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

Cerebral hemispheric blood flow and metabolism were measured before and after therapy with intracarotid infusion of combined PBZ and PPL in 15 patients with recent cerebral infarction. HBF was unaltered despite decrease in cerebral perfusion pressure. Cerebral hemispheric oxygen comsumption and carbon dioxide production decreased while cerebral hemispheric lactate production increased. Biphasic cerebral uptake of tyrosine was observed during and immediately after PBZ and PPL infusion. CSF HVA increased, indicating altered DA turnover. CSF 5HIAA levels also increased, suggesting altered 5HT turnover after PBZ and PPL. Release of cyclic AMP from ischemic brain into cerebral venous blood seen in the steady state was abolished after therapy. Cerebral hemodynamic studies suggest a functional balance between monaminergic neurogenic influences in the control of cerebral circulation. Imbalance of such controlling factors in ischemic brain may lead to paradoxical vascular responses to induced hypertension and hypotension. PBZ and PPL enhance such responses perhaps by increasing central neurotransmitter turnover and release. Further shift toward cerebral anaerobic metabolism may occur in ischemic brain following the use of phenoxybenzamine and propranolol. Worsening of neurological deficit occurred in four cases. Combined therapy with PBZ and PPL does not appear beneficial in the therapy of patients with recent stroke.
Stroke
PMID:Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients. 0 7

Cardiovascular and metabolic parameters were studied in dogs anesthetized with pentobarbital sodium, and while awake resting or exercising for 30 min at either 6.4 km/h, 10% grade (32% VO2 max) or 8.0 km/h, 16% grade (50% VO2 max). The anesthetized dogs had lower cardiac outputs, stroke volumes, arterial-mixed venous oxygen differences, oxygen uptakes, rectal temperatures, and higher diastolic and mean arterial pressures than awake resting dogs. Heart rates and arterial systolic pressures were similar in the two conditions. The increased oxygen uptakes during exercise were associated with approximately equal percentage increments in cardiac outputs and oxygen extractions. Cardiac output increases during exercise were largely due to increases in heart rates. Arterial CO2 tension and CO2 contents as well as venous O2 and CO2 gas tensions and contents declined, and pH and rectal temperatures increased during exercise. The dogs became alkalotic during exercise. Elevated central body temperatures appeared to be the major factor controlling respiration.
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PMID:Cardiovascular, respiratory, and metabolic adjustments to exercise in dogs. 1 2

The effect of local hypercapnic acidosis or local hypocapnic alkalosis on pial arterioles were studied in anesthetized cats equipped with a cranial window for the direct observation of the pial microcirculation of the parietal cortex. Changes in PCO2 and pH of the extracellular fluid were induced by perfusing the space under the cranial window with artificial cerebrospinal fluid equilibrated with different concentrations of CO2, while PaCO2 was maintained constant. Hypercapnic acidosis dilated and hypocapnic alkalosis constricted pial arteioles markedly. The results indicate that a basis exists for considering CO2 as a mediator for local regulation of brain blood flow. The vasodilation associated with arterial hypercapnia was abolished by a reduction in CSF PCO2 equal in magnitude to the rise in arterial blood PCO2, suggesting that the action of CO2 is entirely local.
Stroke
PMID:Local mechanism of CO2 action of cat pial arterioles. 1 34

The mechanism by which the local effect of CO2ON pial arterioles is exerted was examined in anesthetized cats equipped with a cranial window for the direct observation of the microcirculation of the parietal cortex. The dilation of pial arterioles in response to application of artificial cerebrospinal fluid with low pH was the same whether or not the PCO2 of the solution was maintained in the normal range or markedly increased. The constriction of pial arterioles in response to application of artificial cerebrospinal fluid with high pH was the same whether or not the PCO2 of the solution was maintained in the normal range or markedly decreased. Finally, pial arterioles did not change their caliber in response to application of cerebrospinal fluid with unchanged pH but markedly increased or decreased Pco, or bicarbonate ion concentration. These results show that the action of CO2 on cerebral vessels is exerted via changes in extracellular fluid pH and that molecular CO2 and bicarbonate ions do not have independent vasoactivity on these vessels.
Stroke
PMID:Analysis of vasoactivity of local pH, PCO2 and bicarbonate on pial vessels. 1 63

Peripheral vascular and myocardial effects of increasing concentrations of nitrous oxide (0 to 70 per cent) in oxygen were determined in 15 unanaesthetized calves before and after replacement in their natural heart (NH) with a pneumatically driven artificial heart (AH). Nitrous oxide produced concentration-related decreases in arterial and mixed venous pH and increases in minute ventilation and arterial and mixed venous carbon dioxide tensions in both NH and AH calves. Nitrous oxide resulted in significant increases in cardiac output, stroke volume and mean aortic, pulmonary artery and right atrial pressures in NH and AH calves, but did not significantly change systemic vascular resistance in either group of animals. Heart rate was increased in NH calves but was fixed in AH calves. Elevations in heart rate and cardiac output at nitrous oxide concentrations greater than 30 per cent and aortic pressure at 70 per cent nitrous oxide were significantly greater in NH than AH animals (P less than 0.05). These data demonstrate that nitrous oxide stimulates the cardiovascular system in spontaneously breathing mammals and that the changes result from improved venous return and an increase in myocardial chronotropy. Our findings also suggest that cardiovascular stimulation during nitrous oxide breathing may be related to increased concentrations of arterial and/or venous carbon dioxide.
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PMID:Peripheral vascular and cardiac effects of nitrous oxide in the bovine. 2 Feb 5

The influence of sympathetic nervous activity on cerebral circulation and cerebrovascular CO2 reactivity was investigated through inhibition of dopamine beta-hydroxylase (DBH). A PO2 electrode, a PCO2 electrode and a plate-type thermocouple-flowmeter were placed on the pial surface of the cat brain. Cerebrocortical PO2, PCO2, cerebrocortical blood flow and arterial blood pressure were continuously recorded before, during and after intracarotid infusion of 10 mg/kg of fusaric acid, a potent DBH inhibitor. The effects of 5% CO2 inhalation and hyperventilation were measured before and after the inhibition of DBH. Following the intracarotid infusion of fusaric acid, cerebrocortical PO2 and cerebrocortical blood flow increased significantly. After the inhibition of DBH, the degree of the increase in cerebrocortical PO2 during 5% CO2 inhalation was enhanced while the degree of the decrease in cerebrocortical PO2 during hyperventilation did not show any significant change. The cerebral vasodilatation caused by fusaric acid suggests that the sympathetic nervous system takes part in the resting tone of cerebral blood vessels. The increase in the cerebrovascular CO2 reactivity produced by the inhibition of DBH suggests that the sympathetic nervous system modifies cerebrovascular CO2 reactivity.
Stroke
PMID:Modification of cerebrovascular CO2 reactivity by inhibition of dopamine beta-hydroxylase. 4 44

Experiments were performed on 2 groups of baboons anesthetized with Sernylan. One group served as control and the other was premedicated with 5 mg/kg phenoxybenzamine (PBZ). A 2-step hypovolemic shock model was used followed by retransfusion of the shed blood. Cerebral blood flow was measured by the 133Xe clearance method. Arterial and cerebral venous samples were taken and analyzed for blood gases as well as glucose and lactate content. The cerebral metabolic rates of oxygen, glucose, and lactate were calculated. In addition, the effect of CO2 inhalation was studied before shock was induced. PBZ produced no effect on either CBF or the flow response to CO2 prior to bleeding. PBZ pretreatment prevented the fall in cerebral blood flow and CMRO2 produced by systemic hypotension due to bleeding. Lactic acid showed no evidence of change either in production or uptake by the brain during the experimental procedure. The cerebral metabolic pathway of glucose, however, seemed to be affected by PBZ both before and during shock.
Stroke
PMID:Effect of phenoxybenzamine on cerebral blood flow and metabolism in the baboon during hemorrhagic shock. 11 93

The purpose of this study is to determine the effect of propranolol on the cardiovascular response to carbon dioxide (0-20%) during anaesthesia with 1% halothane in oxygen (blood level 16.3 mg/100 ml S.D. +/- 5) in dogs each with a chronically implanted electromagnetic flow probe on the ascending aorta. Cardiac output, stroke volume; heart rate, mean arterial pressure (MAP) and total peripheral resistance (TPR) were obtained and paired with arterial blood gas determination after each step of increased concentration of carbon dioxide with or without propranolol. Propranolol (0.06-0.9 mg/kg) prevented the response to elevation of inspired carbon dioxide of increased heart rate, stroke volume, and cardiac output, TPR and MAP were reduced by CO2 and only slightly changed in the propranolol series.
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PMID:Modification by propranolol of cardiovascular response to hypercapnia during halothane anaesthesia. 12 29

The stroke volume and cardiac output changes in twenty-four patients undergoing laparoscopy were measured using the non-invasive technique of impedance cardiography. There was a moderate fall of stroke volume and cardiac output during intraperitoneal insufflation of carbon dioxide which was directly related to the volume of gas used. The need for caution during laparoscopy particularly in ill patients is emphasised.
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PMID:Cardiovascular changes during laparoscopy. Studies of stroke volume and cardiac output using impedance cardiography. 13 Aug 11

Cardiac output in the horse was measured before and at predetermined times during 2-hour periods of thiopentone-halothane and thiopentone-diethyl ether anaesthesia. Left ventricular stroke volume was decreased to a similar extent during anaesthesia with each volatile agent, but a greater reduction in cardiac output occurred during halothane anaesthesia. This finding reflected the differing effects of halothane and ether on heart rate, a slight bradycardia occurring with the former agent while ether produced a small degree of tachycardia. The latter effect was attributed to enhanced sympathoadrenal activity. Changes in cardiac output and stroke volume were considered in relation to other factors, including arterial blood pH and tensions of oxygen and carbon dioxide. Positive correlations between some of these variables and cardiac function were established. With both volatile agents the reductions in stroke volume and cardiac output were related to the duration of anaesthesia, being greatest during the early stages. Possible reasons for the tendency of stroke volume and cardiac output to return towards control levels are discussed.
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PMID:Cardiac output in the conscious and anaesthetised horse. 23 42


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