Biomedical subjects

S E Ricksten

Publications and source records attributed to S E Ricksten.

At least 73 records · Page 4Linked to original sources

PubMed1989

Thoracic epidural anesthesia and central hemodynamics in patients with unstable angina pectoris.

The effects of high thoracic epidural anesthesia (TEA) on central hemodynamics as measured by pulmonary arterial catheterization were studied in nine patients with severe coronary artery disease and unstable angina pectoris. The patients were also treated with a combination of beta-blockers, calcium antagonists, and nitrates, as well as salicylates, low-dose heparin, and nitroglycerin infusion for greater than 24 hr. Management of pain with high TEA was started with the bolus epidural injection of 4.3 +/- 0.2 mL bupivacaine (5 mg/mL), which induced a sympathetic blockade from Th. During ischemic chest pain, pulmonary artery and pulmonary capillary wedge pressures were significantly increased. TEA, while relieving the chest pain, significantly decreased systolic arterial blood pressure, heart rate, and pulmonary artery and pulmonary capillary wedge pressures, without any significant changes in coronary perfusion pressure, cardiac output, stroke volume, and systemic or pulmonary vascular resistances. In some patients, ST-segment depression was less pronounced during TEA. Thus, during ischemic chest pain, TEA has beneficial effects on the major determinants of myocardial oxygen consumption, without jeopardizing coronary perfusion pressure. TEA may therefore favorably alter the oxygen supply/demand ratio within ischemic myocardial areas.

Aged↗

PubMed1988

Effects of naloxone and verapamil in experimental amitriptyline poisoning in rats.

The effects of verapamil and naloxone as potential antidotes for amitriptyline-induced cardiotoxicity were investigated in an experimental rat model. Amitriptyline was infused continuously at a dose of 37.5 mg/kg/h. After 15 minutes, the animals were given either naloxone (2 mg/kg + 3 mg/kg/h), verapamil (0.08 mg/kg + 0.08 mg/kg/h), or physiological saline. In the group given naloxone, a significant decrease in heart rate was seen. Although MAP and max dP/dT increased, there was no significant difference from controls. Naloxone did not decrease mortality. When the bolus dose of verapamil was given, a significant decrease in MAP and max dP/dT was obtained. Although the mean blood pressure was significantly higher in those animals treated with verapamil who survived 60 minutes, verapamil did not change the course of the amitriptyline poisoning. In conclusion, our findings indicate that naloxone lacks significant positive effects and that verapamil has an additional negative inotropic effect. Neither drug can be recommended for the treatment of amitriptyline poisoning.

Amitriptyline↗

PubMed1988

Effects of halothane, enflurane, and isoflurane on coronary vascular tone, myocardial performance, and oxygen consumption during controlled changes in aortic and left atrial pressure. Studies on isolated working rat hearts in vitro.

The effects of equi-anesthetic concentrations of halothane (HAL, n = 11), enflurane (ENF, n = 11) and isoflurane (ISO, n = 10) on cardiac function were studied and compared with a control group (n = 12) in isolated paced rat hearts by means of an antegrade heart perfusion technique. Left atrial pressure (LAP) and mean aortic pressure (MAP) could be altered independently of each other, and aortic flow, coronary flow (CF), and po2 in venous coronary effluent were continuously recorded. Stroke volume (SV), myocardial oxygen consumption (MVO2), and myocardial oxygen extraction were calculated: 1) MAP was altered from 60 to 120 mmHg at a constant LAP (7.5 mmHg), and 2) LAP was varied from 4 to 12.5 mmHg at a constant MAP (80 mmHg). Left ventricular function curves (LVFC) were constructed and the maximal SV (SVmax) was obtained. The LAP needed to perform 75% of the maximal SV (LAP0.75) was estimated to assess the effect of the anesthetics on diastolic function. HAL ENF and ISO decreased SVmax significantly compared to control. This decrease was more pronounced for HAL (41%) compared to both ENF (26%) and ISO (26%). Accordingly, SV, at various levels of MAP, at a constant LAP, was significantly lower for HAL than for both ENF and ISO, while there was no significant difference between the latter two. None of the anesthetics shifted the LVFC to the right, i.e., did not affect diastolic properties. HAL induced the most pronounced decrease in MVO2, while there was no significant difference between ENF and ISO in this respect. Coronary flow (CF), at controlled perfusion pressures, decreased significantly with HAL but not with ENF or ISO compared to control. CF was significantly higher with ISO compared to both ENF and HAL. HAL and ISO, but not ENF, decreased myocardial oxygen extraction significantly compared to control and, thus, increased the myocardial oxygen supply-to-demand ratio.

Animals↗

PubMed1988

Thoracic epidural anesthesia in conscious and anaesthetized rats. Effects on central haemodynamics compared to cardiac beta adrenoceptor and ganglionic blockade.

A simple technique for cannulation of the thoracic epidural space in rats was described. 40-50 microliter of epidural bupivacaine 5 mg/ml induced a distribution of sensory analgesia from lower cervical to lower thoracic segments. With this model, effects of thoracic epidural anaesthesia (TEA) on mean arterial pressure (MAP), cardiac output (CO), systemic vascular resistance (SVR), stroke volume (SV), heart rate (HR), central venous pressure (CVP), left ventricular end-diastolic pressure (LVEDP) and maximal increase of pressure in the left ventricle (max dp/dt) were studied in six groups of animals: 1) In conscious animals (n = 10) MAP, CO, SV and HR decreased significantly by 12%, 25%, 10% and 16%, respectively, while SVR increased significantly by 20% during TEA; 2) In chloralose-anaesthetized animals (n = 7) the reduction in CO during TEA was less pronounced and there were no significant changes in SV or SVR; 3) In conscious animals (n = 6) LVEDP, CVP and max dp/dt decreased significantly during TEA; 4) Hexamethonium, when administered to pharmacologically vagotomized conscious animals during TEA (n = 8), induced a significant decrease in SVR (23%) but no change in HR; 5) Changes in haemodynamics after cardiac adrenoceptor blockade with metoprolol, in conscious animals (n = 12), did not differ significantly from those seen during TEA, except for an unchanged SV after metoprolol; 6) 50 microliters of bupivacaine (5 mg/ml) when given i.v. to conscious animals (n = 8) did not affect CO, SV, HR or TPR significantly, while MAP increased slightly but significantly. Thus, in this conscious animal model, TEA almost completely and rather selectively blocked probably mediated by a reflex activation of unblocked sympathetic efferents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed1988

Thoracic epidural anaesthesia decreases the incidence of ventricular arrhythmias during acute myocardial ischaemia in the anaesthetized rat.

The aim of the present investigation was to study the effect of high thoracic epidural anaesthesia (TEA) on the incidence of ventricular arrhythmias after ligation of the left coronary artery in chloralose-anaesthetized rats. Forty animals were randomly assigned to receive either 40-50 microliter of bupivacaine (5 mg/ml) or saline in implanted thoracic epidural catheters. TEA decreased mean arterial pressure (MAP) from 118 +/- 5 mmHg to 72 +/- 4 mmHg and heart rate (HR) from 450 +/- 9 to 387 +/- 8 beats/min, while epidural saline did not affect MAP and HR. In both groups coronary artery ligation induced a transient decrease in MAP within the first 5-10 min after ligation. In the control group HR increased, during the 30-min post-ligation period, from 453 +/- 9 to 474 +/- 10 beats/min (P less than 0.05) while no significant change was seen in the TEA group. In both groups the mortality rate was 10%. In the TEA group 30% and in the control group 0% had normal sinus rhythm during the recording period (P less than 0.001). The incidence of ventricular fibrillation and/or tachycardia was significantly lower (P less than 0.05) in the TEA group (20%) compared to the control group (53%). The incidence of ventricular extrasystoles did not differ between the two groups. We conclude that TEA-induced blockade of sympathetic afferents and efferents may offer protection against malignant ventricular arrhythmias in the early phase of acute myocardial infarction.

Anesthesia, Epidural↗

PubMed1988

Postganglionic sympathetic nerve activity in halothane-anaesthetized rats during controlled and spontaneous ventilation.

The aim of the study was to compare the effect of halothane anaesthesia on sympathetic nerve discharge in mechanically normoventilated and spontaneously breathing rats. Renal sympathetic nerve activity (rSNA), mean arterial pressure (MAP) and heart rate (HR) were measured in the conscious state and at the inspiratory halothane concentrations of 0.6%, 1.2% and 2.4% in one mechanically normoventilated and one spontaneously breathing group, while a third group was subjected to controlled hypoventilation at 1.2% halothane concentration. Halothane in blood was determined in two separate groups at 1.2%. In an additional group of spontaneously breathing rats, PaCO2 was analysed during consciousness and the halothane concentrations of 1.2% and 2.4%. There was a pronounced decrease in rSNA, MAP and HR at all levels of anaesthesia in the mechanically ventilated rats. However, rSNA, HR and MAP were significantly higher in the spontaneously breathing rats at increasing levels of halothane anaesthesia. Controlled hypoventilation at 1.2% halothane increased the variables significantly. In spontaneously breathing animals, PaCO2 increased significantly during the halothane exposure. The concentration of halothane in blood was significantly higher in the spontaneously breathing rats. Thus, the halothane-induced respiratory depression in the spontaneously breathing rats preserved rSNA during halothane anaesthesia, possibly via CO2-mediated chemoreceptor stimulation.

Anesthesia, Inhalation↗

PubMed1988

Haemodynamics and plasma ANP (atrial natriuretic peptide) after acute blood volume expansion in normotensive and spontaneously hypertensive rats.

Atrial natriuretic peptide (ANP) was measured in plasma during acute volume load in conscious, spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. During basal conditions immunoreactive ANP were similar in the SHR (630 +/- 56 pmoles l-1) and the WKY (657 +/- 114 pmoles l-1) groups. An acute 10% and 20% whole blood volume expansion resulted in a linear increase in immunoreactive plasma ANP in the WKY. In the SHR the increase in plasma ANP was attenuated during the 20% volume load. During the 10% and 20% volume load central venous pressure (CVP), central blood volume (CBV) and cardiac output increased relatively more in the SHR compared with the WKY group. In contrast, the increase in peripheral blood volume (PBV) and decrease in heart rate (HR) was attenuated in the SH rats. In the SHR group there was a shift of the ANP vs. CVP and ANP vs. CBV curves to the right compared with the WKY. We conclude that acute volume loading is a potent stimulus for ANP release in WKY as well as SHR. However, in the SHR, ANP release was blunted in spite of the increased centralization of the volume load in this rat strain. Thus, the decreased responsiveness of the ANP hormonal system may contribute to the development and maintenance of hypertension in this genetic form of hypertension.

Animals↗

PubMed1988

Effects of hypovolaemia or isoprenaline infusion on the sympathetic reflex response to PEEP ventilation in rats.

The aim of this investigation was to study vagally mediated sympathetic reflex responses to mechanical ventilation with positive end-expiratory pressure (PEEP), during hypovolaemia or during high inotropic stimulation of the heart by isoprenaline infusion. Renal sympathetic nerve activity (RSNA), heart rate and mean arterial pressure were studied during mechanical ventilation with zero end-expiratory pressure (ZEEP) and 5 and 10 cmH2O PEEP in chloralose anaesthetized Wistar rats. Experiments were performed on two groups of rats: eight animals were subjected to 10% blood volume depletion, and seven animals to infusion of isoprenaline. PEEP ventilation was applied during control conditions and during hypovolaemia or isoprenaline infusion before and after vagotomy. In the intact (control) situation, there was a significant increase in RSNA from ZEEP to 10 PEEP in both groups (+75%, +51%). During hypovolaemia or isoprenaline infusion, PEEP ventilation did not induce any significant increase in RSNA in both groups after vagotomy, 10 PEEP induced a significant increase in both groups (+56%, +54%). These results indicated that under conditions of hypovolaemia or increased cardiac inotropism, PEEP ventilation may elicit a vagally mediated reflex with an inhibitory action on sympathetic activity, in turn probably caused by an activation of left ventricular receptors.

Animals↗

PubMed1988

Differential haemodynamic effects of atrial natriuretic peptide (ANP) in normotensive and spontaneously hypertensive rats.

Central haemodynamic parameters and cardiac performance were measured in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) control rats after a 10-min infusion of rat ANP (103-125), 1 micrograms kg-1 min-1. Mean Arterial blood pressure (MAP) decreased by approximately 10% in both groups of rats. Heart rate (HR) increased slightly in both strains during the infusion. In the normotensive group the fall in MAP was due to a reduction in cardiac output (CO) while in the SHR there was a decrease in CO as well as in total peripheral resistance (TPR). The ANP infusion also reduced central blood volume (CBV) and stroke volume (SV) in both groups of rats. The reduction in CBV and CO was significantly more pronounced in the WKY strain. Left ventricular end diastolic pressure (LVEDP) and cardiac contractility (dP/dt) did not change while central venous pressure (CVP) was slightly decreased in the WKY group as a result of the ANP infusion. We conclude that ANP reduces MAP in normotensive animals by a reduction in CO. In the SHR a reduction in TPR also contributes to the fall in MAP. Atrial natriuretic peptide did not exert any negative inotropic effects, but the reduction of CO was due to an increased venous compliance.

Animals↗

PubMed1988

Renal sympathetic nerve activity during morphine abstinence in sino-aortic baroreceptor-denervated rats.

This study was undertaken to investigate the influence of the arterial baroreceptors on the response of renal sympathetic nerve activity (rSNA) during naloxone-precipitated morphine abstinence in rats. In chronically baroreceptor-denervated, morphine-dependent rats, rSNA, mean arterial pressure (MAP) and heart rate (HR) were studied before and after repeated i.v. bolus doses of naloxone (0.005-5 mg kg-1), during chloralose anaesthesia or in the conscious state. In the anaesthetized animals, naloxone doses of 0.05-5 mg kg-1 caused a pronounced inhibition of rSNA, reaching a level 61% below pre-naloxone activity. This was accompanied by increases in MAP and HR. In the conscious rats, the lower doses of naloxone elicited an initial state of increased somatomotor activity. This was paralleled by slight increases in rSNA and MAP. After 4-5 min, the behavioural excitation faded and was replaced by lethargy. The rats exhibited still signs of withdrawal in the form of piloerection, chromodacryorrhoea and defaecations. Concomitantly, rSNA returned towards the pre-naloxone level, while MAP showed a sustained increase. The higher naloxone doses exacerbated the hypertension without any further changes in rSNA or in behaviour. We conclude that the influence of the baroreceptors is of minor significance for the inhibition of rSNA during naloxone-precipitated abstinence in anaesthetized rats. In conscious, intact rats, however, the baroreceptors seem to contribute to rSNA inhibition since no significance decrease of rSNA occurred in baroreceptor-denervated rats in the present study. This is in contrast to our previous finding of a marked inhibition of rSNA in rats with intact baroreceptors.

Animals↗

PubMed1988

Central haemodynamics during morphine abstinence in anaesthetized rats.

Central haemodynamics were studied in one group of morphine-dependent rats, and in a non-dependent control group, before and after administration of repeated bolus doses of naloxone. Dependence was induced by s.c. morphine pellet implantations. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO) and mean transit time (MTT) were measured in the conscious state, after induction of chloralose anaesthesia and after the administration of naloxone (0.005, 0.05, 0.5 and 5 mg kg-1 i.v.). Total peripheral resistance (TPR), stroke volume (SV) and central blood volume (CBV) were subsequently calculated. The haemodynamic variables did not differ significantly in the conscious state, except for a lower SV, when compared with the non-dependent control group. However, in response to anaesthesia the dependent rats exhibited a greater fall in MAP, mainly due to a TPR decrease. Naloxone elicited a marked increase in MAP in the morphine-dependent group, which was mainly caused by an increase in TPR. Naloxone induced no significant change compared with the control group in CO and CBV, while SV increased concomitantly with a lowered HR after naloxone in the morphine-dependent group. These results suggest that the withdrawal hypertension during morphine abstinence was mainly explained by an increase in TPR, reflecting an augmented tone of the resistance vessels. The minor changes in CBV indicate that the tone of the venous capacitance vessels was largely unaffected by naloxone-induced morphine abstinence.

Animals↗

PubMed1988

Clonidine interaction in amitriptyline poisoning.

The effect of clonidine on amitriptyline-induced cardiotoxicity was investigated in an experimental rat mode. A continuous infusion of amitriptyline (30 mg/kg/h) was given until the animal died, usually within 2 hours. Fifteen minutes after starting the amitriptyline infusion, 50 micrograms/kg of clonidine was given intravenously over five minutes. This led to an increase in blood pressure and left ventricular end-diastolic pressure. There was no significant change in cardiac contractility. Heart rate decreased. These changes can be explained by an increase in afterload due to peripheral vasoconstriction. No signs of reduced sympathetic outflow were seen on the ECG. The peripheral effects of clonidine dominated over the central effects, which may be due to a competitive inhibition of amitriptyline at central noradrenergic sites. An increased afterload pushes the heart towards failure and increases mortality. In this model, clonidine did not reverse amitriptyline-induced cardiovascular toxicity. It may even be potentially harmful if used to treat tricyclic antidepressant poisoning.

Amitriptyline↗

PubMed1988

Pre- and postganglionic sympathetic nerve activity during induced hypotension with adenosine or sodium nitroprusside in the anesthetized rat.

The aim of this study was to examine the effects of adenosine (AD)-induced hypotension on preganglionic adrenal (aSNA) and postganglionic renal (rSNA) sympathetic nerve activity. rSNA (n = 10) and aSNA (n = 6) were recorded together with mean arterial pressure (MAP) and heart rate (HR) in chloralose-anesthetized, artificially ventilated rats. In each experiment, hypotension was induced by equihypotensive doses of AD (0.03-2.0 mg.kg-1.min-1) and sodium nitroprusside (SNP) (1-10 micrograms.kg-1.min-1). SNP induced a progressive reflex tachycardia and a reflex increase in rSNA to levels 159 +/- 35% above control at a MAP reduction of 55% of the normotensive control value. Equipotent doses of AD induced a decrease in HR and significantly less pronounced reflex increase in rSNA. The maximal increase in rSNA with AD was 55 +/- 19% at a MAP reduction of 30%. At higher infusions rates of AD, rSNA progressively declined toward the normotensive control values. However, AD elicited a progressive increase in preganglionic aSNA that was not significantly different from the increase seen during SNP infusion. It is concluded that AD-induced hypotension is associated with a suppression of postganglionic sympathetic nerve activity caused by an inhibition of ganglionic neurotransmission.

Adenosine↗

PubMed1988

Changes in renal sympathetic nerve activity during experimental septic and endotoxin shock in conscious rats.

Changes in postganglionic renal sympathetic nerve activity, arterial pressure, and heart rate were measured in conscious rats during intravenous infusion of live E. coli bacteria (10(9)/h) or bolus injection of E. coli endotoxin (20 mg/kg). Bacteria infusion was associated with a marked and parallel increase in heart rate and sympathetic activity with only minor changes in mean arterial pressure. The early response to bolus injection of endotoxin was a short-lasting decrease in mean arterial pressure combined with a marked increase in sympathetic activity and heart rate, probably due to baroreceptor unloading. However, when mean arterial pressure returned to pre-endotoxin levels, sympathetic activity and heart rate remained markedly elevated, indicating a partly nonreflexogenic increase in central sympathetic outflow. This study using direct nerve recordings of sympathetic activity in conscious animals confirms earlier clinical observations of an increased activity of the sympathetic nervous system in septic shock.

Animals↗

PubMed1987

Reflex changes in sympathetic nerve activity during mechanical ventilation with PEEP in sino-aortic denervated rats.

The aim of this study was to evaluate the role of cardiopulmonary receptors with vagal afferents in the reflex control of sympathetic nerve activity during mechanical ventilation with positive end-expiratory pressure (PEEP). Experiments were performed on 17 chloralose-anaesthetized rats. Changes in renal sympathetic nerve activity (RSNA), heart rate and mean arterial pressure were studied at zero end-expiratory pressure (ZEEP) and at 5 and 10 cm H2O PEEP in intact animals (n = 8), after sino-aortic denervation (n = 17) and after sino-aortic denervation plus vagotomy (n = 10). In the intact animals, 10 cm H2O PEEP induced a significant increase in RSNA (+66%) and heart rate (+10%) while the mean arterial pressure did not change significantly. Sino-aortic denervation increased baseline levels of RSNA, heart rate and mean arterial pressure. After sino-aortic denervation, 10 cm H2O PEEP still induced a significant increase in RSNA (+22%) and heart rate in 13 animals. In four animals, 10 cm H2O PEEP elicited a depressor reflex with a significant decrease in both RSNA (-32%) and heart rate. Bilateral vagotomy after sino-aortic denervation at ZEEP significantly increased RNSA (+15%) and heart rate, indicating an ongoing tonic inhibitory influence on RSNA from vagal afferents in sino-aortic denervated rats. The PEEP did not induce any significant change in RSNA or heart rate after sino-aortic denervation plus vagotomy. The results indicate that cardiopulmonary receptors with vagal afferents contribute to the reflex excitation of the sympathetic nervous system during mechanical ventilation with PEEP. Under certain circumstances, PEEP may also trigger powerful depressor reflexes, mediated by vagal afferents.

Animals↗

PubMed1987

Changes in central hemodynamics during experimental septic shock in conscious rats.

This study describes the hemodynamic, metabolic, and respiratory effects of a 4-h continuous intravenous infusion of live Escherichia coli bacteria (10(9)/h) in conscious, unrestrained rats. The early response to bacterial infusion was moderate hypotension and a marked and sustained increase in heart rate and respiratory rate. During later stages of bacteria infusion a marked decrease in stroke volume and cardiac output was observed, while total peripheral resistance increased. Arterial blood gas measurements showed an early primary respiratory alkalosis, while later stages of bacteria infusion were accompanied by progressive development of metabolic acidosis. This small-sized animal shock model may be useful for further studies, particularly since conscious rats were used to avoid the influence of anesthesia upon the development of septic shock.

Animals↗

PubMed1986

Acute volume expansion as a physiological stimulus for the release of atrial natriuretic peptides in the rat.

The concentration of immunoreactive atrial natriuretic peptide(s) (ANP) was measured in normovolemic conscious rats and 15 min after 10% and 20% blood volume expansion. A 20% blood volume expansion caused a 2-fold increase in plasma ANP. While plasma ANP increased linearly, atrial levels of ANP remained unaltered. The increase in plasma ANP parallelled increases of central blood volume and central venous pressure. It is concluded that acute blood volume expansion is a major physiological stimulus for the release of atrial natriuretic peptides into the circulation.

Animals↗

PubMed1986

Estimation of central venous pressure by measurement of proximal axillary venous pressure using a "half-way" catheter.

The pressure in the proximal axillary vein (AVP) was compared with central venous pressure (CVP) in eight patients during and after elective abdominal surgery. Both pressures were recorded from soft, elastic, polyurethane catheters inserted in the basilic or cephalic veins ("half-way" catheters), punctured at the fossa cubiti (AVP), and via the right jugular vein (CVP). The AVP and CVP were recorded simultaneously using hydrostatic, conventional disposable venous pressure measurement sets. The measurements were performed during intermittent positive pressure ventilation with positive end-expiratory pressure from 0 to 7.5 cmH2O (0-0.74 kPa), as well as during spontaneous breathing. During both controlled and spontaneous respiration, small mean differences (0.2-1.0 cmH2O) (0.02-0.1 kPa), and a highly significant (P less than 0.001) positive correlation between CVP- and AVP-values were found. An increase of 1 cmH2O (0.10 kPa) in the CVP was associated with an increment of practically identical order (0.99-1.04 cmH2O) (0.10-0.11 kPa) in the AVP. The results suggest that monitoring of the AVP by a basilic "half-way" catheter produces diagnostic information similar to that from the measurement of the CVP from subclavian, external or internal jugular, as well as "long-way" brachial catheter, with no risk of the major mechanical complications which accompany the use of the latter catheters.

Adult↗