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

Observations were made before and 3-5 days after prolonged endurance jogging an average of 42 miles/day, 6 days/wk for 2.5 mo by a young male adult who voluntarily initiated a run across the United States. Both arterial PO2 and lactic acid increased. In each instance, the first limitation in circulatory delivery of oxygen was a plateau in stroke volume and cardiac output. Afterward, pulse deficit and systemic arterial pressure fell with exercise and heart rate accelerated. Although there was no change in oxygen transport (Q X CAO2), a reduction in stroke volume was exactly balanced by a rise in arterial oxygen content. Vital capacity, residual volume, and total lung capacity and diffusion capacity for carbon monoxide, hematocrit, and red cell mass increased, while plasma volume diminished and heart size and total blood volume were unchanged.
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PMID:Cardiac limitation to maximal oxygen transport and changes in components after jogging across the US. 121 77

The purpose of this study is to develop a reliable method for obtaining information about "spontaneous respiration" in paralysed cats. Therefore action potentials from one of the phrenic nerves are recorded. In a spontaneously breathing animal, a CO2 rebreathing experiment is performed in order to obtain a relationship between phrenic nerve activity and tidal volume. This phrenic nerve activity is corrected for the noise measured during expiration and quantified proportional to the square root of the mean impulse rate of the whole nerve bundle. Thus, high correlation coefficients (0.95 or more) between phrenic nerve activity and tidal volume can be obtained. After paralysing the cat this relationship can be used to estimate "spontaneous tidal volume" from the phrenic nerve activity. It appears to be necessary to perform unilateral phrenicotomy on the nerve from which recordings are taken, because there is a condiserable amount of afferent signals in the phrenic nerve which is dependent on the stroke volume of the respirator, on the alveolar PCO2 and somewhat on the alveolar PO2. It is concluded that after vagotomy and phrenicotomy and if suitably quantified, the electrical activity in the phrenic nerve gives accurate information on "spontaneous ventilation" in a paralysed cat.
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PMID:Ventilation estimated from efferent phrenic nerve activity in the paralysed cat. 123 28

The cerebrovascular response to hypercapnia and hyperventilation was studied in normal and jaundiced baboons by the intracarotid 133Xe injection technique. The baboons with bile duct ligation were found to have decreased CBF at all levels of PaCO2. This difference between normal and jaundiced baboons was 13% at normocapnia rising to 33% with hypercapnia and 37% with hypocapnia. The CBF values all were increased toward normal by use of an alpha-adrenoreceptor blockade (phentolamine). It is suggested that the obstructive jaundice potentiated an inherent vasoconstrictor alpha-adrenergic mechanism to oppose the effects of CO2. Also, alteration of the PaCO2 may have produced its effects on the cerebral vessels by altering this adrenergic mechanism.
Stroke
PMID:Abnormal cerebrovascular response to altered PaCO2 in baboons with obstructive jaundice. 126 12

Hypobaric hypoxia causes hypocapina and alkalosis, hemoconcentration and increased hematocrit, and a decreased cardiac stroke volume. To assess the role of the hypocapnic alkalosis in causing these other changes, five men were exposed to hypobaric hypoxia at a barometric pressure (PB) of 440 torr with an alveolar O2 tension of 55 torr for 5 days with 3.77% CO2 added to the atmosphere to prevent alkalosis. They did not lose weight, and arterial CO2 tension, pH, and cardiac stroke volume were unchanged. An unchanged hematocrit implied an unchanged plasma volume. During exercise to maximum, stroke volumes equaled sea level values but arterial hypoxemia was profound, the arterial O2 tension being 39 torr. By contrast, three men at high altitude without CO2 supplementation (PB=455 torr; alveolar PO2=56 torr) had weight loss, hypocapnia, alkalosis, and decreased stroke volume. Increased hematocrits suggested decreased plasma volumes. During exercise, arterial PO2 (48 torr) was higher than in the group receiving CO2. Maximum oxygen uptakes were decreased to a similar degree in the two groups. Catecholamine excretion doubled in the group with CO2 but in the group without CO2 catechoamine excretion was unchanged. A normal pH at high altitude apparently maintained plasma volume, which, with the increased catecholamine excretion, may have prevented a decrease in stroke volume. However, the subjects with CO2 added did not have enhanced oxygen transport, because their arterial oxygenation was impaired.
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PMID:Maintained stroke volume but impaired arterial oxygenation in man at high altitude with supplemental CO2. 126 78

Cigarette smoking causes significant exposure to nicotine, which increases heart rate, blood pressure, and thus myocardial oxygen demand, and to carbon monoxide, which decreases the oxygen-carrying capacity of the blood because of carboxyhemoglobin formation. Cigarette smoking also predisposes the patient to coronary vasoconstriction. Smoking cessation results in the early elimination of nicotine and carbon monoxide from the system and decreases the risks of ischemia based on these mechanisms. Over the long term, smoking cessation results in elimination of the increased risk of myocardial infarction in patients without previous heart disease as early as 2 years after smoking stops. In addition, for patients with known coronary artery disease, smoking cessation results in an increase in HDL level, which may result in a retardation of atherogenesis and reduced cardiovascular morbidity and mortality. It is important for all physicians to reiterate both the short- and long-term risks of cigarette smoking as well as the good news-that smoking cessation results in a substantial, if not complete, reversal of the risk of myocardial infarction and death, particularly for patients with established coronary artery disease. In light of those established facts, efforts to develop more effective methods to help patients quit smoking must be increased so patients can realize these important health benefits.
Heart Dis Stroke
PMID:Cardiovascular benefits of smoking cessation. 134 4

We studied the effects of laparoscopic cholecystectomy on respiratory and hemodynamic function in eight adult pigs. Minute ventilation was adjusted to normalize baseline arterial blood gases, then fixed throughout carbon dioxide insufflation. A metabolic measurement cart recorded total CO2 excretion, oxygen consumption, and minute ventilation. Carbon dioxide pneumoperitoneum was maintained at a constant pressure of 15 mm Hg as cholecystectomy was performed. After 1 hour of insufflation, CO2 excretion increased from 115 +/- 10 mL/min to 149 +/- 9 mL/min but O2 consumption remained unchanged. The PaCO2 increased from 35 +/- 2 mm Hg to 49 +/- 3 mm Hg and arterial pH fell from 7.47 +/- 0.02 to 7.35 +/- 0.03. Systemic and pulmonary hypertension occurred and stroke volume dropped from 35.5 +/- 3.5 mL to 28.6 +/- 2.2 mL with compensatory tachycardia. Right atrial pressure remained unchanged as inferior vena cava pressure increased to reflect the intraperitoneal pressure. We conclude that CO2 pneumoperitoneum resulted in significant transperitoneal CO2 absorption, with secondary hypercapnia and acidemia. The accumulation of CO2 was also associated with an increase in systemic and pulmonary arterial pressure. Heart rate increased to compensate for the decreased stroke volume to maintain cardiac output.
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PMID:Intraperitoneal carbon dioxide insufflation and cardiopulmonary functions. Laparoscopic cholecystectomy in pigs. 138 6

Sick preterm infants may, under certain conditions, demonstrate blood pressure passive cerebral blood flow in response to changes in arterial carbon dioxide tension. Blood pressure in turn depends on cardiac output and peripheral resistance. A Doppler technique for assessing cardiac output compared favourably in terms of reproducibility to a thermodilution technique in a group of infants undergoing cardiac catheterization for congenital heart disease. Doppler was subsequently used to monitor changes in cardiac output following an increase in arterial carbon dioxide tension of 1 kPa in 25 ventilated preterm infants. Blood pressure increased significantly (p = 0.006). However, heart rate did not change significantly (p = 0.16) and, in addition, both stroke and minute volume decreased (p = 0.023, p = 0.02, respectively). This suggests that accompanying changes in components of peripheral resistance exert important effects on blood pressure in the preterm neonate in response to changes in arterial carbon dioxide tension.
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PMID:Cardiovascular effects of carbon dioxide in ventilated preterm infants. 139 61

The purpose of this study was to assess hemodynamic and respiratory measures of submaximal and maximal exercise performance in patients with chronic atrial fibrillation, before and one month after cardioversion to sinus rhythm. Restoration of sinus rhythm (n = 16) produced significant reductions in resting and exercise heart rates, 14 percent to 20 percent (p < 0.01). Due to a proportionately larger increase in stroke volume, cardiac output increased by 9 percent during low-level exercise (p < 0.01) and by 7 percent during exercise above the anaerobic threshold (p < 0.05). Minute ventilation was reduced by 7 percent during low-level exercise (p < 0.01) and by 9 percent above the anaerobic threshold (p < 0.05). The ratio between minute ventilation and carbon dioxide elimination was significantly reduced (p < 0.01). Maximum oxygen uptake (+8 percent; p < 0.01) and maximal tolerated work load (+6 percent; p < 0.05) increased. Hemodynamic changes during exercise were similar in patients with (n = 7) or without (n = 9) disopyramide prophylaxis. Restoration of sinus rhythm induced improvement in hemodynamics and in efficiency of ventilation, thereby reducing the ventilatory demand during submaximal exercise.
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PMID:Improved ventilatory response to exercise after cardioversion of chronic atrial fibrillation to sinus rhythm. 139 36

Eight young men underwent an 8-month endurance exercise training program. Prior to and following the training program, the subjects' maximal oxygen uptake (VO2max), total blood volume (TBV) and plasma volume (PV), tolerance to lower body negative pressure (LBNP) assessed by the cumulative stress index (CSI) to presyncope, and their hemodynamic responses to 0 to -45 torr LBNP was determined. Hemodynamic measures included rebreathe carbon dioxide cardiac output (Qc), heart rate (HR), directly measured arterial blood pressures (ABP), and strain gauge determination of forearm blood flow (FBF) and leg volume changes (delta LgV). Calculated values of stroke volume (SV), forearm, vascular resistance (FVR), and peripheral vascular resistance (PVR) were made. Following training, each subject had an increased VO2max (mean = +27.4%, P < 0.001), TBV (mean = +15.8%, P < 0.02), and PV (mean = +16.5%, P < 0.02) and each subject had a decreased tolerance to LBNP (mean CSI = -24%, P < 0.001). Stepwise linear regression identified that the major factors to significantly predict the decreased CSI pre- to post-training were a reduced response of PVR to LBNP from -15 to -45 torr (Model R2 = 0.853), the delta TBV (model R2 = 0.981), and the greater post-training reduction in SBP to LBNP of 0 to -45 torr (model R2 = 1.0). These data suggest that physiologic adaptations associated with the increased VO2max and TBV resulting from a prolonged endurance exercise training program can alter the reflex control of vasomotion and cardiac output during LBNP and reduce the LBNP tolerance.
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PMID:Reduction in LBNP tolerance following prolonged endurance exercise training. 143 75

The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.
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PMID:Carbon monoxide and pulmonary circulation in an ovine model. 146 25


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