (100 mg). Pulmonary artery pressure and pulmonary vascular resistance increased significantly in group 1 after protamine neutralization of heparin. This was accompanied by significant increases in plasma concentrations of the cyclooxygenase products thromboxane B2, 6-keto-prostaglandin F1 alpha, and prostaglandin F2 alpha. Cyclooxygenase products increased to comparable degrees in group 2, but without hemodynamic effects. Leukocyte counts decreased comparably in both groups. Hemodynamic reactions, as well as changes in plasma prostanoid levels were absent in group 3, and group 4, but leukocyte counts were less affected in animals that received protamine alone. The results indicate that the hemodynamic side-effects of protamine are mediated by prostanoids and that thromboxane A2 release is the pivotal step, because side effects were effectively prevented by pretreatment with a thromboxane receptor antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Left ventricular oxygen tensions in dogs during coronary vasodilation by enflurane, isoflurane and dipyridamole.

The purpose of this study was to investigate the effects of the anesthetics enflurane and isoflurane and of the coronary vasodilator dipyridamole on myocardial oxygen balance and myocardial tissue oxygen tensions. The studies were performed in 24 open-chest dogs during basal anesthesia with a narcotic. Myocardial blood flow (MBF) was measured using radioactive microspheres, myocardial surface tissue PO2 by means of a platinum multiwire surface electrode. One control group and three experimental groups were studied: enflurane (1.1 vol%), isoflurane (0.7 vol%, both end-tidal concentrations), and dipyridamole (0.4 mg/kg). Mean arterial pressure significantly decreased to an average of 70 mm Hg in all three experimental groups. Although MBF was unchanged during enflurane (-18%) and isoflurane (+20%), it increased during dipyridamole (+304% p less than 0.05 vs baseline and control, enflurane, and isoflurane groups). Myocardial oxygen consumption decreased significantly during enflurane and isoflurane but remained unchanged during dipyridamole. Thus, the ratio between myocardial oxygen delivery and consumption increased 6% with enflurane (p less than 0.05 vs baseline), 47% with isoflurane (p less than 0.05 vs baseline and control group) and 280% with dipyridamole (p less than 0.05 vs baseline and control, enflurane, and isoflurane groups). Coronary venous PO2 remained unchanged during enflurane but increased significantly during isoflurane and dipyridamole. Left ventricular surface tissue PO2 was unchanged in enflurane and isoflurane animals and decreased slightly, yet significantly, during dipyridamole. All variables remained unchanged in the control group. Thus, isoflurane and dipyridamole interfered with MBF autoregulation and increased myocardial oxygen delivery out of proportion to myocardial demands.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Pulmonary kinetics of fentanyl and alfentanil in surgical patients.

The pulmonary kinetics of fentanyl and alfentanil were studied quantitatively in two groups of five and six surgical patients, respectively, after the induction of anaesthesia. A mixture of one of the opioids and indocyanine green was administered as a bolus. From measurements of the concentrations of the dye in plasma and the opioids in blood, central blood volume and the amount of drug which passed through the pulmonary circulation were calculated. The pulmonary release of fentanyl and alfentanil was calculated from the arterial-mixed venous blood concentration differences. Fentanyl 43.0-86.9% (median 70.9%) and 35.9-79.8% of alfentanil (median 58.6%) were sequestered by the lung on first passage of the opioid-containing blood through the pulmonary capillaries. During the following 14 min, fentanyl was released, apparently from two binding sites (T1/2fast: 0.22 (0.16-0.27) min; T1/2slow: 5.78 (3.65-13.86) min). Initially, there was a rapid release of alfentanil (T1/2: 0.28 (0.08-0.51) min). However, 1-3 min after injection, the arterial-mixed venous blood concentration differences of alfentanil disappeared, although considerable amounts of drug were still present in the lung of five of the six patients studied. It may be expected that a temporary pulmonary sequestration of fentanyl and alfentanil has considerable impact on the time course of their pharmacological effects, on the time necessary to reach their maximum effect and on the intensity and (in case of fentanyl) the duration of these effects.

Adult↗
PubMed1988

Splanchnic oxygen consumption and hepatic surface oxygen tensions during isoflurane anesthesia.

Blood flow to and oxygen consumption of the splanchnic organs were determined together with hepatic surface oxygen tensions in 18 mongrel dogs anesthetized with the long-acting narcotic piritramid. Twelve animals also received 0.7 Vol% and 1.4 Vol% isoflurane; six time-related controls received piritramid only. Surgical preparation consisted of a left thoracotomy for inserting a catheter into the left atrium for microsphere injections and for gaining access to the hepatic surface through an incision in the diaphragm. Parameters in the animals receiving isoflurane were recorded at three stages: stage 1--piritramid anesthesia after surgical preparation; stage 2-60 min after addition of 0.7 Vol% (end-expiratory) isoflurane; stage 3-60 min after addition of 1.4 Vol% (end-expiratory) isoflurane. Hepatic surface oxygen tension was determined at each stage using an eight-channel oxygen sensitive electrode. Mean arterial pressure and cardiac output decreased during both stages with isoflurane; hepatic arterial inflow remained constant. Portal blood flow and, hence, total hepatic inflow decreased significantly. An unchanged splanchnic O2 consumption induced lower hepatic venous pO2 values: 40 +/- 1 mmHg at control, 35 +/- 2 mmHg, and 31 +/- 2 mmHg (mean +/- SEM; both P less than 0.05) during isoflurane. A concomitant decrease of hepatic surface pO2 values indicated an altered tissue oxygenation. The percentage of hepatic surface pO2 values in the lowest pO2 range (0-5 mmHg) increased significantly from 8.4 to 20.3% during 1.4 Vol% isoflurane; the percentage of values of 0 mmHg increased from 2.4 to 9.8% during 1.4 Vol.%. No changes of these parameters were detected in the control animals during the 3-h observation period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Recovery times and side effects after propofol infusion and after isoflurane during ear surgery with additional infiltration anaesthesia.

Two anaesthetic procedures that did not include nitrous oxide were compared in a randomised study of 50 patients for tympanoplasty and tympanoscopy: propofol given for induction and maintenance, and thiopentone-isoflurane given for induction and maintenance, respectively. Induction in the first group was with a bolus injection of propofol and the same agent was given for the duration of anaesthesia by continuous intravenous administration. Thiopentone was given until loss of the eyelash reflex and anaesthesia maintained with isoflurane 0.4-2.0%. Analgesia was achieved in both groups by fentanyl given intravenously and by local injection of mepivacaine with ornipressin. The two patient groups were analysed for age, sex and weight as well as for side effects during the induction, maintenance and recovery periods, such as coughing, vomiting, venous pain, spontaneous movements, singultus, headaches, dysrhythmias and psychic disorders possibly due to anaesthesia. Side effects were moderate in both groups. Recovery time was statistically significantly shorter in the propofol group and the patients in this group appeared to be much more aware after recovery than those in the thiopentone-isoflurane group.

Adolescent↗
PubMed1988

Beneficial effect of cyclooxygenase inhibition on adverse hemodynamic responses after protamine.

The hypothesis that adverse effects observed when heparin is antagonized by protamine are mediated by metabolites of the arachidonic acid cascade was tested during general anesthesia (enflurane, fentanyl) in 16 pigs classified into two groups. In the first group (n = 9), effects of intravenously administered protamine on systemic hemodynamics, blood/gas tensions, and arterial and mixed-venous prostanoid levels were studied. The second group (n = 7) was pretreated with indomethacin 10 mg/kg, and the same measurements were made. All pigs received heparin 150 units/kg. When protamine 1.1 +/- 0.1 mg/kg was administered over 3 minutes, marked hemodynamic alterations were observed in group 1: pulmonary artery pressure and pulmonary vascular resistance increased, and left ventricular end-diastolic and systemic arterial pressures decreased. Arterial and mixed-venous PO2 values deteriorated in all pigs in group 1 at the end of protamine infusion. These alterations were accompanied by significantly elevated prostanoid levels in arterial and mixed-venous plasma samples: Thromboxane A2, prostaglandin F2 alpha, KH2-PGF2 alpha (a metabolite of prostaglandin F2 alpha), and prostacyclin were maximally elevated at completion of protamine and remained significantly above control values at 5 minutes but were not significantly different from control after 10 minutes. Blocking the cyclooxygenase cascade by pretreatment of the pigs with indomethacin (group 2) prevented hemodynamic and blood gas alterations. It is concluded that in pigs the detrimental side effects associated with the use of protamine to reverse heparin are mediated by metabolites of the cyclooxygenase cascade.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1988

[Water-electrolyte balance and kidney function for 3 weeks following severe trauma].

A study on water-electrolyte metabolism and renal function was performed in 32 patients (mainly young to middle-aged males) over three weeks after severe accidental trauma (mainly brain trauma), who did not suffer from acute renal failure. With a mean water input of 4 l/day the difference of water input and urine volume was positive over the whole observation time. Patients had a mean osmolar excretion of 1800 mosm/day which was twice normal and was mainly caused by a high urea excretion. They were almost invariably in the state of antidiuresis and achieved unusually high values for negative free-water clearance around 2 ml/min. This, however, was adequate in terms of normotonicity of body water. Cumulated sodium balance over 21 days was negative and, on the average, amounted to minus 440 mmol. The median value for creatinine clearance was in the range of predicted normal (156 ml/min.) between day 5 and 10 and a little less before and thereafter. We frequently observed an elevation of creatinine clearance to 120-150% of normal. Renal clearance of urea was around 100 ml/min. during the phase of maximal protein catabolism. Therefore the reasonable increases in urea production up to a mean of 60 g/day resulted only in moderately elevated levels of plasma urea (40-50 mg/100 ml). In 14 patients we performed a total of 83 measurements of plasma volume (Evans-Blue). In patients with intact renal function mean plasma volume amounted to 110% normal. This, in combination with a reduced red all volume on the average, resulted in mild hypovolaemia (blood volume about 90% of predicted normal).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1988

[Anesthesia for magnetic resonance tomography].

Monitoring of the vital signs and the possibility of respiratory support are necessary conditions for the application of magnetic resonance imaging to infants and geriatric patients as well as during intensive care therapy. Since April 1986, 73 patients have been scanned under general anesthesia with controlled artificial ventilation in the Grosshadern University Hospital. For the first time, the ventilator could be placed in the vicinity of the magnetic resonance imaging scanner. With this system, the anesthesiologist is able to inspect the patient, ventilator, and monitoring unit from one place in the examination room.

Adolescent↗
PubMed1987

Prevention of colonization and respiratory infections in long-term ventilated patients by local antimicrobial prophylaxis.

In a randomized clinical trial the prophylactic effects of locally administered antimicrobials on quantitative colonization and respiratory infections were studied in intubated patients with an expected period of mechanical ventilation of greater than 6 days. Nineteen patients received 50 mg of polymyxin B and 80 mg of gentamicin distributed among nose, oropharynx and stomach at 6-h intervals, as well as 300 mg of amphotericin B in the oropharynx. Twenty untreated patients served as controls. In the control group colonization by respiratory pathogens was more common (oropharynx 19 vs 6 patients (p less than 0.001); trachea 19 vs 11 (p less than 0.01)), and the number as well as the count of the colonizing species was usually higher. Fourteen patients of the control group developed respiratory infections, including nine cases of pneumonia, as compared to four patients with prophylaxis, including one case of pneumonia (p less than 0.01). Pneumonia-associated deaths were prevented with prophylaxis; however, the overall mortality remained unchanged. Respiratory infections in the prophylaxis group were associated with organisms resistant to the agents used, but the overall occurrence of resistance was not increased, as compared to the control group. We conclude that unrestrained upper airway colonization by respiratory pathogens and respiratory tract infection were causally related. Local antimicrobial prophylaxis proved to be a highly effective strategy for the prevention of potentially life-threatening pneumonias in critically ill patients, but in the present study the host setting appeared to be the major determinant of outcome.

Administration, Intranasal↗
PubMed1987

Induced hypotension: action of sodium nitroprusside and nitroglycerin on the microcirculation. A micropuncture investigation.

Sodium nitroprusside (SNP)-induced hypotension is associated with tissue hypoxia in liver and skeletal muscle, suggesting a redistribution of nutritional capillary flow. To test this hypothesis, the effects of SNP and nitroglycerin (NTG) on striated muscle vessels were studied in 42 hamsters using intravital microscopy, quantitative video image analysis, a platinum multiwire electrode for local Po2 measurements, and a micropuncture system for the determination of microcirculatory pressure. A transparent chamber was implanted in a dorsal skin fold. When the mean arterial pressure was reduced to 70 or 40 mmHg by SNP, the precapillaries dilated and precapillary resistance decreased, but significant changes in venular diameter were not observed. However, SNP-induced hypotension was associated with a consistent increase in intravascular pressure within the venules. As a result, the arteriolar-venular pressure gradient was reduced by more than 50%. Furthermore, the functional capillary density was less, and tissue hypoxia was present during SNP hypotension. In contrast, NTG dilated both arterioles and venules in the microvascular network. Despite a lower blood cell velocity in all segments, the functional capillary density and local Po2 remained unchanged during NTG, principally because there was only a 10% reduction of the arteriolar-venular pressure gradient. These findings suggest that, in terms of tissue oxygenation, NTG may be preferable to SNP for deliberate hypotension.

Animals↗