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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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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.
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PMID:Analysis of vasoactivity of local pH, PCO2 and bicarbonate on pial vessels. 1 63

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.
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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.
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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 circulatory response to different ventilatory patterns during artificial ventilation was examined in 17 sternotomized piglets. A constant CO2-tension level was maintained in all investigations by reference to analyses of the end-tidal infra-red CO2 fraction and arterial CO2-tension. The greatest variation in mean values for end-tidal CO2-tension was 0.2 kPa. Total compliance and lung compliance were lower at a ventilator volume/pressure quotient of 20 compared to those at 80 ml/kPa, and at f = 30 compared to f = 11 cycles/min. Higher cardiac output, lower pulmonary vascular resistance and systemic vascular resistance were measured at f = 11 (inspiration 20%) than at f = 30 (inspiration 50%). An increase in inspiration time by about 100% at the lower ventilatory frequency (f = 11) resulted in a significant but uncompensated decrease in cardiac output and stroke volume. These results demonstrate the value of a rapid insufflation in order to give longer expiration time per minute for the benefit of the venous return and cardiac output.
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PMID:The circulatory response to specific ventilatory patterns using a tidal volume ventilator. 29 Dec 73

A double-blind cross-over trial of the non-selective beta-blocker propranolol and the beta1-selective blocker metoprolol was carried out in 8 hypertensive patients. At the end of each 4-week period of treatment haemodynamic and respiratory indices and perceived exertion were studied during moderate exercise. Both beta-blockers resulted in reduced heart rate, cardiac output, and blood pressure, whereas the stroke volume increased. Total peripheral resistance did not change. During exercise the expiratory peak flow rate equally increased in every period. However, the peak flow rate at rest, as well as during exercise, was reduced by propranolol, while metoprolol had no such influence. Neither of the beta-blockers changed O2 consumption, CO2 production, tidal volume, or respiratory rate. Moreover, they did not influence perceived exertion. These results suggest that the arteriolar and bronchiolar beta2-receptors do not play a major role in the alteration of circulation and ventilation during exercise. As far as their practical use as antihypertensive agents is concerned, this study shows no advantage in the use of either of these beta-blockers.
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PMID:Effects of propranolol and metoprolol on haemodynamic and respiratory indices and on perceived exertion during exercise in hypertensive patients. 37 43

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.
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PMID:Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates. 37 15

A comparison was made between the effects of two different anesthetics, alpha-D-gluco-chloralose and 1-1-phenylcyclohexyl piperidine hydrochloride (Sernylan), on cerebral blood flow (CBF), brain metabolism and cerebrovascular CO2 responsiveness in primates. The experiments were carried out on immobilized and artificially ventilated baboons. Anesthesia was induced either with 100/mg/kg chloralose (i.p.) or with 1 mg/kg Sernylan (i.m.). CBF in 8 different brain regions was measured by the intra-arterial 133Xe clearance technique. The CO2 responsiveness of the cerebrovascular bed was tested by a gas mixture containing 5% CO2. Chloralose depressed total as well as regional CBF compared to the effect of Sernylan. A significant shift occurred toward lower CBF values in the grey matter while white matter flow was identical in the two groups. Brain O2 consumption was significantly higher during Sernylan analgesia (3.35 +/- 0.34 ml/100 g/min) than during chloralose anesthesia (2.42 +/- 0.22 ml/100 g/min). There were no differences in glucose uptake, lactate and pyruvate production, or in arterial and cerebral venous blood gases in the two types of anesthesia. The cerebrovascular CO2 sensitivity of the Sernylan-treated baboons was higher than that of the chloralose-anesthetized animals, in both the grey and white matter.
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PMID:Comparative effects of chloralose anesthesia and Sernylan analgesia on cerebral blood flow, CO2 responsiveness, and brain metabolism in the baboon. 40 48


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