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

Acupuncture, needling with electrostimulation, at Tsu San Li (St-36) produced (1) significant decrease in cardiac output, (2) decrease in stroke volume, (3) increase in total peripheral resistance, and (4) minimal changes in heart rate, mean arterial pressure, pulse pressure, and central venous pressure in dogs under halothane anesthesia. Atropine given alone and given before acupuncture at Tsu San Li (St-36) produced (1) early significant increase in cardiac output, (2) early significant increase in heart rate, (3) increase in mean arterial pressure, (4) decrease in total peripheral resistance, and (5) minimal changes in stroke volume, pulse pressure, and central venous pressure in anesthetized dogs. It was concluded that the effects of acupuncture at Tsu San Li (St-36) were parasympathomimetic-like and that these effects could be blocked by atropine, a parasympatholytic drug.
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PMID:Cardiovascular effects of atropine on acupuncture, needling with electrostimulation, at Tsu San Li (St-36) in dogs. 87 81

Immediate haemodynamic changes during electrical cardioversion were compared in 30 patients anaesthetized either with thiopental or with Althesin. The systolic arterial pressure, heart rate, stroke and cardiac indices were measured before atropine premedication, after atropine, during anaesthesia, and 3 and 10 minutes after defibrillation. The stroke index was estimated by transthoracic impedance method. Both anaesthetics caused a significant but similar decrease in systolic arterial pressure. The cardiac index remained relatively stable in both groups during all stages of the procedure. Atropine induced an expected increase in heart rate and a decrease in stroke index. while both variables tended to approach the baseline values after cardioversion with no difference between thiopental and althesin groups. No significant difference in the haemodynamic response to cardioversion was seen in patients with heart volumes exceeding 650 ml/m2 BSA as compared to those with smaller hearts. It is concluded that both thiopental and althesin can be considered as safe anaesthetics for cardioversion.
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PMID:Anaesthesia for cardioversion: immediate haemodynamics in patients anaesthetized with thiopental or althesin. 99 10

Effects of the drug xylazine were determined on arterial pH, arterial oxygen pressure (PaO2), arterial carbon dioxide pressure (PaCO2), aortic blood pressure, aortic flow, heart rate, pulse pressure, stroke volume, and peripheral resistance of dogs. The drug was given intravenously (IV) with and without atropine and was given intramuscularly (IM) without atropine. After IV administration of xylazine (1.1 mg/kg), arterial pH, PaO2, and PaCO2 values were not changed from control values. However, the drug did produce a statistically significant decrease in heart rate, decrease in aortic flow, initial increase in blood pressure followed by decrease, and increase in peripheral resistance. Stroke volume and pulse pressure were not significantly changed. Atropine (0.02 mg/kg, IV) did not significantly change any of the effects produced by xylazine. Intramuscular administration of xylazine (2.2 mg/kg) did not produce significant changes in arterial pH, PaO2, or PaCO2. Heart rate and aortic flow decreased significantly, but statistically significant changes did not occur in aortic blood pressure or peripheral resistance; however, the changes in these last 2 values were in the same direction and were of similar magnitude as those which occurred afger IV administration of xylazine.
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PMID:Cardiopulmonary effects of xylazine in dogs. 114 58

In anesthetized dogs, methysergide (1 and 3 mg/kg i.v.) caused reductions in systolic and diastolic blood pressure, heart rate, left ventricular pressure and peripheral resistance. Caardiac output was unchanged because of an increase in stroke volume. Methysergide exhibited no alpha-receptor, ganglion, or adrenergic neuron-blocking properties nor did it have marked direct vasocilator action. The BCO, but not the orthostatic, reflex was severely inhibited by the drug, evidence for a central inhibitory action. Atropine, vagotomy or carotid sinus debuffering had little or no effect on the hypotension and bradycardia produced by methysergide, whereas guanethidine pretreatment essentially abolished these effects. Direct intracerebronventricular administration of small doses of methysergide (0.2 mg/kg) caused significant hypotension and bradycardia. It is concluded that methysergide causes centrally mediated hypotension and bradycardia, the mechanism of which is not clearly understood.
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PMID:Centrally mediated hypotension and bradycardia by methysergide in anesthetized dogs. 117 77

Atropine can have a place during cardiopulmonary resuscitation (CPR) in the management of asystole, where parasympathetic influence might be excessive. However, the beneficial effects of atropine in electromechanical dissociation (EMD) have not been clearly demonstrated. The authors studied the effects of atropine in combination with epinephrine on an experimental model of EMD in the closed-chested dog. In 15 pentobarbital-anesthetized, mechanically ventilated dogs (mean weight 20 kg), EMD was induced by ventricular fibrillation followed by an external countershock, and was observed for 2 minutes before CPR was started. After 5 minutes of chest compression using a CPR thumper, either atropine 0.5 mg or D5W was administered, and the same injection was repeated every 5 minutes until recovery. Epinephrine 1 mg was administered in alternans. Each dog was submitted to two successive episodes of CPR, using either atropine or D5W, in a randomized order. Of a total of 28 CPRs, five were successful with chest compression alone. In the treatment groups, 10 of 11 were successful with atropine, but only eight of 12 with D5W (P < .01). The duration of CPR was also significantly shorter when atropine was used (9 minutes 56 seconds +/- 14 seconds versus 12 minutes 08 seconds +/- 43 seconds, P < .001). During the recovery period, atropine-treated animals had higher arterial pressure, heart rate, cardiac output and stroke volume. On this experimental model, the administration of high doses of atropine together with epinephrine enhances the recovery from EMD and results in a better cardiac function during recovery.
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PMID:Atropine administration in experimental electromechanical dissociation. 848 81

Oxymorphone was administered intravenously (IV) to 10 dogs (0.4 mg/kg initial dose followed by 0.2 mg/kg three times at 20-minute intervals). Four hours after the last dose of oxymorphone, heart rates were less than 60 bpm in six dogs. After atropine (0.01 mg/kg IV) was administered, heart rate decreased in five dogs and sinus arrhythmia or second degree heart block occurred in four of them. A second injection of atropine (0.01 mg/kg IV) was administered 5 minutes after the first and the heart rates increased to more than 100 bpm in all six dogs. Ten minutes after the second dose of atropine, heart rate, cardiac output, left ventricular minute work, venous admixture, and oxygen transport were significantly increased, whereas stroke volume, central venous pressure, systemic vascular resistance, and oxygen extraction ratio were significantly decreased from pre-atropine values. The PaCO2 increased and the PaO2 decreased but not significantly. The oxymorphone-induced bradycardia did not produce any overtly detrimental effects in these healthy dogs. Atropine reversed the bradycardia and improved measured cardiovascular parameters.
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PMID:Cardiovascular and pulmonary effects of atropine reversal of oxymorphone-induced bradycardia in dogs. 141 73

1. Beat-by-beat changes in cardiac performance in response to arterial baroreceptor stimulation induced by phenylephrine were evaluated by pulsed-wave aortic Doppler ultrasound in eighteen subjects. Stroke distance was used as an index of stroke volume and minute distance as an index of cardiac output; peak velocity was also measured. 2. The sensitivity of the baroreceptor-cardiac reflex was assessed by calculating the slope of the regression lines relating the changes in heart period (R-R interval), peak velocity and stroke distance in response to the rise in systolic blood pressure (SBP) induced by phenylephrine. In ten subjects the experiment was repeated after vagal blockade by atropine. Since the tachycardia induced by vagal blockade could alter the sensitivity of the baroreflex, we compared the results obtained after atropine with those obtained during pacing at similar rates in six subjects with cardiac pacemakers. 3. As R-R interval lengthened in response to the rise in SBP, stroke distance and peak velocity fell sharply. The subjects with a highly sensitive baroreceptor-heart rate reflex showed the greatest fall in peak velocity and stroke distance. The slope of the relationship between R-R interval and SBP for each subject correlated closely with that of peak velocity/SBP (correlation coefficient, r = 0.88) and stroke distance/SBP (r = 0.93) relationships. 4. Atropine virtually abolished all the cardiac reflex changes, despite a considerable increase in SBP induced by phenylephrine. At comparable heart rates achieved by pacing the sensitivity of the baroreceptor-cardiac reflex (calculated from the slopes of the regression lines relating changes in stroke distance and in peak velocity to the rise in SBP) was maintained and was significantly greater when compared to that obtained after vagal blockade. 5. These results show that the stimulation of arterial baroreceptors is accompanied by a fall in the Doppler-derived indices of stroke volume and cardiac output. This response is neural and is abolished by atropine, which indicates that it is mediated through the efferent vagus.
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PMID:Baroreflex control of stroke volume in man: an effect mediated by the vagus. 159 76

The cardiovascular changes induced by several sedatives were investigated in five ponies with a subcutaneously transposed carotid artery by means of cardiac output determinations (thermodilution technique), systemic and pulmonary artery pressure measurements (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). The cardiovascular depression (decrease in systemic blood pressure and cardiac output) was long lasting (greater than 90 min) after administration of propionylpromazine (0.08 mg/kg intravenous (i.v.)) together with promethazine (0.08 mg/kg i.v.). The phenothiazine-induced sedation was not optimal. alpha 2-Agonists (xylazine (0.60 mg/kg i.v.) and detomidine (20 micrograms/kg i.v.)) induced initial but transient cardiovascular effects with an increase in systemic blood pressure and a decrease in cardiac output for about 15 min. Second degree atrioventricular blocks and bradycardia were seen during this period. The cardiovascular depression was more pronounced during detomidine sedation. Atropine (0.01 mg/kg i.v.) induced a tachycardia with a decrease in stroke volume but did not alter the cardiac output or other cardiovascular parameters. It prevented the occurrence of the bradycardia and heart blocks normally induced by xylazine or detomidine. Atropine potentiated the initial hypertension induced by the alpha 2-agonistic sedatives (especially detomidine). The decrease in cardiac output induced by xylazine, and to a lesser extent by detomidine, was partially counteracted when atropine was given in advance. The atropine-xylazine combination seemed the best premedication protocol before general anaesthesia as it only resulted in minor and transient cardiovascular changes.
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PMID:Haemodynamic changes during sedation in ponies. 239 24

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two-dimensional echocardiographic dimensions of the left ventricle and pulmonary artery blood flow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg.kg-1 IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in both groups, but decreases in EF (32 +/- 5 per cent vs 18 +/- 5 per cent) and increases in LVEDV (18 +/- 7 per cent vs 7 +/- 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 +/- 6 per cent), than during isoflurane anaesthesia (18 +/- 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 +/- 4 per cent) following atropine in both groups, and CO returned to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children. 272 Aug 67

Respiratory and circulatory (measured and calculated) variables were obtained at the same time in resting eels, during normoxia and after 1 h exposure to environmental hypoxia (water PO2 of 40 torr). In normoxia, values of respiratory and circulatory variables appeared less than those reported for most other fish. These differences could be partly explained by a lower level of standard metabolism and a greater uptake of O2 through the skin. Hypoxia caused a marked decrease in heart rate (40%), cardiac output (37%), ventral and dorsal arterial blood pressures (22% and 32%), associated with a constriction of prebranchial veno-venous shunt, and an increase in branchial vascular resistance (30%). Atropine treatment during hypoxia reduced, but did not abolish, bradycardia, and branchial vascular resistance remained unchanged. The lack of increase in cardiac stroke volume as well as the slowing of the heart in atropine-treated eel, could be regarded as metabolic effects of sustained hypoxia. The increase in branchial resistance and constriction of prebranchial veno-venous shunt could be regarded as a direct myogenic effect of hypoxia. Hypoxic exposure resulted in an increase in ventilatory water flow Vg (more than twofold), a decrease in gill O2 uptake (50%) and oxygen partial pressure in arterial (PaO2 80%) and mixed venous blood (PvO2 78%), and in increase in the transfer factor for O2 of the gills, TO2, (+66%). The ventilatory convection requirement increased (fivefold) while extraction (EwO2%) and effectiveness (Eff%) of gill oxygen transfer were maintained in spite of hyperventilation. Hypoxic hyperventilation reduced partial pressure of CO2 (PaCO2 from 3.4 to 0.7 torr) and markedly raised pH (pHa from 7.98 to 8.33) in arterial blood, thus causing a typical respiratory alkalosis, which resulted in increased O2 affinity and capacity of eel haemoglobin.
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PMID:Ventilatory and circulatory adjustments in the European eel (Anguilla anguilla L.) exposed to short term hypoxia. 292 Aug 10


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