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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular responses during a graded lower body negative pressure (LBNP) protocol were compared before and after atropine and propranolol administration to test the hypothesis that both sympathetic and parasympathetic control of cardio-acceleration are associated with syncopal predisposition to orthostatic stress in healthy subjects. Eleven men were categorized into two groups having high (HT, N = 6) or low (LT, N = 5) tolerance based on their total time before the onset of presyncopal symptoms. HT and LT groups were similar in physical characteristics, fitness, and baseline cardiovascular measurements. Atropine treatment had no effect on LBNP tolerance or mean arterial pressure at presyncope, despite an atropine-induced increase in heart rate. Propranolol treatment reduced (p<0.05) LBNP tolerance in both groups. Diminished LBNP tolerance after propranolol administration was associated with reductions in cardiac output, whereas increase in systemic peripheral resistance from baseline to presyncope was unaffected by propranolol. Reduction in cardiac output and LBNP tolerance after beta blockade reflected a chronotropic effect because lower LBNP tolerance for the HT (-50%) and LT (-39%) groups was associated with dramatic reductions (p <0.05) in the magnitude of LBNP-induced tachycardia without significant effects on stroke volume at presyncope. Absence of an atropine-induced difference in cardiac output and systemic peripheral resistance between HT and LT groups failed to support the notion that cardiac vagal withdrawal represents a predominant mechanism that could account for differences in orthostatic tolerance. Because a reduction in LBNP tolerance in both HT and LT groups after propranolol treatment was most closely associated with reduced tachycardia, the data suggest that a primary autonomically mediated mechanism for maintenance of mean arterial pressure and orthostatic tolerance in healthy subjects is beta adrenergic-induced tachycardia.
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PMID:Effects of cholinergic and beta-adrenergic blockade on orthostatic tolerance in healthy subjects. 1132 87

A 14monthold female beagle had ventricular preexcitation (VP).The finding was characterized by a wide positive QRS complex with a tall notched R wave in leads I, II, III, and aVF, an inverted QRS complex in leads aVR and aVL, a Q wave in lead I, and a short PR interval. Compression of the carotid sinus caused an anticipated marked decrease in heart rate, but did not reveal latent electrocardiographic abnormalities. We did not detect evidence of ventricular hypertrophy during echocardiography. Examination of the M-mode image indicated abnormal movements of the septum. There were 2 sharp waves at each systole instead of a single wider wave that is seen for clinically normal dogs. To further characterize this ECG finding, the affected dog and 2 clinically normal female beagles (positive control dogs) were given atropine (0.025 mg/kg of body weight, i. v.) Increases in heart rate, relative to values obtained before atropine administration, were evident in all 3 dogs. Increase in heart rate in the dog with VP appeared sooner after injection than in the clinically normal dogs; it was evident at the conclusion of the atropine injection. When the increase in heart rate was maximal in the affected dog (3 min after atropine administration), notching of the R wave disappeared, and the QRS duration decreased to about 60 ms. Echocardiographically, atropine produced a decrease in end diastolic, end systolic and stroke volumes in all treated dogs, which was similar between clinically normal dogs and the dog with VP. Atropine administration also was associated with a decrease in the percentage of thickening of the septum in the dog with VP, but not in the clinically normal dogs. We did not detect histopathologic abnormalities in the heart of the dog with VP.
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PMID:Type B Ventricular Preexcitation With Abnormal Contraction of the Ventricular Septum in a Dog. 1245 38

Forty three children ranged from 1 yr. to 6 yr. were randomly assigned to non-atropinized group (n = 20; A(-)) and atropinized group (0.015 mg.kg(-1) i.m., n = 23; A(+)). Control hemodynamics were measured under 0.5% halothane and 67% nitrous oxide and 33% oxygen for three minutes, and then halothane was increased to 2.5% and maintained for 15 min. In the A(-) group, stroke volume (SV) decreased to 64%, heart rate (HR) increased from 100/min to 111/min, and blood pressure (BP) decreased from 65 mmHg to 62 mmHg. Skin blood flow (SBF) concomitantly measured by a laser doppler flowmeter decreased to 48% and total peripheral resistance (TPR) increased to 128%. In the A(+) group, HR increased from 117/min to 132/min ( P < 0.05, vs. A(-) group), BP decreased from 67 mmHg to 66 mmHg. SV decreased to 71% ( P < 0.05, vs. A(-) group). Changes in SBF and TPR were 68% and 128% respectively. End-expired halothane concentration in the A(+) group increased slower than in the A(-) group but not significantly. The results indicate increased sympathetic tone would work as a compensating mechanism for decreased SV and CO. Atropine premedication attenuated cardiovascular depression by maintaining HR and possibly by delaying induction speed of anesthesia. In conclusion, halotane-nitrous oxide anesthesia decreased SV without a marked decrease in heart rate and blood pressure in children. This decrease in SV and BP was attenuated by atropine premedication.
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PMID:Hemodynamic responses during induction of anesthesia with halothane-nitrous oxide in children with or without atropine premedication. 1527 85

Hypoxia and increased temperature alter venous blood pressures in teleosts through active changes in venous tone. Elasmobranchs possess a capacious venous system but have limited adrenergic vascular innervation and subambient central venous pressure (P(cv)). In this study, we explored venous hemodynamic responses to acute temperature increase and moderate (6.9 kPa) and severe (2.5 kPa) hypoxia in the dogfish (Squalus acanthias). Normoxic dogfish at 10 degrees C had a P(cv) between -0.08 and -0.04 kPa and a mean circulatory filling pressure (P(mcf)) of approximately 0.12 kPa. At 16 degrees C, heart rate (f(H)), cardiac output (Q), and P(mcf) increased but P(cv) and plasma epinephrine and norepinephrine levels were unchanged. In contrast, moderate and severe hypoxia increased P(cv) and decreased Q and stroke volume (V(S)). f(H) decreased in severe hypoxia, whereas P(mcf) was unaffected despite elevated catecholamine levels. Atropine abolished hypoxic reductions in Q, V(S), and f(H), but P(cv) still increased. In contrast to the response in teleosts, this study on dogfish suggests that venous capacitance changes associated with warming and hypoxia are minimal and likely not mediated by circulating catecholamines. Thus hemodynamic status of the capacious elasmobranch venous circulation is potentially regulated by blood volume shifts from passive flow-mediated events and possibly through myogenic mechanisms.
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PMID:The role of venous capacitance, circulating catecholamines, and heart rate in the hemodynamic response to increased temperature and hypoxia in the dogfish. 1917 85

Results showed that autonomic nervous system (ANS) and blood circulation system (BCS) dysfunction in 3rd trimester pregnant women with gestosis are more pronounced, than in healthy pregnant women, despite the prescribed treatment. The most significant disturbances were vagotonia and hypokinetic haemodynamics type (often iatrogenic). Spinal anaesthesia (SA) during Cesarean section in pregnant women is accompanied by blood pressure decrease to the level demanding on vasopressors use. Considering normal indicators of SI, CI, oxygen transportation and electrocardiogram vasopressor was not introduced Apgar score assessment of newborns was within normal. However, vagotonia and hypokinetic haemodynamics type during anaesthesia that certifies autoregulation reserves insufficiency. Atropine introduction in pregnant women with vagotonia and hypokinetic haemodynamics type (often iatrogenic, owing to irrational therapy) before SA beginning of promoted neurovegetative inhibition optimization and haemodynamics stabilization in eukinetic range. Vagus blockade (elimination of ANS dysfunction) was accompanied by more physiologic sympathicotonia development with smaller decrease of blood pressure (without stroke index reduction!), absence of bradycardia and vomiting. Research showed that the blood pressure cannot be the only objective criterion of vasopressors use.
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PMID:[Neuro-autonomic inhibition and haemodynamics management optimization during cesarean section under spinal anaesthesia in pregnant women with gestosis]. 2366 21

Emodin, an active anthraquinone constituent isolated from the rhubarb, a traditional Chinese herbal medicine which is widely used in clinical treatment, has cardiovascular protective properties. However, it remains unclear whether the cardiovascular protective actions of emodin are related to an activation of cardiac natriuretic hormone secretion. The purpose of the present study was to explore the effect of emodin on the secretion of ANP, a member of the family of cardiac natriuretic hormones, and its mechanisms involved. Experiments were performed in isolated perfused beating rabbit atria allowing measurement of ANP secretion, atrial pulse pressure, and stroke volume. Emodin increased ANP secretion concomitantly with a decrease in atrial pulse pressure and stroke volume in a concentration-dependent manner. These effects were reversible. Inhibition of K(+) channels with tetraethylammonium and glibenclamide attenuated the emodin-induced changes in ANP secretion and atrial dynamics. Furthermore, the emodin-induced changes in ANP secretion and atrial dynamics were attenuated by inhibition of L-type Ca(2+) channels with nifedipine. Atropine, methoctramine, tertiapin-Q, and pertussis toxin had no significant effect on the emodin-induced changes in ANP secretion and mechanical dynamics. The present study demonstrates that emodin increases ANP secretion via inhibition of L-type Ca(2+) channels through an activation of K(+)ATP channel in isolated beating rabbit atria. The results also provide a rationale for the use of emodin in the treatment of impairment of the regulation of the cardiovascular homeostasis.
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PMID:Emodin accentuates atrial natriuretic peptide secretion in cardiac atria. 2475 13

FOLFIRINOX is a standard chemotherapeutic regimen for patients with advanced pancreatic cancer who have a good performance status. In this study, we present the case of a 64-year-old male who developed dysarthria following FOLFIRINOX treatment, and review all four cases of dysarthria encountered among the nine patients who received this treatment in our hospital. In all cases, dysarthria occurred during the infusion of irinotecan in the first course of treatment, persisted for several hours, and then resolved rapidly without any sequelae. Physical and neurological examinations at the onset of dysarthria revealed no other abnormalities. Imaging studies revealed no abnormal findings. Atropine was prophylactically administered in the second and subsequent courses of treatment and effectively prevented or alleviated dysarthria. This acute neurological symptom is surprising and uncommon in traditional cancer chemotherapy, and medical oncologists may initially suspect the onset of stroke or cerebrovascular disease. However, consistent with our experience, all reported cases resolved completely, with no need for dose reduction or treatment interruption.
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PMID:FOLFIRINOX-induced reversible dysarthria: A case report and review of previous cases. 2662 8


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