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Biomedical subjects

M Delle

Publications and source records attributed to M Delle.

At least 19 recordsLinked to original sources
PubMed2006

Remodeling of the thoracic aorta after stent grafting of type B dissection: a Swedish multicenter study.

AIM: Endovascular repair of complicated type B dissections has evolved as a promising alternative to open repair. Previous studies have indicated that continued false lumen flow is a predictor of continued aortic dilatation and risk of rupture during follow-up. This multicenter study was conducted to analyze the postoperative changes of the false lumen after endografting of complicated type B dissections. METHODS: All patients treated with endovascular stent grafts for thoracic type B dissections at 5 major Vascular Centers in Sweden were identified through local databases. Review of charts and all available pre- and postoperative CT scans were performed to identify demographics, indications for repair as well as postoperative changes of the aorta and false lumen. RESULTS: A total of 129 patients treated for type B dissections between 1994 and December 2005 were identified. Median radiological follow-up was 14 months. Fourteen patients died perioperatively leaving 115 patients available for analysis. Seventy-four of these had CT imaging of sufficient quality for morphological analysis. The vast majority of acute patients were treated for rupture or end-organ ischemia whereas most chronic patients were treated for asymptomatic aneurysms. In 80% of patients, the false lumen thrombosed along the stent graft but it remained perfused distal to the stent graft fixation in 50% of patients. Only 5% of patients presented with aortic enlargement of the stent grafted area when adequate proximal sealing was achieved. The distal, uncovered aorta displayed expansion in 16% of patients. CONCLUSIONS: The stent grafted thoracic aorta after type B dissection appears to be stabilized by covering the primary entry site with a stent graft in the majority of both acute and chronic dissections. The uncovered portion of the aorta distal to the stent graft, however, remains at risk of continuous dilatation. Stent grafting for complicated type B thoracic dissections seems to be a treatment option with reasonable morbidity and mortality even though the incidence of severe complications is still significant.

Adult↗
PubMed2002

Treatment of femoral pseudoaneurysms. Percutaneous US-guided thrombin injection versus US-guided compression.

PURPOSE: Thrombin injection in femoral pseudoaneurysms has been suggested to be superior to traditional US-guided compression. Our aim was to evaluate results with compression therapy with special reference to use of thrombin in case of failure. We also studied 7 patients who underwent primary thrombin injection. MATERIAL AND METHODS: We retrospectively reviewed all (n=44) femoral artery pseudoaneurysms diagnosed at our department during October 1998-May 1999. US-guided compression with the Femostop device or US-guided thrombin injection (100-1000 IU) was the first choice according to the physicians' preference, followed by the other regime if the first choice was non-successful. RESULTS: Thirty-nine (89%) of the patients received anticoagulation treatment and/or concomitant antiplatelet drugs. Out of the 44 patients, 37 were treated with compression as the first choice. This regime was successful in 22 (59%). This group included 2 lesions that resolved spontaneously after initially failed compression and 1 deep venous thrombosis after treatment. The persistent 15 pseudoaneurysms after failed compression received thrombin injection, and it was also the primary therapy in 7 patients. Complete thrombosis within the pseudoaneurysm was immediately induced after treatment. One early recurrence required a second injection. No complication of thrombin was noted and no surgery was required. CONCLUSION: US-guided thrombin injection is an effective treatment for embolisation of pseudoaneurysms. The technique is superior to compression therapy.

Aged↗
PubMed2001

Esomeprazole 20 mg maintains symptom control in endoscopy-negative gastro-oesophageal reflux disease: a controlled trial of 'on-demand' therapy for 6 months.

BACKGROUND: Most patients with gastro-oesophageal reflux disease (GERD), regardless of endoscopic status, suffer symptomatic relapse within 6 months of stopping acid suppressant therapy. AIM: To assess the efficacy of 'on-demand' treatment of GERD with esomeprazole, the first proton pump inhibitor developed as an optical isomer. METHODS: In this multicentre, double-blind study, 342 endoscopy-negative GERD patients demonstrating complete resolution of heartburn during the final week of a 4-week treatment period with esomeprazole 20 mg or omeprazole 20 mg once daily were randomized to receive esomeprazole 20 mg or placebo on demand (maximum of one dose per day) for a further 6 months. Use of rescue antacids was permitted. RESULTS: All 342 patients (191 males), aged 19-79 (mean 49) years, were evaluable in the intention-to-treat analysis. The proportion of patients who discontinued treatment due to insufficient control of heartburn was significantly higher among placebo compared to esomeprazole recipients (51% vs. 14%; P < 0.0001). Patients randomized to esomeprazole on-demand therapy remained in the study longer than those in the placebo group (mean 165 vs. 119 days). Over 50% took the study medication for periods of 1--3 consecutive days (esomeprazole) or 4--13 consecutive days (placebo). Use of antacids was > 2-fold higher among placebo recipients. The frequency of adverse events was similar in the two groups, when adjusted for time spent in the study, as were the clinical laboratory profiles. CONCLUSIONS: On-demand therapy with esomeprazole 20 mg is effective and well tolerated in maintaining symptom control in endoscopy-negative GERD.

Administration, Oral↗
PubMed2001

Aneurysm sac hygroma: a cause of endotension.

PURPOSE: To describe a new pathophysiological mechanism for endotension. CASE REPORTS: Four patients developed aneurysm sac expansion after repair of abdominal aortic aneurysms, one with a conventional polytetrafluoroethylene (PTFE) graft and the others with a variety of commercially made endografts (2 PTFE, 1 Dacron). Pressures within the sacs were nonpulsatile and approximately half the systemic blood pressure. Attenuation on computed tomography (CT) was significantly less in the sac than in the graft in 3 of the patients. A clear, highly viscous fluid was aspirated from all 4 sacs, supporting the diagnosis of aneurysm sac hygroma. Prominent local hyperfibrinolysis in the sac was combined with signs of local coagulation activation. CONCLUSIONS: A new mechanism for continued sac expansion based on aneurysm sac hygroma is proposed. Measurement of attenuation may be of diagnostic value. It is further proposed that local hyperfibrinolysis/coagulation may promote rebleeding, liquefaction, and continued expansion analogous to the chronic subdural hematoma.

Aged↗
PubMed1996

Differential responses in adrenal and renal nerves to CNS osmotic stimulation.

Hypertonic solutions act in the central nervous system (CNS) to increase mean arterial blood pressure (MAP) by activation of the sympathoadrenal axis. However, adrenal nerve activity (pre- and postganglionic nerve fibers) has not been determined during central osmotic stimulation. Therefore, these experiments evaluated adrenal (AdSNA) and renal (RSNA) sympathetic nerve activity, MAP, and heart rate (HR) following CNS administration of isotonic, hypertonic, and hypotonic sodium chloride solutions in chloralose-anesthetized rats. Injection of isotonic saline (5 microliters) did not alter MAP, HR, RSNA, or AdSNA. However, injection of hypertonic saline (5 microliters of 0.5 M) into the anteroventral portion of the third cerebral ventricle increased MAP (12 +/- 2 mmHg) and decreased HR (16 +/- 6 bpm). In addition, hypertonic saline significantly decreased RSNA (58 +/- 5% control), whereas AdSNA increased (158 +/- 10% control). Injection of hypotonic (5 microliters of 0.05 M) NaCl produced the opposite responses in RSNA (119 +/- 7% control) and AdSNA (86 +/- 5% control) and had no significant effect on MAP or HR. Furthermore, pre- and postganglionic adrenal nerve fibers responded similarly to changes in CNS osmolality. These results demonstrate that osmotic stimulation produces differential responses in RSNA and AdSNA, but not in pre- and postganglionic adrenal nerve fibers.

Adrenal Medulla↗
PubMed1996

The effects of hexamethonium on cerebral blood flow and cerebral function during relative cerebral ischaemia in rats.

Cerebral blood flow in either the cortex, thalamic region or the brain stem, as well as somatosensory evoked potentials were measured in a model of moderate cerebral ischaemia in three groups of anaesthetized spontaneously hypertensive rats. The rats were bled to reduce evoked potential amplitudes to approximately 50-60% of pre-haemorrhage control. The consequent blood pressure fall reduced blood flow to approximately 65, 80 and 85% of pre-haemorrhage control in the cortical, thalamic and brain stem regions, respectively, as measured with a laser Doppler flowmeter. Hexamethonium (10 mg kg-1 i.v.), an autonomic ganglion blocker, caused vasodilation and a slight (7-13 units of prebleeding control) increase in blood flow in all the three regions, and the somatosensory evoked potentials normalized. In addition, the latency of the first evoked potential component decreased toward prebleeding values. Heart rate decreased and a transient decrease was also observed in mean arterial pressure despite an attempt to keep it constant with a pressure regulating reservoir. It is possible that the slightly increased regional cerebral blood flow after hexamethonium injection can explain the improved cerebral function as indicated by the enhanced somatosensory evoked potentials. However, the results might also indicate an autonomic regulation of afferent sensory pathways.

Animals↗
PubMed1992

Reflex changes in post- and preganglionic sympathetic adrenal nerve activity and postganglionic sympathetic renal nerve activity upon arterial baroreceptor activation and during severe haemorrhage in the rat.

The aim of the study was to compare pre- (pre-aSNA) and postganglionic adrenal sympathetic nerve activity (post-aSNA) and postganglionic renal sympathetic nerve activity (rSNA) in rats during arterial baroreceptor activation and haemorrhage. Adrenal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar rats. To test for pre-aSNA or post-aSNA in adrenal nerves, a ganglionic blocker, trimethaphan (10 mg kg-1), was administered i.v. If the nerve activity in the adrenal nerve decreased or increased the nerve was considered to contain predominantly post- or preganglionic fibres, respectively. In contrast, the renal nerves exhibit an almost pure postganglionic activity. Baroreceptor activity was tested by activation of baroreceptors, with an alpha-receptor agonist, phenylephrine, which was slowly infused (0.5-2 micrograms kg-1 min-1), and to deactivate the baroreceptors the rats were bled down to 50 mmHg for 8 min. The experiments showed that all tested nerve types were baroreceptor dependent. There were no significant differences between the slopes relating nerve activity inhibition to increase in blood pressure (infusion of phenylephrine). During maximal inhibition there was a difference between the rSNA and pre-aSNA, 87 +/- 4%, n = 6, and 68 +/- 6%, n = 10 (P less than 0.01) of the control value, respectively. The maximal inhibition of post-aSNA was 80 +/- 3%, n = 7, of the control value. During haemorrhage there was a difference between the nerve populations. Pre-aSNA responded with a marked increase within 1.5 min (159 +/- 29% of control, n = 7) and was then maintained at that level until retransfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1992

Differential responses in post- and pre-ganglionic adrenal sympathetic nerve activity and renal sympathetic nerve activity after injection of 2-deoxy-D-glucose and insulin in rats.

The aim of the study was to compare pre-ganglionic adrenal nerve activity (pre-aSNA) to post-ganglionic adrenal nerve activity (post-aSNA) in rats after administration of 2-deoxy-D-glucose (2-DG, 500 mg kg-1, i.v.), which mimicks a central hypoglycaemia or to the response in pre-aSNA and post-aSNA to hypoglycaemia after injection of insulin (5U). Renal postganglionic sympathetic nerve recordings (rSNA) in a separate group was used as a reference. Adrenal or renal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar-rats. Trimethaphan, a short-lasting ganglionic blocker, was administered i.v. (10 mg kg-1) in order to test for pre- or post-aSNA in the adrenal nerves. The adrenal nerves was considered to contain predominantly post or preganglionic fibres, respectively if the nerve activity in the adrenal nerve decreased (post-aSNA) or increased (pre-aSNA). In contrast, all renal nerves showed almost a pure postganglionic activity. Post-aSNA responded with a tendency to increase after the 2-DG injection. The highest value (percentage change from control) 5 min after injection was 12 +/- 9%. The pre-aSNA increased with values of 99 +/- 52% at 3 min and 86 +/- 31% at 5 min (percentage change from control). The activity in the rSNA was only slightly decreased after the injection of 2-DG when compared to pre-drug control activity. There was a significant difference between the pre-aSNA vs. post-aSNA at 1 min (P less than 0.05), 3 min (P less than 0.01) and 5 min (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1990

Electrical stimulation of the gastrocnemius muscle in the spontaneously hypertensive rat increases the pain threshold: role of different serotonergic receptors.

In a previous study, prolonged low-frequency muscle stimulation in the hind leg of the fully conscious spontaneously hypertensive rat (SHR) was shown to induce a long-lasting reduction of blood pressure. It was also shown that opioid and serotonergic (5-HT) systems were involved. More recently, we have shown that the 5-HT1 receptors are involved in the post-stimulatory decrease in blood pressure. In the present study, the influence of this type of muscle stimulation on the pain threshold was investigated. Pain perception was measured as the squeak threshold to noxious electric pulses. After cessation of the stimulation, an analgesic response was elicited within 60 min and peak analgesia developed after 120 min, being 139 +/- 10% (P less than 0.01) of the prestimulatory control value. The increased pain threshold lasted for another 2 h. One group of SHR was pretreated with PCPA, a serotonin synthesis blocker, which completely abolished the post-stimulatory analgesia. To analyse further the involvement of different serotonin systems, drugs with selective affinity for 5-HT receptors were used. In one group a prestimulatory dose of metitepine maleate (a 5-HT1&2 receptor antagonist) abolished the post-stimulatory elevation of the pain threshold. The prolonged analgesic response was still present after prestimulatory treatment with ritanserin or ICS 205-930 (5-HT2 and 5-HT3 blocking agents respectively). In another group of experiments, the serotonin receptor antagonists were administered post-stimulation to animals with fully elicited analgesia. None of the antagonists used could reverse the elevation of pain threshold towards prestimulatory levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed1990

Vascular adrenergic responses in morphine-dependent rats.

The circulatory effects of morphine abstinence have recently been found to involve decreased renal sympathetic nerve activity and increased mean arterial pressure, induced by vasoconstriction. A direct influence of morphine withdrawal on the peripheral vasculature could possibly contribute to the increased resistance. Therefore, contractile responses to transmural nerve stimulation and to applied noradrenaline of peripheral arteries from morphine-dependent and untreated rats were examined in vitro under paired conditions. No increase in contractile response was observed after chronic morphine treatment, either on nerve stimulation or on applied noradrenaline. Instead the smooth muscle sensitivity to adrenergic stimulation was reduced. Consequently, the present study does not support a peripheral adrenergic origin of the vasoconstriction during naloxone-precipitated morphine abstinence.

Animals↗
PubMed1990

Role of opioid receptors in the long-lasting blood pressure depression after electric muscle stimulation in the hind leg of the rat.

In a previous study, electrically induced contractions of the gastrocnemius muscle in conscious spontaneously hypertensive rats were shown to induce a blood pressure reduction of 15-20 mmHg lasting several hours. We showed in that study that endogenous opioid systems were involved. In this study, drugs with selective affinity for different opioid receptors were used to analyse further the involvement of endogenous opioid systems in the post-stimulatory drop in blood pressure in spontaneously hypertensive rats. Prestimulatory intracerebroventricular administration of beta-FNA (a mu-receptor antagonist) did not significantly influence the response at all, nor did a lower intravenous dose of naloxone reverse the post-stimulatory drop in blood pressure. High-dose naloxone (15 mg kg-1) increased post-stimulatory blood pressure by around 10 mmHg. About 50% of the drop thus remained after this treatment. A similar, partial reversal of the decreased blood pressure was seen after intravenous administration of a delta-receptor antagonist, ICI 154,129. However, the depressor response was completely reversed by a low intravenous dose of MR 2266 BS (a kappa-receptor antagonist). These results suggest that the reduction in blood pressure after muscle stimulation is mainly mediated by the opioid kappa-receptor. A certain involvement of the delta-receptor is also indicated.

Animals↗
PubMed1990

Neurophysiological evidence for and characterization of the post-ganglionic innervation of the adrenal gland in the rat.

The aim of this study was to examine and characterize the post-ganglionic innervation of the adrenal gland, using a neurophysiological nerve recording technique. Adrenal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar rats. To test for post-ganglionic nerve activity, trimethaphan, a ganglionic blocker, was given intravenously. About 60% of the adrenal nerve preparations tested responded with a marked decrease in nerve activity (to 52 +/- 11% of pre-trimethaphan activity, P less than 0.01), while other nerves responded with an increase in activity (to 152 +/- 29% of pre-trimethaphan activity, P less than 0.01). Based on these responses, the nerves were considered to contain predominantly post- or preganglionic fibres respectively, and the difference in response to an intravenous injection of trimethaphan between the two groups was significant (P less than 0.01). It was also demonstrated that the post-ganglionic adrenal nerve activity had a greater variability in firing pattern than preganglionic adrenal nerve activity. We also examined whether there was any cardiac rhythmicity in the investigated nerves. There was a weak cardiac rhythmicity in six out of 12 post-ganglionic adrenal nerves, but there was no cardiac rhythmicity in the remaining six post-ganglionic nerves, and we observed no cardiac rhythmicity in preganglionic nerves. In contrast, renal sympathetic nerves showed a profound cardiac rhythmicity. Our results might explain recent histological findings of a direct post-ganglionic innervation of the adrenal cortex. We speculate that this nerve population is involved in steroid synthesis indirectly via regulation of the cortical blood flow or directly via a direct innervation of parenchymal cells in the adrenal cortex.

Adrenal Glands↗
PubMed1990

Differentiated responses of renal and adrenal sympathetic nerve activity to intravenous morphine administration in anesthetized rats.

The aim of this study was to examine the effect of i.v. morphine on sympathetic nerve activity (SNA) in the rat. Adrenal SNA and renal SNA were recorded simultaneously, together with mean arterial pressure and heart rate, in chloralose-anesthetized, artificially ventilated rats. Separate groups of rats were subjected to vagotomy. In intact rats, i.v. injection of morphine (1 mg/kg) caused an immediate transient depressor response. Within 1-3 sec, renal SNA was markedly inhibited in parallel with hypotension and bradycardia. After a few minutes, mean arterial pressure and renal SNA returned toward base-line levels, and subsequently they declined gradually again below base line. Adrenal SNA, however, showed an immediate brief increase. In the vagotomized rats, an extended renal SNA excitation occurred, accompanied by a rise in mean arterial pressure. After about 15 min, these variables returned toward base-line levels. The adrenal SNA excitation still occurred in the vagotomized rats. The renal depressor and the renal and adrenal pressor responses were all abolished by naloxone pretreatment. It is concluded that i.v. injection of morphine induces a highly differentiated response of SNA. A pronounced immediate increase in adrenal SNA occurs in parallel with renal SNA inhibition. The renal nerve inhibition is mainly reflexly obtained by opioid receptor-mediated activation of vagal afferents. The predominant central action of morphine seems to be sympathetic excitation which is also mediated through opioid receptors.

Animals↗
PubMed1990

Regional changes in sympathetic nerve activity and baroreceptor reflex function and arterial plasma levels of catecholamines, renin and vasopressin during naloxone-precipitated morphine withdrawal in rats.

The aim of the study was to examine regional changes in sympathetic nerve activity (SNA) and baroreceptor function and arterial plasma catecholamines, arginine vasopressin (AVP) and plasma renin activity during morphine withdrawal in chloralose-anesthetized rats. Dependence was induced by s.c. morphine base pellets. Adrenal, renal and splanchnic SNA and SNA from the lumbar sympathetic chain were recorded before and after i.v. injections of naloxone. Baroreceptor function was examined with phenylephrine-induced increases in mean arterial pressure. In separate experiments, arterial plasma norepinephrine, epinephrine, dopamine, plasma renin activity and AVP were measured before and after naloxone-precipitated withdrawal. Naloxone administration elicited an increase in mean arterial pressure and heart rate. Although renal SNA was inhibited by approximately 50%, adrenal SNA and lumbar SNA increased by approximately 400 and 80%, respectively. Splanchnic SNA did not change significantly. The baroreceptor-mediated inhibition of adrenal SNA was facilitated while that for renal SNA was attenuated. The arterial plasma level of norepinephrine was doubled and epinephrine increased almost 20-fold. AVP increased about 15-fold, whereas plasma renin activity showed only a minor increase after naloxone. This study shows that a marked differentiation of the SNA response occurs during morphine withdrawal in rats, which suggests an interaction between opioid receptors and the control of regional sympathetic output. Furthermore, large amounts of AVP and epinephrine are released, which probably contribute to the cardiovascular changes seen in the withdrawal phase.

Animals↗
PubMed1989

The effects of naloxone on cerebral blood flow and cerebral function during relative cerebral ischemia.

CBF and somatosensory evoked potentials (SEPs) were measured in a model of moderate cerebral ischemia in anesthetized spontaneously hypertensive rats. The rats were bled to reduce SEP amplitudes to about 50% of prebleeding control. The consequent blood pressure fall reduced CBF to 77% of control as measured by the laser-Doppler technique. Naloxone (5 mg kg-1 i.v. plus 25 mg kg-1 h-1 i.v. for 30 min) caused a significant increase in SEP amplitudes, while CBF did not change significantly. In addition, the latency of the first SEP component decreased toward prebleeding values. Heart rate (HR) decreased, but MABP was held constant by a pressure-regulating reservoir. In unbled rats, naloxone (5 mg kg-1 i.v.) caused a transient small increase in MABP and SEP amplitudes and decrease in HR. These results indicate that sensory input is regulated by opioid systems. Increased opioid activity may inhibit ascending sensory pathways during relative cerebral ischemia and thereby depress SEP responses. Thus, naloxone can release this inhibition and enhances SEP independently of CBF during relative cerebral ischemia. Similar mechanisms might explain the apparently beneficial effects of naloxone in some stroke models.

Animals↗
PubMed1989

The opiate antagonist naloxone counteracts the inhibition of sympathetic nerve activity caused by halothane anesthesia in rats.

The study was undertaken to examine if endogenous opioid systems mediate the response of the sympathetic nervous system to halothane anesthesia. Steady state values of renal sympathetic nerve activity (rSNA), mean arterial pressure (MAP), and heart rate (HR) were continuously recorded in the conscious state and at three depths of halothane anesthesia (0.6%, 1.2%, and 2.4%) in rats. Halothane caused an inhibition of rSNA and hypotension and a decrease in HR at the three halothane concentrations. Repeated bolus doses of the opiate antagonist (-)naloxone given iv during 1.2% halothane anesthesia did not significantly increase any of the variables. However, pretreatment with (-)naloxone (2 or 15 mg.kg-1) induced an increase in rSNA at 0.6% halothane, and subsequently the rSNA inhibition was less pronounced at the two higher halothane concentrations compared with control. HR showed a similar pattern, whereas the hypotension was essentially unaffected. Pretreatment with the pharmacologically inactive compound (+)naloxone had no effect on the halothane-induced depression of rSNA. The ED50 halothane concentration concerning nociceptive aversive behavior was not significantly changed with (-)naloxone pretreatment (2 mg.kg-1). In order to determine if sympathoinhibitory bulbospinal serotonin pathways are activated during halothane anesthesia, rSNA, MAP, and HR were recorded in rats pretreated with the serotonin synthesis inhibitor parachlorophenylalanine (PCPA). However, PCPA pretreatment did not affect the rSNA response to halothane compared with control. These findings indicate that the halothane-induced inhibition of rSNA might partially result from a stereospecific activation of opioid receptors, whereas halothane analgesia does not seem to be mediated by opioid mechanisms.

Anesthesia, Inhalation↗
PubMed1989

[Differentiated changes in the activity of the sympathetic nerves induced by glycopenia in spontaneously hypertensive rats].

2-deoxy-D-glucose (2-DG) evokes an increase in the efferent discharge rate of the adrenal nerve in anesthetized rats and rabbits. A 63% increase in adrenal sympathetic nerve activity (adrSNA) occurred within 15 min after 125 mg/kg 2-DG administration in alert animals, no changes being revealed 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 500 mg/kg) led to an over 120% increase in the adrSNA and the 20 mm Hg increase in the BP, whereas renSNA only increased by 30%. These results indicate that 2-DG-induced neuroglycopenia evokes highly differential changes in adrenal and renSNA in alert SHR rats. Whether this explains an obvious response of the BP in SHR to 2-DG, remains to be determined.

Adrenal Glands↗