Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1,4-Dihydro-2,6-dimethyl-4(3-nitrophenyl)-3,5-pyridine carboxylic acid, 3-ethyl-5-methyl ester (nitrendipine, Bay e 5009) is a new vasodilatory calcium antagonist with pronounced hypertensive efficacy. Doses of 0.3-31.5 mg/kg p.o. lower the blood pressure of rats with spontaneous, renal and desoxycorticosterone acetate (DOCA)-hypertension. Doses of 0.03-10.0 mg/kg p.o. lower the blood pressure of dogs with renal hypertension. The hypotensive effect is about 10 times less in normotensive rats. No increase in tolerance occurred during therapeutic studies lasting 5 weeks in hypertensive rats and several days in hypertensive dogs. There were no signs either of acquired tolerance developing during these studies. Dogs in fentanyl analgesia respond to i.v. administration of 0.001-0.03 mg/kg with a reduction in peripheral vascular resistance and an increase in cardiac output and heart rate. The stroke volume remains unchanged. The vasodilatory effect occurs at different degrees in different vascular beds. The most pronounced increases in vascular flow were measured in the muscular vessels of the hind quarters and in the coronary vessels. The mesenterical, skin and brain blood flows were much less affected.
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PMID:Pharmacological studies of the antihypertensive effect of nitrendipine. 719 97

To assess the effects of i.v. injection of morphine, 0.5 mg/kg, hemodynamic studies were performed on 24 critically ill patients under controlled ventilation. An esophageal balloon was used to estimate intrapleural pressure and transmural cardiac filling pressures were calculated. After injection of morphine, there were significant decreases in heart rate (13%), cardiac index (18%), stroke index (17%) and arterial pressure (15%) and there was a nonsignificant increase in esophageal pressure (15%). Transmural cardiac filling pressures decreased significantly (21% for the pulmonary wedge pressure); intravascular filling pressures were unchanged. Oxygen consumption decreased significantly, by 21%, in 10 patients with initially elevated oxygen consumption and by 9% in 14 patients with initially normal oxygen consumption. The oxygen extraction ratio was unchanged, suggesting that the decrease in oxygen consumption was caused by decreased oxygen demand rather than by inadequate oxygen delivery. These results indicate that the hemodynamic effects of morphine (0.5 mg/kg) administered to critically ill patients were associated with a significant decrease in oxygen consumption, which probably reflected sedation and analgesia.
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PMID:Hemodynamic and metabolic effects of morphine in the critically ill. 723 25

The existence of a posterolateral thalamic relay nucleus for pain and temperature sensation was postulated in 1911, on the basis of the stroke-induced analgesia and thermanaesthesia found paradoxically in patients with thalamic pain syndrome. Pain or temperature sensations can be evoked in humans by electrical stimulation in a vaguely defined region of the posterolateral thalamus. Here we use anterograde tracing and single unit recordings to demonstrate that there is a distinct nucleus in the posterior thalamus of the macaque monkey that receives a dense, topographic input from spinothalamic lamina I neurons and in which almost all neurons are nociceptive- or thermoreceptive-specific. Immunohistochemical staining showed that this nucleus is defined by a dense calbindin-positive fibre plexus in the macaque, so we applied the same staining method to sections of human thalamus. We found a nearly identical fibre plexus localized within a distinct nucleus that is cytoarchitectonically homologous to the lamina I relay nucleus in the macaque thalamus. The stereotaxic coordinates of this nucleus and its location relative to the main somatosensory representation fit clinical descriptions of the pain-producing region in humans. We conclude that this is a specific thalamic nucleus for pain and temperature sensation in both monkey and human.
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PMID:A thalamic nucleus specific for pain and temperature sensation. 780 30

This study characterizes analgesia an hemodynamics after epidural clonidine 8 micrograms/kg (Group C) or clonidine 4 micrograms/kg+morphine 2 mg (Group CM) in comparison to epidural morphine 50 micrograms/kg (Group M). Forty-five patients scheduled for pancreatectomy in combined general/epidural anesthesia were studied. The study drugs were administered 75 min postoperatively and for 10 h pain intensity (visual analog scale [VAS]), heart rate (HR), mean arterial pressure (MAP), and cardiac output (CO) were measured; filling pressures were kept > 5 mm Hg. Adequate analgesia could be achieved within 1 h in all patients of Groups C and CM, but only in six patients of Group M (P < 0.001). Quality of analgesia was comparable in all groups (VAS reduction 82% +/- 20%, mean +/- SD) but duration of analgesic action was longer in Groups CM (586 +/- 217 min) and M (775 +/- 378 min) compared to Group C (336 +/- 119 min) (P < 0.001). In Group M, no hemodynamic alterations occurred. In Groups C and CM, HR, CO, and MAP were reduced significantly compared to baseline within the first 15-90 min, while stroke volume and systemic vascular resistance remained stable. We conclude, that hemodynamic alteration after epidural clonidine under conditions of stable filling pressures is caused mainly by a decrease in HR. It is not an effect of analgesia but of the intrinsic antihypertensive action of clonidine.
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PMID:Analgesic and hemodynamic effects of epidural clonidine, clonidine/morphine, and morphine after pancreatic surgery--a double-blind study. 772 26

The authors analyze the efficacy of midazolam (dormicum, Egys, Hungary) used for induction anesthesia in 35 patients subjected to planned surgery for varicose disease of the lower limbs and on the abdominal organs and in 17 critical patients in intensive care units. To assess the hemodynamics, catheterization of the peripheral and pulmonary arteries was carried out, cardiac output, pressure in cardiac cavities, pulmonary capillary wedging pressure assessed, total peripheral and total pulmonary resistance, cardiac and stroke indexes estimated, gaseous composition of arterial and mixed venous blood analyzed. The drug had virtually no side effects on the function of vital systems of the body. Midazolam fully meets the requirements to drugs used for induction anesthesia and is compatible to such drugs as barbiturates, diazepam, ketamine. The drug can meet pharmacodynamic and pharmacokinetic requirements to sedative agents used in intensive care units, excepting analgesia. However, the need in analgesics and their doses are reduced during sedative therapy with midazolam. Midazolam effects on the lesser circulation hemodynamics permit its use as a sedative agent in patients with respiratory distress syndrome and pulmonary artery thromboembolism; it is also advisable for induction anesthesia in patients operated on for pulmonary artery thromboembolism and in other patients with lesser circulation hypertension.
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PMID:[Clinical experience in the use of dormicum (midazolam) in anesthesiology and intensive care]. 773 88

Efficient analgesia may be the major objective in the cardiovascular risk patient following myocardial infarction, acute occlusion of peripheral vessels, or dissection/perforation of major abdominal vessels. It was the purpose of the study to investigate the haemodynamic and respiratory side effects of eight different opioids in 57 circulatory risk patients prior to major vascular surgery. METHODS. Patients were randomly allocated to eight groups, each receiving a different opioid within a clinical, equipotent dose range (buprenorphine, fentanyl, morphine, nalbuphine, pentazocine, pethidine, tramadol, alfentanil). A complete haemodynamic and blood gas status was obtained prior to as well as 5, 10, 15, and 20 min following opioid administration. Monitoring included a complete invasive haemodynamic and blood gas status. Statistical evaluation was performed by 1- and 2-factorial ANOVA (P < 0.05). RESULTS. Significant time effects (changes from baseline at the time of measurement) were observed for heart rate and total peripheral resistance, while significant group (group-specific differences in the course of values at the different times of measurements) and time effects were noted for mean pulmonary artery pressure, pulmonary capillary wedge pressure, stroke volume index, and PaO2. No major effects were observed following morphine, fentanyl, alfentanil, tramadol, and nalbuphine. Buprenorphine caused distinct respiratory depression accompanied by an increase in pulmonary vascular tone. Pentazocine and pethidine caused a significant increase in MPAP and peripheral vascular resistance while pethidine also produced marked respiratory depression. CONCLUSIONS. For interpretation of the results, factors such as respiratory depression, histamine release, secretion of endogenous catecholamines, and hypoxia-induced pulmonary vasoconstriction have to be discussed. Tramadol, an opioid with moderate potency, seems to offer some advantages due to its minor cardiovascular and respiratory side effects.
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PMID:[Different opioids in patients at cardiovascular risk. Comparison of central and peripheral hemodynamic adverse effects]. 784 Apr 3

Thoracic epidural analgesia combined with chronic beta-adrenergic blocker medication may cause cardiac depression. We investigated the cardiovascular and myocardial metabolic effects of a T1-T12 epidural block in 18 patients (age < 65 yr, ejection fraction > 0.5), receiving chronic beta-adrenergic blocker medication and scheduled for aortocoronary bypass surgery. After randomization into a light or deeper general anesthetic group, the cardiovascular and myocardial metabolic effects of a subsequent general anesthesia induction were investigated. Thoracic epidural analgesia induced a moderate decrease in mean arterial pressure, coronary perfusion pressure, free fatty acids, and myocardial consumption of free fatty acids. General anesthesia with thiopental (2-4 mg/kg) and a low fentanyl dose (5 micrograms/kg) increased heart rate, coronary perfusion pressure, and coronary vascular resistance, whereas mean pulmonary arterial pressure and pulmonary capillary wedge pressure decreased. After thiopental (2-4 mg/kg) and a high fentanyl dose (30 micrograms/kg), mean arterial pressure and left ventricular stroke work index decreased. We conclude that a T1-T12 epidural block in well sedated, beta-adrenergic blocked patients does not induce clinically significant cardiovascular effects. Induction of general anesthesia was well tolerated, but the light general anesthetic could not prevent an increase in heart rate and coronary vascular resistance, whereas the deeper anesthetic induced slight myocardial depression. No effect on the atrioventricular conduction, as measured by the PQ-time, was noted.
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PMID:The influence of thoracic epidural analgesia alone and in combination with general anesthesia on cardiovascular function and myocardial metabolism in patients receiving beta-adrenergic blockers. 810 48

Cardiovascular variables such as heart rate, arterial blood pressure, stroke volume and the shape of electrocardiographic complexes all vary beat-by-beat. This variability occurs because of the dynamic response of cardiovascular regulatory systems to perturbations in cardiovascular function. We applied spectral analysis to the effects of sympathetic vasomotor blockade by epidural analgesia and parasympathetic blockade of the heart by atropine on the beat-to-beat variability of heart rate and blood pressure in humans. High-frequency fluctuations in heart rate (+/- 0.2 Hz) are caused by respiratory induced fluctuations of blood pressure, mediated by the vagus nerve. Low-frequency fluctuations (0.06-0.12 Hz) are related to sympathetic baroreflex control of vasomotor activity and heart rate. In our study, even partial parasympathetic blockade of the heart by atropine decreased the power in the high and low frequency heart rate fluctuations. There were no significant changes in blood pressure fluctuations in either frequency range. Sympathetic blockade by epidural analgesia decreased only low-frequency fluctuations of both heart rate and blood pressure. From a cardiovascular model and our experimental results we support the view that high frequency fluctuations in heart rate are due to the vagal response to blood pressure fluctuations caused by respiration and that the fluctuations around 0.1 Hz in both heart rate and blood pressure have their origin in the sympathetic baroreflex control loop of vasomotor activity.
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PMID:Effects of epidural analgesia and atropine on heart rate and blood pressure variability: implications for the interpretation of beat-to-beat fluctuations. 817 38

A 44-year-old patient, without remarkable medical history, was admitted with a head trauma with initial loss of consciousness and a thoracic trauma. The initial treatment included the insertion of a chest drain for evacuation of a pneumothorax and intrapleural analgesia with bupivacaine. The day after admission, the patient experienced a generalized epileptic crisis, without prodomes. Later, a left proportional hemiplegia with aphasia was recognized. The CT scan obtained immediately after the crisis, as well as the carotid Doppler ultrasonography and echocardiography were normal. The bilateral carotid angiography showed an image of fibromuscular dysplasia of the extracranial segment of the right internal carotid artery. The migration of a carotid thrombus initiated by the trauma was hypothetized. A treatment with a platelet aggregation inhibiting drug was started and associated 20 days later with low molecular weight heparin. The patient recovered a normal motility within 10 days; only the aphasia remained. Trauma of the carotid artery is not a frequent cause of cerebrovascular accident. The occurrence of the latter is favoured by a pre-existing lesion of this artery. This case demonstrates that in a trauma patient not all central nervous system manifestations are initiated by a head trauma.
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PMID:[Post-traumatic hemiplegia in a patient with fibromuscular dysplasia of the carotid artery]. 831 57

Acute myocardial infarction (AMI) recognises no boundaries, and the patient's greatest need occurs at the interface between primary care and hospital system. Ideally, the general practitioner, if summoned, should be able to provide resuscitation, analgesia with opiates, and thrombolytic therapy. Thrombolytics should certainly be given to eligible patients by the general practitioner if an hour could be saved by so doing. Optimising the risk-benefit ratio for thrombolytic therapy given in the community is a challenge to clinical judgement. Experience with this potent treatment is best obtained under a degree of supervision, which could take the form of an audit of the prehospital management of suspected AMI. With prehospital administration of thrombolytic therapy at the first opportunity, the chances of saving a life are better than 1 in 10, while the excess risk of a disabling stroke is about 1 in 1000.
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PMID:Guidelines for general practitioners administering thrombolytics. 853 50


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