Biomedical subjects

V Lischke

Publications and source records attributed to V Lischke.

50 records · Page 3Linked to original sources

PubMed1995

[Prevention of myocardial ischemia. Study following aortocoronary bypass operation with the calcium antagonist diltiazem].

The incidence of postoperative myocardial infarction (MI) is proportional to the incidence of myocardial ischaemic episodes. Therefore, the prevention of such episodes is of great clinical importance. METHODS. In 90 patients undergoing coronary artery bypass grafting (CABG), perioperative i.v. treatment with either nitroglycerin (NTG), diltiazem (DIL), or the combination of DIL/NTG was used until arrival in the intensive care unit. Myocardial ischaemic episodes were monitored with an automatic ECG-ST-trend analyser (Marquette 7010). RESULTS. Significantly less ischaemic episodes were seen in the DIL group (6.7%) compared to the NTG group (13.2%) or DIL/NTG group (13.5%). Furthermore, significantly less ischaemic episodes were associated with relevant haemodynamic alterations in the DIL group (58.1%) compared to the NTG (89.1%) or DIL/NTG group (80.0%). Increases in heart rate were markedly reduced in the DIL group. DISCUSSION. DIL results in marked haemodynamic stabilisation during CABG, especially in the period immediately after extra-corporeal circulation. This might serve as an explanation for the significant reduction in ischaemic episodes in the DIL group compared to the other two groups. Therefore, perioperative prevention of myocardial ischaemia with the calcium antagonist DIL seems to be favourable in patients during CABG.

Adult↗

PubMed1995

Inhalation anesthetics inhibit the release of endothelium-derived hyperpolarizing factor in the rabbit carotid artery.

BACKGROUND: Inhalation anesthetics may interfere with the synthesis or action of endothelium-derived vasoactive factors. We investigated the effects of desflurane, enflurane, halothane, isoflurane, and sevoflurane on the release of nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) in the isolated endothelium-intact carotid artery of the rabbit. METHODS: Isolated segments of the carotid artery were suspended in Krebs-Henseleit solution (37 degrees C) and preconstricted with phenylephrine (1 microM). Relaxations caused by acetylcholine (ACh) (0.03-10 microM) or sodium nitroprusside (0.01-10 microM) were compared in the presence or absence of the nitric oxide synthase inhibitor NG-nitro-L-arginine (0.1 mM) in segments exposed to desflurane (8%), enflurane (2-4%), halothane (2-3.5%), isoflurane (2-4%), or sevoflurane (2%) as well as in NG-nitro-L- arginine-treated segments exposed to enflurane (2%) in combination with the KCa(+)-channel blocker tetrabutylammonium (0.3 mM) or the cytochrome P450 inhibitor clotrimazole (3 microM). RESULTS: Desflurane, enflurane, and sevoflurane selectively inhibited the ACh-induced release of EDHF. Halothane and isoflurane also weakly affected the nitric oxide-mediated relaxant response to ACh. The inhibitory effect of these two anesthetics on EDHF release was concentration-dependent. Relaxations induced by sodium nitroprusside were not inhibited by any of the anesthetics tested. Three structurally unrelated cytochrome P450 inhibitors clotrimazole (0.1 mM), metyrapone (1 mM), and SKF525a (proadifen, 0.1 mM) abolished the EDHF-mediated relaxation elicited by ACh. The pharmacologic profile of the inhibitory effect of enflurane on the release of EDHF closely resembled that of clotrimazole but not that of tetrabutylammonium. Moreover, all anesthetics inhibited the cytochrome P450-catalyzed O-dealkylation of 7-ethoxycoumarin by rabbit liver microsomes in a concentration-dependent manner. CONCLUSIONS: Inhalation anesthetics significantly attenuate the EDHF-mediated relaxant response to ACh in the rabbit carotid artery. This effect appears to be attributable to inhibition of the cytochrome P450-dependent synthesis of EDHF by the endothelium.

Acetylcholine↗

PubMed1995

Selective inhibition by barbiturates of the synthesis of endothelium-derived hyperpolarizing factor in the rabbit carotid artery.

1. Several lines of evidence suggest that both volatile and intravenous anaesthetics may interfere with the synthesis and release of endothelium-derived vasoactive factors. We have investigated the effects of three different barbiturates on the release of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) in phenylephrine (1 microM)-preconstricted, endothelium-intact ring segments of the rabbit carotid artery. The segments were pretreated with the cyclo-oxygenase inhibitor, diclofenac (1 microM), to prevent the formation of vasoactive prostanoids, such as prostacyclin (PGI2). 2. Acetylcholine (ACh) elicited a concentration-dependent relaxation (EC50 0.15 microM) in control segments which was not significantly different from the relaxant responses of segments pretreated with methohexitone (0.03-0.3 mM), phenobarbitone (0.1-0.3 mM) or thiopentone (0.1-0.3 mM). 3. Inhibition of NO synthesis with NG-nitro-L-arginine (0.1 mM) significantly reduced the maximum relaxant response to ACh from 96 to 40%. This NO/PGI2-independent relaxation appeared to be mediated by the release of EDHF, since it was strongly diminished in the presence of the K+Ca inhibitors, tetrabutylammonium (1-3 mM) and charybdotoxin (10 nM), following preconstriction with potassium calcium (40 mM) or removal of the endothelium. Thiopentone or methohexitone markedly attenuated the EDHF-mediated relaxant response to ACh, while phenobarbitone had no effect. The endothelium-independent relaxation elicited by sodium nitroprusside (0.01-10 microM), on the other hand, was only marginally affected by these anaesthetics. 4. The cytochrome P450 inhibitor, clotrimazole (3-100 microM), mimicked the inhibitory effect of thiopentone and methohexitone on the NO/PGI2-independent relaxant response to ACh. Moreover the cytochrome P450-catalyzed O-dealkylation of 7-ethoxycoumarin by rabbit liver microsomes was inhibited in the presence of thiopentone or methohexitone (0.3-1 mM), while phenobarbitone was without effect.5. These findings suggest that thiopentone and methohexitone selectively attenuate the EDHF-mediated relaxant response to ACh in the rabbit carotid artery, presumably by interfering with its synthesis from arachidonic acid via the cytochrome P450 epoxygenase pathway.

Acetylcholine↗

PubMed1994

Prolongation of the QT-interval during induction of anesthesia in patients with coronary artery disease.

During induction of anesthesia in 60 patients undergoing coronary artery bypass grafting (CABG), we measured the QT-interval (QTI) in the ECG, heart rate (HR) and mean arterial pressure (MAP). Based on the HR, we corrected the QT-interval (QTcI). Prior to induction, six patients (10%) already had abnormal prolongation of QTcI (> or = 440 ms). After injection of fentanyl and vecuronium, the QTcI increased significantly (P < 0.01); to a far lesser extent after injection of hypnotics (i.e. etomidate, midazolam or propofol). Orotracheal intubation caused significant shortening of QTcI (P < 0.01). HR decreased markedly after injection of fentanyl. MAP decreased, however, only after injection of hypnotics. In the immediate post intubation period, HR and MAP increased significantly. The various hypnotics produced no significant difference in HR and QTcI at any measurement point. MAP changed only after injection of hypnotics. The decrease of HR and MAP during induction of anesthesia is thought to result from a corresponding reduction of adrenosympathetic stimulation. We believe that QTcI is similarly influenced.

Anesthesia, Intravenous↗

PubMed1994

Droperidol causes a dose-dependent prolongation of the QT interval.

To further investigate possible prolongation of the frequency-corrected QT interval (QTc interval) after administration of droperidol (DRO), we studied 40 surgical patients who were randomly assigned to one of three groups, receiving an intravenous (IV) injection of either 0.1 mg/kg (Group 1, n = 10), 0.175 mg/kg (Group 2, n = 10), or 0.25 mg/kg (Group 3, n = 20) of DRO at induction of anesthesia. The QTc interval, heart rate, and arterial pressure were registered before and 1, 2, 3, 4, 5, 7.5, and 10 min after the respective dose injection. Significant prolongations of the median QTc interval were found in patients from all groups, ranging from 37 ms (8.0%) in Group 1, to 44 ms (10.6%) in Group 2, to 59 ms (14.9%) in Group 3, when compared with control. The heart rate showed a significant increase in all groups. Mean arterial pressure (MAP) was slightly but significantly decreased in Groups 1 and 3. Prolongation of the QTc interval is a predictable and dose-dependent side effect after injection of high-dose DRO.

Blood Pressure↗

PubMed1993

[ST segment changes in the ECG. Anesthesia induction with propofol, etomidate or midazolam in patients with coronary heart disease].

Induction of anaesthesia with propofol and fentanyl can lead to marked reductions in mean arterial pressure (MAP) and heart rate (HR). Thus, the application of propofol in patients with severely reduced coronary artery perfusion is controversial. METHODS. The study group consisted of 60 patients undergoing coronary artery bypass grafting (CABG). Anaesthesia was induced over 30 s with propofol (P 1.5 mg/kg), etomidate (E 0.3 mg/kg), or midazolam (M 0.15 mg/kg) following a bolus dose of fentanyl (5 micrograms/kg). Vecuronium was used as a muscle relaxant. During induction we continuously measured MAP and HR and recorded the occurrence of myocardial ischaemia using an automatic ST-segment analyser (Marquette 7010). ST-segment deviations of more than 1 mm in leads II and V5 were interpreted as significant signs of myocardial ischaemia. RESULTS. All groups showed reductions in MAP and HR on induction that were marked in the P group. Intubation caused elevation of MAP and HR to pre-induction levels (HR: all groups) or slightly above (MAP: E, M). Four patients in the P group and 3 in each other group showed significant ST-segment deviation prior to induction. In the P group these deviations disappeared in 2 patients after injection while they remained unchanged in the M group. In the E group injection had no effect on the ischaemic ECG changes but produced another case of significant ST-segment deviation. Laryngoscopy and intubation produced no further significant ST-segment deviation in either group. DISCUSSION. Induction is a critical phase of anaesthesia, especially in patients with limited coronary reserve. Induction agents should alleviate the stress response while causing minimal haemodynamic changes. Despite marked reductions in MAP in the P group, the number of patients with ischaemic ECG changes was cut by half. Their number was unchanged or even raised in the other groups. After application of P, with an alleged reduction of coronary perfusion, a compensational reduction in myocardial oxygen consumption may occur.

Aged↗

PubMed1991

[Cardiac adverse effects following an intravenous injection of pirenzepine are an expression of deficient receptor sensitivity].

Under the aspect of life-threatening pneumonias in long-term ventilated patients receiving ant-acids or H2-antagonists the prophylaxis of stress ulcer with pirenzepine gains new importance. This study was aimed at detecting cardiac side effects of pirenzepine due to low receptor specificity. Pirenzepine (10 mg) was given via the peripheral or central venous route at an injection velocity of 5 or 30 seconds as well as a control of 2 ml normal saline solution via the central venous route for 5 seconds, 20 times each. Heart rate and blood pressure were determined before and after the injection. Independent of the injection site or velocity, an increase in the heart rate was found after the injection of pirenzepine. The increase was more marked if the central venous route was used. The percentage rise in heart rate was up to the thirteenth minute highly significant when comparing pirenzepine to normal saline solution. There were no changes in blood pressure. If M1-cholinoceptors are blocked, a reduction of the heart rate is seen. Blocking M2-cholinoceptors causes a rise in the heart rate. Injecting 10 mg of the M1-antagonist pirenzepine results in a significant increase in the heart rate, independent of site or velocity of injection which can be explained by blocking M2-cholinoceptors at the same time. To prevent this probably dose-dependent effect, pirenzepine should be given slowly over a couple of minutes.

Adult↗

PubMed1991

[Characteristics of the QT interval in the ECG following reconstructive surgery of the common carotid artery].

In 40 patients undergoing thrombendarterectomy of the common carotid artery, the frequency-corrected QT interval in the ECG, as well as the serum sodium, potassium and total calcium were studied. Examination took place preoperatively 1.-3. hour postoperative and the 1. and 5. day postoperative. In 13 patients, pathological prolongation of QT interval (greater than 440 msec) was already found pre-operatively. Postoperative significant QT interval prolongations could not be found in any patient, independent of the site of operation or pre-operative findings. The total serum calcium concentration was postoperatively significantly reduced (P less than 0.01). There was no correlation between the reduced total serum calcium and the QT interval in the ECG. The findings contradict the assumption that clinically relevant reduction of the autonomous cardial innervation is frequent in patients undergoing thromboendarterectomy of the common carotid artery.

Aged↗

PubMed1989

[The plasma histamine level during anesthesia induction using midazolam].

Midazolam has not yet been investigated for its possible properties as a histamine releaser. The aim of the following study was to ascertain whether histamine release follows the i.v. injection of midazolam. METHODS. Twenty patients between 18 and 58 years of age were split into two groups at random. Either 0.15 mg/kg midazolam or 0.15 ml/kg NaCl 0.9% were injected i.v. Venous blood was drawn 2 min before and 2, 5, and 10 min after each injection. The content of histamine in plasma was determined by HPLC. RESULTS. In the midazolam group, histamine levels decreased from 0.37 ng/ml to 0.29 ng/ml after 5 min (P less than 0.05). The kinetics typical of histamine release could not be observed in any of the patients. We observed a slight decrease in the blood pressure or tachycardia in 3 patients, but even in these cases there was no increase in histamine level. In the NaCl group, the histamine level decreased from 0.34 ng/ml to 0.23 ng/ml after 2 min (P less than 0.05). The hemodynamics of these patients remained unchanged. One patient had an abnormally high histamine level prior to the injection (2.33 ng/ml). CONCLUSION. Our results show that midazolam is not a histamine releaser. The relevance of 1 patient having a high baseline level of histamine remains unclear.

Adult↗

PubMed1989

[Prolongation of the QT interval in the ECG following surgery of the neck (neck dissection)].

The QT interval on the ECG was determined in 40 patients undergoing major resection plus neck dissection. The readings were taken before operation, between 1 and 3 h after operation, and the 1st and the 7th day after the operation. The QT interval was prolonged significantly more often and more intensively in patients undergoing surgery on the right side (from 411 +/- 17 to 459 +/- 50 ms) than in those operated on the left side (409 +/- 14 to 431 +/- 32 ms; all values mean +/- SD). The cause of the prolongation of QT interval is thought to be either direct surgical damage to the sympathetic cardiac nerves during the operation, or a temporary disturbance of nerve function due to pressure, tension or oedema in the wound. An explanation for the observed side difference might be differing functional effects of right- and left-sided sympathetic innervation of the heart. Attention is drawn to the meaning of these findings as a predisposing factor for ventricular tachyarrhythmias.

Adult↗

PubMed1988

[Effect of glycopyrrolate and atropine on the behavior of heart rate and pH value of gastric juice during microlaryngoscopies].

In a prospective study a total of 51 patients were given either a premedication with atropine (10 micrograms/kg) (n = 17), with glyopyrrolate (5 micrograms/kg) (n = 15) or no anticholinergic premedication (n = 19). In the group of patients premedicated with glycopyrrolate the pH levels of the gastric juice were more often above 2.50 than in the group without anticholinergic premedication (p less than 0.05). During the microlaryngoscopic interventions there was a trend to fewer A-node rhythms or bradycardias in the group premedicated with glycopyrrolate than in the other groups. Reduction of salivary gland secretion by anticholinergics made intervention easier. Glycopyrrolate has advantages over atropine as far as the induction of anaesthesia for microlaryngoscopic interventions is concerned.

Aged↗

PubMed1984

Effects of acetylsalicylic acid on human platelet function in vivo at salicylate steady state.

The results of clinical trials concerning the use of acetylsalicylic acid (ASA) as antithrombotic drug are contradictory. Inhibition by ASA of platelet prostaglandin synthesis and aggregation is prevented by its metabolite salicylic acid (SA) in animals and in human platelets in vitro. It was suggested that ASA might produce its own inhibitor, thereby diminishing its efficiency in thromboembolic disease. In four healthy male subjects there was no difference in inhibition of collagen-induced platelet aggregation after the administration of 500 mg ASA alone or at salicylate steady state (3 g SA daily). But the inhibition of tissue-extract-induced platelet shape change was diminished and shortened by pretreatment with SA. We conclude that SA does not inhibit the effects of ASA on human platelet aggregation in vivo in therapeutic dose ranges. The clinical importance of the SA/ASA-interaction on tissue-extract-induced platelet shape change remains to be clarified.

Adult↗

PubMed1984

[Effects of acetylsalicylic acid on partial functions of human thrombocytes are not inhibited in vivo by salicylic acid].

Acetylsalicylic acid inhibits platelet function. In plasma acetylsalicylic acid is rapidly deacetylated to salicylic acid which is slowly eliminated and has no direct inhibitory effects on platelet function. However, salicylic acid prevents the inhibition by acetylsalicylic acid of collagen-induced aggregation of human thrombocytes in vitro. It was suggested that salicylic acid might inhibit the antiplatelet effects of acetylsalicylic acid in vivo and therefore low-dose acetylsalicylic acid would be more effective for antithrombotic therapy. A 500-mg tablet of acetylsalicylic acid applied 90 min after oral administration of 500 mg salicylic acid to six healthy male volunteers led to the same inhibition of collagen-induced platelet aggregation and tissue-extract-induced platelet stimulation as 500 mg acetylsalicylic acid alone. These results cannot give additional support to the recommendation of low-dose acetylsalicylic acid in the prevention of thromboembolic disease.

Administration, Oral↗

PubMedDate not supplied

Midazolam does not antagonize fentanyl-mediated analgesia in surgical patients.

STUDY OBJECTIVE: To determine whether midazolam possesses a clinically significant antianalgesic action in surgical patients. DESIGN: Randomized, controlled study. SETTING: Inpatient anesthesia at a university department of neurosurgery. PATIENTS: 2 groups of 10 patients each who were scheduled for supratentorial brain surgery, did not have elevated intracranial pressure, and were free from systemic disease. INTERVENTIONS: Patients underwent anesthesia induction with hexobarbital, succinylcholine, and pancuronium; anesthesia was maintained with injections of droperidol-fentanyl (Group 1) or with midazolam-fentanyl (Group 2) following a predetermined repetitive dosing schedule, such that fentanyl 0.1 mg was injected upon predominant increases in heart rate, whereas droperidol 2.5 mg or midazolam 2.5 mg was injected upon increases in blood pressure. MEASUREMENTS AND MAIN RESULTS: Duration of anesthesia and invasiveness of surgery were similar in both groups. The amount of fentanyl required was 0.55 +/- 0.18 mg/hr (mean +/- SD) in Group 1 and 0.53 +/- 0.17 mg/hr in Group 2. Injections of droperidol 7.5 +/- 3.4 mg/hr (Group 1) and midazolam 5.9 +/- 2.3 mg/hr (Group 2) were administered intraoperatively. This redosing regimen was associated with uninterrupted hemodynamic stability, indicating comparable and adequate anesthetic depth. Plasma concentrations of metabolites and hormones indicative of humoral stress activation did not differ between groups. CONCLUSION: Under these clinical conditions, the administration of midazolam, when compared with droperidol, was not associated with signs of any antagonistic or antianalgesic action toward fentanyl-mediated analgesia.

Adolescent↗