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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. We have previously shown that the cytosolic acid concentration changes in skeletal muscle during contraction in spontaneously hypertensive rats and normotensive Wistar-Kyoto rats in vivo. We have now found that this change was unaffected by 20% inhaled CO2 or by 4,4'-di-isothiocyanostilbene-2,2'-disulphonate. This is evidence that HCO3- exchange in vivo is not important in the control of cytosolic acid concentration during skeletal muscle contraction in either spontaneously hypertensive or Wistar-Kyoto rats. 2. We have also previously shown that the difference in cytosolic acid response during contraction between spontaneously hypertensive and Wistar-Kyoto rats is due to increased Na+/H+ antiporter activity in the spontaneously hypertensive rats. Our current findings suggest that this increase in Na+/H+ antiporter activity is more likely to be due to a change in the Km of the antiporter than to a change in the Vmax. We estimate that the Km of the antiporter changes in hypertension from pH 7.16 to 7.33. 3. We did not find any differences between adult spontaneously hypertensive and Wistar-Kyoto rats with regard to resting intracellular and extracellular pH and resting intracellular and extracellular HCO3- concentrations. In addition, we did not find any evidence of a difference in skeletal muscle HCO3-/Cl- exchange between adult spontaneously hypertensive and Wistar-Kyoto rats. 4. At rest, skeletal muscles of the spontaneously hypertensive and Wistar-Kyoto rats have the same lactate production, HCO3-/Cl- exchange and arterial partial pressure of CO2. In addition, we can also calculate that at a resting intracellular pH of 7.05 in the spontaneously hypertensive rats, the antiporter is 66% saturated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na+/H+ and HCO3-/Cl- exchange in the control of intracellular pH in vivo in the spontaneously hypertensive rat. 166 80

In anaesthetized rats, ventilatory stimulation induced by phentolamine, an alpha sympatholytic agent, emphasizes the role of some adrenergic mechanisms in the control of the respiratory centres activity. Phentolamine (5 and 10 mg.kg-1, iv) stimulates ventilation after a 4 s latency, tidal volume and respiratory rate being both increased. A same response can also be provoked 10 min later, by a second identical iv administration, systemic blood pressure remaining then stable at its previous low level. Hyperventilation is also observed when phentolamine is injected in totally denervated rats, without any remaining baro- or chemosensitivity. Stimulation is thus due to a central activity in relation with the release of inhibitory influences. Phentolamine also causes hyperventilation after prazosin pretreatment indicating that the alpha 1 adrenergic blockade is not involved in the post-phentolamine stimulation. This is an alpha 2 adrenergic transmission dependent mechanism. Variation of the systemic blood pressure is not the main mechanism involved in the hyperventilation induced by phentolamine. Meanwhile, baroreceptor activity modulates the central response to the drug, as shown by the negative influence of the post-vasopressin arterial hypertension. Hyperoxia is also a modulating factor acting by two ways: an inhibition of the peripheral chemoreceptors activity is added to an arterial hypertension. On the other side, activation of these chemoreceptors by almitrine bismesilate increases the respiratory responses to phentolamine. As already shown by one of us (Lagneuax, 1986), phentolamine pretreated rats are more responsive to hypoxia and to almitrine. Moreover, these phentolamine pretreated rats are protected against cardiovascular collapses and against apnea, frequently observed during hypoxia without CO2 compensation.
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PMID:[Alpha 2 adrenergic control of ventilation in the rat]. 170 84

Previous studies using the xenon-133 cerebral blood flow (CBF) method have documented the impairment of CO2 vasoresponsivity after a severe head injury, but only global values can be obtained reliably with this technique. We studied CO2 vasoresponsivity using the stable xenon-enhanced computed tomographic CBF method, which provided information about well-defined cortical regions and deep brain structures not available with the xenon-133 method. In 17 patients with admission Glasgow Coma Scale scores of 8 or less, hemispheric CO2 vasoresponsivity ranged from 1.3 to 8.5% per mm Hg change in partial CO2 pressure. Lobar, cerebellar, basal ganglia, and brain stem CO2 vasoresponsivity frequently varied from the mean global value by more than 25%. In all but one patient, local CO2 vasoresponsivity in one or more of these areas differed from the mean global value by more than 50%. The greatest variability occurred in patients with acute subdural hematomas and diffuse (bihemispheric) injuries. This variability in CO2 vasoresponsivity has important implications for the effective and safe management of intracranial hypertension that frequently accompanies severe head injury.
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PMID:The use of stable xenon-enhanced computed tomographic studies of cerebral blood flow to define changes in cerebral carbon dioxide vasoresponsivity caused by a severe head injury. 175 99

Exposure to carbon monoxide in our society is a frequent occurrence, from auto exhaust, industrial effluents, and cigarette smoke, and takes place over a wide range of concentrations. It has been suggested that chronic CO inhalation may alter blood pressure, even possibly provoking hypertension by acting alone or in combination with other environmental stressors. Some studies examining the response to CO exposure have reported decreases in blood pressure, whereas others have found increases or no change. Blood pressure in long-term cigarette smokers is generally decreased relative to nonsmokers, albeit a slight decrease. The strength of this finding is somewhat clouded by the effect of the lower body weight in smokers. The increases in blood pressure observed acutely with smoking are mainly due to nicotine. Chronically, the hypertensive action of nicotine is largely offset by the hypotensive action of CO. Several studies support the notion that environmental CO exposure or smoking accelerates or exacerbates hypertension in some people. It has been asserted that chronic CO exposure increases the development of atherosclerotic disease; however, convincing evidence from animal experiments is lacking. Nevertheless, CO may elevate plasma cholesterol and does appear to enhance atherosclerosis when serum cholesterol is greatly elevated by diet. Using the borderline hypertensive rat, an animal model reputed to have increased sensitivity to environmental stimuli, we found no evidence to suggest a provocatory role for CO in the development of hypertension; instead, CO exposure produced hypotension. On the whole, the human and animal literature, as well as our studies, fail to support the hypothesis that long-term CO exposure is capable of provoking an increase in blood pressure, even in borderline hypertensive or sensitive individuals.
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PMID:Is there a connection between carbon monoxide exposure and hypertension? 182 71

Laparoscopy performed with carboperitoneum in 30 women of infertility was studied to evaluate the changes of systemic blood pressure and end-tidal carbon dioxide (CO2) and their relationship. The patients were randomly divided into 2 groups. In group I (n = 15), the patient's respiration was set to maintain a nearly constant end-tidal CO2 by adjusting the minute ventilation. In group II (n = 15), the minute ventilation was kept constant to monitor the changes of end-tidal CO2. Perioperative measurements included end-tidal CO2, systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) which were recorded the moment just before intra-abdominal CO2 administration and every 2 min thereafter for at least 10 min. The data showed that in both groups there were time-related changes of blood pressure with a maximum increase about 20-30% of baseline level found at 6 min later after the beginning of intra-peritoneal CO2 insufflation, and no significant change of HR was noted. The intergroup comparisons of SBP, DBP and HR were not statistically significant. With regard to end-tidal CO2 change in group II, it also appeared in a time-related fashion. A maximum increase was found 6 min later after the intra-abdominal CO2 administration. Our results disclosed that carboperitoneum during laparoscopy might consistently induce systemic arterial hypertension, and hypercarbia might not be the major determinant factor of hypertension.
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PMID:Hypercarbia is not the determinant factor of systemic arterial hypertension during carboperitoneum in laparoscopy. 183 24

Single lung transplantation was performed in several steps: laparotomy to prepare an omentopexy, followed by pneumonectomy and implantation of a pulmonary graft, both by postero-lateral thoracotomy. The patients suffered from lymphangiomyomatosis (1), panacinar emphysema (2) and idiopathic pulmonary fibrosis (1). Immunosuppressive treatment was started before surgery. Anaesthesia was induced and maintained with alfentanil, midazolam and vecuronium. The patients were intubated with a Carlens endotracheal tube. Ventilation was carried out using an oxygen-air mixture, without any nitrous oxide or halogenated anaesthetic agent. Besides the usual parameters, expired CO2 concentrations, and oxygen saturation in the pulmonary artery were monitored. Partial femoro-femoral cardiopulmonary bypass was not required. Three major problems were encountered: hypoxia, hypercapnia, and pulmonary arterial hypertension. Hypoxia first occurred during the period of one-lung ventilation, during pneumonectomy, and again after unclamping of the graft vessels before the bronchus had been anastomosed. It was treated either by increasing the FiO2, inflating the lungs with pure oxygen, or partial clamping of the homolateral pulmonary artery. Hypercapnia occurred in three of the four patients until the graft was ventilated again. Except in one patient with preoperative pulmonary hypertension, the increase in pulmonary vascular resistances remained moderate after clamping of the pulmonary artery. Sufficient oxygen delivery, with more than 50% venous oxygen saturation, was maintained at this time by the infusion of dopamine and dobutamine. Two other specific problems were encountered in the emphysematous patients: severe hypotension following the start of artificial ventilation and after placing the patient in lateral position; thoracic asymetry with overdistension of the emphysematous lung, and mediastinal shift.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia in unilateral pulmonary transplantation]. 185 49

The cardiovascular effects of xylazine and detomidine in horses were studied. Six horses were given each of the following 5 treatments, at 1-week intervals: xylazine, 1.1 mg/kg, IV; xylazine, 2.2 mg/kg, IM; detomidine, 0.01 mg/kg, IV; detomidine, 0.02 mg/kg, IV; and detomidine, 0.04 mg/kg, IM. All treatments resulted in significantly decreased heart rate, increased incidence of atrioventricular block, and decreased cardiac output and cardiac index; cardiac output and cardiac index were lowest following IV administration of 0.02 mg of detomidine/kg. Mean arterial pressure was significantly reduced for various periods with all treatments; however, IV administration of 0.02 mg of detomidine/kg caused hypertension initially. Systemic vascular resistance was increased by all treatments. Indices of ventricular contractility and relaxation, +dP/dt and -dP/dt, were significantly depressed by all treatments. Significant changes were not detected in stroke volume or ejection fraction. The PCV was significantly reduced by all treatments. Respiratory rate was significantly decreased with all treatments, but arterial carbon dioxide tension did not change. Arterial oxygen tension was significantly decreased briefly with the 3 IV treatments only.
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PMID:Cardiovascular effects of xylazine and detomidine in horses. 185 87

The effects of endothelin 1 on the internal maxillary artery blood flow, measured as an index of cerebral blood flow, were examined in six unanesthetized goats under control conditions, hypercapnia induced by inhalation of 10% CO2 in air, hypertension by intravenous infusion of norepinephrine, and hypotension by intravenous injection of diazoxide. Under control, administration of endothelin (0.01-0.3 nmol) into the internal maxillary artery produced dose-dependent sustained decreases in cerebral blood flow and increases in cerebrovascular resistance; higher doses (0.1 and 0.3 nmol) also caused hypertension and bradycardia. During hypercapnia or hypertension, endothelin did not significantly affect cerebral blood flow, and only higher doses (0.1 and/or 0.3 nmol) increased cerebrovascular resistance, but this was lower than under control. However, under hypotension endothelin evoked a higher reduction in cerebral blood flow and increment in cerebrovascular resistance, and systemic effects were also more marked than under control. Therefore endothelin is a potent cerebral vasoconstrictor, and this effect is very attenuated during hypercapnia and hypertension but is increased under hypotension.
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PMID:Endothelin action on cerebral circulation in unanesthetized goats. 188 47

During an 18-month period 33 patients in whom there were contraindications to the use of iodinated contrast arteriography underwent 40 carbon dioxide/digital subtraction arteriograms for lower extremity ischemia (19), severe hypertension and renal insufficiency (12), or arterial aneurysm (2). Contraindications to iodinated contrast agents included renal insufficiency, congestive heart failure, and contrast hypersensitivity. Sixteen aortic, 15 iliac-femoral-popliteal-tibial, five aorta-iliac-femoral and four aorta-iliac-femoral-popliteal-tibial carbon dioxide/digital subtraction arteriography studies were performed. In 11 studies, imaging of selected arterial segments required the addition of 10 to 60 ml of dilute nonionic contrast. Guided by carbon dioxide/digital subtraction arteriography studies four femoral-tibial bypasses, three aneurysmorrhaphies, two aortorenal bypasses, one aortofemoral bypass and one femoral-femoral bypass were successfully performed in 11 patients. In addition, carbon dioxide/digital subtraction arteriography directed angioplasties of the common iliac (4), superficial femoral (6), popliteal (3), or tibioperoneal trunk (1) were performed in 10 patients. Complications of carbon dioxide/digital subtraction arteriography included transient deterioration in renal function in three patients in whom 20 ml of nonionic contrast was used, a nonfatal myocardial infarction after a popliteal percutaneous transluminal angioplasty in one patient, and transient tachypnea and tachycardia during a carbon dioxide/digital subtraction arteriography study in one patient. Diagnostic arteriograms are obtainable using carbon dioxide as the contrast agent. Carbon dioxide/digital subtraction arteriography permits patients with symptomatic arterial disease at high risk for contrast related complications to safely undergo arteriography and subsequent arterial reconstruction or endovascular intervention.
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PMID:Clinical applications of carbon dioxide/digital subtraction arteriography. 189 74

A Commercially available, non-invasive system for estimation of cardiac output by the CO2-rebreathing method (Sensormedicus MMC4400) was evaluated to determine its reliability in clinical practice. Values of cardiac output were obtained at rest and during mild to moderate bicycle ergometer work in patients with ischemic heart disease or hypertension. Cardiac output measured by the CO2-rebreathing method was significantly correlated with that measured simultaneously by dye dilution or thermodilution methods. Cardiac output values determined by the CO2-rebreathing method were the same as those obtained by the two invasive methods in reproducibility. When cardiac output and Vo2 were normalized for body weight, they were significantly correlated with each other. This result was obtained both by the CO2-rebreathing method, and by the two invasive methods. These results indicate that MMC4400 will provide a value for cardiac output substantially the same as that obtained by using more laborious invasive methods. Clinical use of the CO2-rebreathing method has been limited by technical difficulties. However, the recently developed non-invasive cardiac output measurement system (MMC4400) uses a microcomputer to analyze the results, and the operator can determine the values for cardiac output easily. Furthermore, it simultaneously measures VO2, VCO2 and VE, so the operator can estimate the measured values for cardiac output with background information on ventilatory gas analysis. Determination of cardiac output through the use of the CO2-rebreathing method is suitable particularly for exercise studies, and it is expected to be a useful device, in the near future, for evaluating cardiac function of patients with primary cardiac diseases.
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PMID:[Non-invasive measurement of cardiac output by the CO2 rebreathing method and its reliability in clinical practice]. 190 14


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