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Biomedical subjects

M Zimpfer

Publications and source records attributed to M Zimpfer.

124 records · Page 7Linked to original sources
PubMed1981

Verapamil as a hypotensive agent during neuroleptanaesthesia.

The haemodynamic effects of verapamil were investigated in 11 patients anaesthetized with thiopentone, fentanyl and dehydrobenzperidol. Suxamethonium and pancuronium bromide were used for muscle relaxation. Verapamil 0.07 mg kg-1 given as a single intravenous bolus decreased mean arterial pressure from 108 +/- 18 mm Hg to 84 +/- 20 mm Hg (P less than 0.001) and total peripheral resistance by 29 +/- 10% from 1662 +/- 399 dyne s cm-5 (P less than 0.001) while heart rate and mean pulmonary artery pressure showed only minor changes. The decrease in arterial pressure was caused by reduction in total peripheral resistance while cardiac output was increased.

Aged↗
PubMed1981

Bainbridge reflex in conscious, unrestrained, and tranquilized baboons.

The effects of volume loading were examined in conscious, unrestrained, and tranquilized baboons (20-25 kg) 1-3 mo after instrumentation with miniature left ventricular pressure and diameter gauges. The response to volume loading was accompanied by significant increases (P less than 0.01) in cardiac rate (32 +/- 4 beats/min) in tranquilized baboons. When rapid saline infusion was accomplished in conscious unrestrained baboons by means of activating a remote-controlled interrogator, heart rate also rose significantly (41 +/- 8 beats/min, P less than 0.01). After cholinergic blockade with atropine, ganglionic blockade with hexamethonium, bilateral vagotomy, or combined cholinergic and beta-adrenergic blockades, volume loading failed to increase heart rate. In two smaller (12-14 kg) intact conscious baboons with relatively high spontaneous heart rates, volume loading did not alter heart rate. These experiments suggest that the Bainbridge reflex exists in larger primates with relatively low spontaneous heart rates.

Animals↗
PubMed1981

Cardiovascular effects of dihydroergotamine during epidural anaesthesia in dogs.

The haemodynamic changes during epidural anaesthesia and following the administration of dihydroergotamine (DHE; 10 micrograms/kg i.v.) were studied in 7 dogs (epidural group). Epidural anaesthesia was associated with reductions in mean arterial, mean pulmonary arterial and mean right atrial pressures. Femoral flow was increased by 119.9 +/- 35.0% and femoral resistance fell by 62.7 +/- 7.2%. All these changes were abolished by additional administration of DHE during epidural anaesthesia. In a second group of dogs (control group, n = 8) with intact innervation, i.e. without epidural block, DHE (10 micrograms/kg iv.) also decreased femoral flow and increased femoral resistance which, however, was significantly less pronounced ( p less than 0.01). It is concluded that DHE in epidural anaesthesia constricts arteriolar resistance vessels, mainly within the blocked areas.

Anesthesia, Epidural↗
PubMed1981

Effects of anesthesia on the canine carotid chemoreceptor reflex.

We studied the effects of alpha-chloralose (100 mg/kg, iv), Na pentobarbital (25 mg/kg, iv) and halothane (1 vol% and 2 vol%) on the response to carotid chemoreceptor stimulation (CCRS) in eight chronically instrumented dogs. CCRS was accomplished by means of intracarotid injections of nicotine while ventilation was held constant in the unanesthetized state and following administration of one of three different anesthetics. In the conscious state, CCRS elicited intense bradycardia and peripheral vasoconstriction as reflected by a 173 +/- 14% increase in initial cardiac cycle length and a 216 /+- 22% increase in mean iliac vascular resistance. Each anaesthetic, studied on separate days, attenuated these responses to CCRS strikingly (P less than 0.01). For instance, after alpha-chloralose, CCRS increased iliac resistance by only 55 +/- 14% and cardiac cycle length by only 27 +/- 13%. After Na pentobarbital, CCRS increased iliac resistance by 12 +/- 4% and cardiac cycle length by 8 +/- 5%. After inhalation of halothane (1 vol%), CCRS increased iliac resistance by 28 +/- 7% and cardiac cycle length by 11 +/- 5%, whereas halothane (2 vol%) abolished these responses to CCRS. Thus, general anesthesia interferes severely with carotid chemoreceptor control of the circulation. Whereas halothane and Na pentobarbital altered responses to CCRS the most, we found that even alpha-chloralose, which has been thought to maintain or augment reflex responses, was able to depress the response to CCRS strikingly.

Anesthesia↗
PubMed1981

Effects of acute increases in left ventricular preload on indices of myocardial function in conscious, unrestrained and intact, tranquilized baboons.

The effects of acute volume loading were examined on indices of left ventricular (LV) function in conscious, unrestrained and intact, tranquilized baboons. Experiments were conducted 1-3 mo after implantation of ultrasonic transducers to measure LV internal diameter and wall thickness, and miniature LV pressure gauges and aortic and left atrial catheters. In 10 intact, tranquilized baboons, rapid volume loading with saline increased LV end-diastolic pressure by 23.7+/-2.6 mm Hg, LV end-diastolic diameter by 7.8+/-1.5%, LV stroke work by 37.5+/-7.8%, while mean arterial pressure and peak LV wall stress did not change significantly. Despite the increase in preload and activation of the Frank-Starling mechanism, LV dP/dt(max) and the maximum velocity of myocardial fiber shortening (LV dD/dt(max)) did not change. Volume loading after beta-adrenergic or combined beta-adrenergic and cholinergic blockades or volume loading with blood instead of saline also failed to augment LV dP/dt(max) and LV dD/dt(max) despite the increase in preload. In order to volume load the baboons in the conscious state, a radiofrequency (RF) interrogator system was devised, which upon receipt of a radio command, activated a battery operated pump to infuse 1,000 ml of saline i.v. to the baboons. In these experiments, preload rose, i.e., LV end-diastolic diameter increased by 13.9+/-2.1% and the Frank-Starling mechanism could be demonstrated, i.e., stroke work rose by 42.8+/-7.4%, but LV dP/dt(max) and LV dD/dt(max) did not change. After preload was depressed by hemorrhage, the rapid infusion of either blood or saline increased LV dP/dt(max) by 92.7+/-18.5% and LV dD/dt(max) by 64.3+/-10.1%. Thus, acute volume loading in the conscious baboons increased LV end-diastolic size and even stroke work substantially. However, preload dependency of LV dP/dt(max) and the maximum velocity of myocardial fiber shortening was only encountered at low levels of LV preload.

Animals↗
PubMed1981

[Haemodynamic changes during intracoronary infusion of norepinephrine. A study of the halothane-induced circulatory depression (author's transl)].

The haemodynamic effects of halothane (0.9 vol% = 1 MAC) and of intracoronary infusion of norepinephrine (14.28 +/- 3.28 ng/kg/min) were investigated in anesthetized dogs (n=6). During inhalation of halothane the left ventricular (LV) stroke volume was diminished while heart rate and total peripheral resistance exhibited no significant changes. In spite of this cardiodepressive action, by means of a decrease in both LV-end-diastolic pressure and LV-end-diastolic volume, a backward heart failure could be excluded. Intracoronary infusion of norepinephrine increased the contractility of the left ventricle leading to an increase in LV-dP/dtmax to control values. However, in comparison to the original level, cardiac output and mean arterial blood pressure remained decreased. Thus, selective inotropic stimulation failed to antagonize the halothane-induced circulatory depression. In a second series of experiments performed on chronically instrumented dogs (n=5) the haemodynamic effects of piritramide (0.3 mg/kg/h i.v.), i.e. the anaesthetic used for preparation of the animals in the acute experiments, were studied during anaesthesia with halothane (1 MAC). While dipidolor failed to elicit significant changes under these conditions, haemodynamic side effects cannot generally be excluded since there is evidence that narcotic analgesics interfere with the neural control of the cardiovascular system.

Anesthesia↗
PubMed1980

Plasma concentrations of noradrenaline and adrenaline and plasma renin activity during extradural blockade in dogs.

Anaesthetized dogs (pentobarbitone 25 mg kg-1 + 3 mg kg-1 h-1) with a Teflon catheter inserted to the femoral artery for pressure and heart rate measurement and blood sampling were studied. Extradural puncture was carried out at L7--S1 under x-ray control and 2% lignocaine (1 ml min-1) infused for approximately 10 min. During extradural block a decrease in arterial pressure was accompanied by a simultaneous decrease in plasma noradrenaline concentration (NA) and a compensatory increase in plasma renin activity (PRA), which became significant 15 min after commencing the block when the arterial pressure was at the minimum. Dihydroergotamine (DHE) led to a rapid reversal of the hypotension with no change in heart rate and a decrease in PRA. Hypovolaemia (blood loss 5 ml kg-1) was induced before and during block, respectively, in two further experimental groups. Increased NA and PRA were found under hypovolaemia without extradural block, but only PRA increased with hypovolaemia and a block. The effects of DHE in the later studies were comparable to those observed in the initial study.

Anesthesia, Epidural↗
PubMed1980

[Plexus analgesia in childhood with special consideration of the "loss of resistance"-method and psychic care of children (author's transl)].

The possibility of a brachial plexus block in children is discussed and presented as a relatively safer method than general anaesthesia. 10 cases aged between 4 and 13 years are reported. Intensive verbal communication with the child during the procedure is essential and sedation may have disadvantages. Prolonged post-operative pain prevention can be achieved by in an indwelling Venflon cannula.

Adolescent↗
PubMed1980

[Cardiovascular effects of two synthetic enkephalin analogues following intracoronary administration in dogs (author's transl)].

Haemodynamic changes following intracoronary injection of two synthetic Met5-enkephalin analogues (FK 33-824 and DALA) with prolonged action as compared with "natural" enkephalines were investigated in anaesthetized dogs (n = 5; dosage; 200, 400, 600 micrograms of both substances i. cor.). DALA led to a shortlasting (5 minutes) rise in heart rate associated with an increase in cardiac output and left ventricular dp/dt max. Besides, a fall in mean arterial blood pressure was noted. No alterations in the pulmonary circulation were encountered. FK 33-824 elicited similar, but unpronounced changes. Direct influences on baroreceptor activity or endogenous release of vasoactive substances as the cause of circulatory effects occuring primarily under DALA were discussed. It is concluded that the cardiovascular effects of synthetic opioids resemble those of morphine and its related compounds.

Animals↗
PubMed1979

[Abolition of hypotension following spinal anaesthesia by dihydroergotamine (DHE) (author's transl)].

The conduction block of the preganglionic sympathetic fibres in spina anaesthesia leads to peripheral vasodilation. Such a loss of tone in blood vessels is also pronounced on the venous side. Therefore the effects of intravenously administered DHE (10 microgram/kg i.v.) on 25 healthy patients undergoing spinal anaesthesia were studied. Though all patients were preinfused with 500 ml Ringer there was a sustained decrease in arterial and pulmonary artery pressures (p less than 0.001). However, the heart rate remained unaffected. After DHE the pressure changes were completely reversed whereas heart rate was significantly decreased (p less than 0.001). The effects of DHE can largely be explained by its powerful and selective action on the capacitance vessels in the peripheral circulation. The increased venous return to the heart augments ventricular filling. Perfusion pressure is increased without any concomitant myocardial stimulation. The results indicate that DHE can have a beneficial effect in patients undergoing spinal anaesthesia.

Adult↗
PubMed1977

Haemodynamic and coronary actions of ouabain during coronary infusion.

The investigations were carried out on 24 mongrel dogs which were anaesthetized with chloralose or sodium pentobarbital. Ouabain was added to the coronary blood (50, 100 and 200 ng/ml coronary blood or 0.7, 1.4 and 2.8 X 10(-7) M) over periods of 30 or 60 min by intracoronary infusion of the glycoside. Under chloralose anaesthesia, ouabain at concentrations of 100 and 200 ng/ml coronary blood augmented left ventricular dp/dt significantly. No significant changes were observed in coronary resting flow and flow per beat at the same time. Likewise, the maximum reactive hyperaemic blood flow remained constant, indicating the absence of any changes in the tone of the large extramural arteries. Under sodium pentobarbital anaesthesia small decreases in heart rate and increases in left ventricular dp/dt were seen only at the highest ouabain concentration (200 ng/ml). All flow parameters remained unchanged. These experiments provide evidence that concentrations of ouabain which 100- and 200-fold exceed therapeutic maintenance levels and 10- and 20-fold exceed the concentrations that produce constriction of helically cut pig and rabbit coronary arteries in vitro, do not diminish the coronary blood supply of the anaesthetized dog in vivo.

Animals↗
PubMed1977

Effect of aminophylline on coronary reactive hyperaemia following brief and long occlusion periods.

The effects of an intracoronary aminophylline infusion, adjusted to give a constant concentration of 25 microgram.cm-3 coronary blood, on the reactive hyperaemic responses following coronary occlusion for 4, 10, and 25 heart beats were investigated in anaesthetised, open-chest dogs. The vasodilator effect of intracoronarily-administered adenosine and the hyperaemic response after coronary occlusion for 10 and 25 heart beats were both significantly diminished under the influence of aminophylline. However, the decrease in the coronary dilator effect of adenosine amounted to 80%, whereas the hyperaemic response was diminished by only 20%. The hyperaemic response following a coronary occlusion for only 4 heart beats remained unchanged. The present results obtained with aminophylline suggest at least a partial involvement of adenosine in mediating reactive hyperaemia after sufficiently long periods of coronary artery occlusion.

Adenosine↗
PubMed1976

Blood flow in intact and constricted coronary arteries under the influence of ouabain.

The effects of ouabain on intact and experimentally constricted coronary arteries were investigated in anaesthetized, thoracotomized dogs. Ouabain decreased the blood flow in the intact artery without changing the flow per beat values and increased flow in the constricted artery. Since ouabain decreased left ventricular enddiastolic pressure, it is proposed that the drug-induced augmentation of flow in the constricted artery is related to an elevation of driving pressure to the endocardial layers of the myocardium which are supplied by the constricted artery.

Animals↗
PubMedDate not supplied

The influence of dihydroergotamine on adenosine-induced and reactive coronary vasodilation. Interaction of dihydroergotamine and coronary vasodilation.

The influence of dihydroergotamine on adenosine-induced and reactive vasodilation after long and short periods of coronary artery occlusion was investigated in thoracotomized dogs. Adenosine-induced vasodilation (intracoronary administration) and vasodilation after long periods of coronary artery occlusion (25-35 beats) were similarly influenced, i.e. decreased by the i.v. administration of 10 mug/kg dihydroergotamine. By contrast vasodilation after short periods of coronary artery occlusion (4-7 beats) tended to be increased. This difference in response is thought to arise from two distinct mechanisms of coronary vasodilation after coronary artery occlusion depending on the duration of the occlusion period. The vasodilation after short periods of coronary artery occlusion possibly corresponds to physiological autoregulation. With longer periods of coronary artery occlusion an additional, consecutive mechanism is called into action.

Adenosine↗
PubMedDate not supplied

Coronary reactive hyperaemia and coronary dilator action of adenosine during intracoronary infusion of angiotensin II.

Investigations were carried out in chloralose-anesthetized, thoracotomized dogs. The effects of an intracoronary infusion of angiotensin II (3 ng/ml coronary blood) on reactive hyperaemic blood flow and adenosine-induced coronary vasodilation were established. Coronary artery occlusions were performed over periods of 5, 10 and 25 heart beats and adenosine was injected intracoronarily at dosages of 2, 4, and 8 microgram/kg body weight. The vasodilator effect of adenosine and reactive hyperaemia after 10 and 25 heart beats were both significantly diminished by angiotensin II. By contrast, reactive hyperaemia after coronary artery occlusion lasting 5 heart beats remained unchanged. The present results obtained with angiotensin II further confirm that adenosine is only partially involved in mediating reactive hyperaemia and that this involvement takes place only after sufficiently long periods of coronary artery occlusion.

Adenosine↗