Biomedical subjects

M Delle

Publications and source records attributed to M Delle.

At least 37 records · Page 2Linked to original sources

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

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

2-Deoxy-D-glucose-induced central glycopenia differentially influences renal and adrenal nerve activity in awake SHR rats.

2-deoxy-D-glucose (2-DG) evokes an increase in the efferent discharge rate of the adrenal nerve in narcotized rats and rabbits. The study reported here was undertaken to determine the sympathetic nerves and blood pressure responses to i.v. 2-DG administration in awake SHR rats. An increase in adrenal sympathetic nerve activity (adrSNA) by 63% was observed 15 min after 125 mg/kg 2-DG administration, but there were no changes in the renal sympathetic nerve activity (renSNA), blood pressure (BP) or the heart rate (HR). Additional administration of 375 mg/kg 2-DG (cumulative dose was 500 mg/kg) led to the increase in the adrSNA by more then 120%, and in BP by 20 mm Hg, whereas renSNA was increased only by 30%. These results indicate that 2-DG-induced neuroglycopenia evokes highly differential changes in adrenal and renSNA in awake SHR rats. Whether this explains the marked response in BP in SHR to 2-DG is to be established.

Adrenal Glands↗

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 sympathetic nerve activity during morphine abstinence in the rat.

The aim of the study was to examine sympathetic nerve activity, heart rate and blood pressure during naloxone-precipitated withdrawal reactions in morphine-dependent rats. In two groups of rats, one group conscious and the other anaesthetized with chloralose, renal sympathetic nerve activity (rSNA), heart rate (HR) and mean arterial blood pressure (MAP) were recorded before and during naloxone-precipitated abstinence. The conscious rats showed a biphasic pattern in the withdrawal responses. Initially, after small doses of naloxone, rSNA and HR increased and increased somatomotor activity including 'wet-dog' shakes were observed. However, upon further administration of naloxone, rSNA and HR promptly decreased while MAP increased. As rSNA was lowered, the withdrawal behaviour of the rats was markedly diminished and the animals rested calmly in the cages. In contrast, the anaesthetized group reacted with an immediate decrease in rSNA after the lowest dose of naloxone, followed by an increase in MAP and HR after higher doses of naloxone, although rSNA was still decreased. In both groups, rSNA remained below pre-naloxone control levels when the increased MAP was lowered to the pre-naloxone level with sodium nitroprusside, indicating a central origin of the sympathetic inhibition. It is concluded that naloxone elicits a biphasic rSNA response in the conscious, morphine-dependent rat. This includes an initial increase upon low naloxone doses followed by a pronounced inhibition of rSNA after higher doses. In chloralose-anaesthetized rats, rSNA declined already after low doses of naloxone. It is suggested that there might be a tonic, excitatory input on rSNA, mediated by the activation of opiate receptors by high levels of circulating morphine in the addicted animal. Naloxone will therefore decrease the tonic sympathetic nerve activity in these rats.

Animals↗

PubMed1975

Alteration of warfarin kinetics in man associated with exposure to an operating-room environment.

The plasma half-life of warfarin (mean +/- SE) in five normal, nonmedicated control subjects given a single 40 mg/m2 oral dose of warfarin was 38.8 +/- 4.1 hours. It was essentially the same (37.7 +/- 2.6 hours) in these subjects when determined again four months later. The effect of the single dose of warfarin on prothrombin complex activity (prothrombin response) was determined by calculating the area under the curve obtained by plotting prothrombin time (seconds) versus time after the warfarin dose (hours). The prothrombin response in control subjects was 1670 +/- 64 sec-hr initially and essentially the same at the end of the four-month interval (1730 +/- 96 sec-hr). Plasma warfarin half-life and prothrombin response in seven anesthesiology residents were 32.1 +/- 3.6 hours and 1337 +/- 78 sec-hr at the start of their training period, i.e., before working in the operating room. Four months later, their plasma warfarin half-lives were significantly prolonged (49.3 +/- 4.8 hours) and the prothrombin responses were significantly greater (1552 +/- 22 sec-hr) compared with their initial values. The alteration of warfarin kinetics appeared to be due mainly to inhibition of warfarin metabolism, presumably related to the repeated exposure of these subjects to an operating room environment.

Administration, Oral↗

PubMed1974