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

Extracorporeal circulation can cause lung damage, which would be especially counterproductive during extracorporeal gas exchange for the treatment of acute respiratory failure. To test the hypothesis that partial venovenous bypass with extracorporeal CO2-removal combined with low-frequency positive pressure ventilation (ECCO2R-LFPPV) can adversely affect lung fluid balance, extravascular thermal lung volume (ETV) and hemodynamics were assessed before, during and after ECCO2R-LFPPV in normal closed chest dogs. In series I dogs (n = 6) subjected to 10 h of ECCO2R-LFPPV, ETV did not change significantly from control (7.1 ml/kg +/- 0.99 SE) during or after bypass. Gravimetric extravascular lung water and lung histology after bypass were found to be normal. In series II dogs (n = 5), subjected to shorter periods of ECCO2R-LFPPV, ETV also remained unchanged. In contrast to previous reports using sheep, pulmonary arterial hypertension during bypass was not observed. Thus, ECCO2R-LFPPV was not associated with increased lung water, pulmonary hypertension or morphological lung changes under the conditions studied and does not seem to cause lung damage in normal lungs.
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PMID:Lung extravascular volume during venovenous bypass with extracorporeal CO2-removal in dogs. 312 77

Previous studies have shown that after experimental neural trauma or acute hypertension the brain produces superoxide anion radicals, and brain arterioles display endothelial lesions, dilation, and loss of normal reactivity in response to a decrease in CO2 tension. Because these abnormalities are prevented by pretreatment with free radical scavengers or inhibitors of the cyclooxygenase component of prostaglandin (PG) H synthase, arachidonic acid metabolism by PGH synthase with concomitant formation of tissue injuring oxygen radicals causes the vascular damage. The purpose of the present experiments was to determine whether kinins, which are known to stimulate arachidonate metabolism and to induce cerebral arteriolar dilation via production of superoxide anion, may be involved in initiating the cerebrovascular abnormalities produced by neural trauma in cats. The diameter and reactivity of untreated in vivo pial arterioles on one cerebral cortex was compared with the diameter and reactivity of pial arterioles on the contralateral cortex, which were pretreated topically with a competitive receptor antagonist, which is specific for kinins. Before fluid percussion neural trauma was induced, arterioles on both cerebral hemispheres constricted normally to a decrease in CO2 tension. After injury, the arterioles on the untreated cortex dilated and did not constrict in response to a decrease in arterial CO2 tension, whereas the arterioles pretreated with the kinin antagonist dilated less and displayed normal reactivity to CO2. These experiments demonstrate that a specific kinin receptor stimulates PGH synthase-dependent, free radical-mediated cerebrovascular injury. Given the ubiquitous distribution of the kallikrein-kinin system, we propose that kinins may be an important common mediator of systemic vascular injury and abnormal vascular reactivity.
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PMID:Kinins induce abnormal vascular reactivity. 313 69

In 9 severe head injuries whose respiration was controlled by a ventilator, continuous measurements of energy expenditure (MEE) were carried out by the ERICA Metabolic Computer. Age was ranged 19 to 69 years old (Mean 48.3 years). Glasgow Coma Scale score was 3 to 11 which were assessed the best score during 6 hours of admission. The MEE was carried out within 7 days of admission and was continued to measure more than 3 days. It measured O2 consumption and CO2 output, and calculated the indirect energy expenditure. The data were displayed and recorded every 1, 15, 60 min. The value of MEE was compared with predicted energy expenditure (PEE) which was calculated by the Harris-Benedict formula. Out of 9 patients, 6 patients were survived. High dose barbiturate therapy was performed in 7 patients to control and decrease the intracranial hypertension. Of them 3 patients died. The value of MEE in all 9 patients was variable from 77% to 212% of PEE. The value of MEE in 6 survived patients was 98.0 to 212.0% of PEE. Out of 6 patients, 4 patients who were administered high dose barbiturate showed variable data of MEE. Two patients showed about 100% of the PEE, one showed about 150%, and another one about 200%. Remaining 2 survivors who were not administered barbiturate showed about 125% of PEE, which was low value. These results were divided into two groups. In 2 patients, the value of MEE was 150% or more in spite of barbiturate therapy. In remaining 7 patients, the value of MEE was 125% or less of PEE.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Continuous measurement of energy expenditure in ventilated patients suffering from severe head injury]. 319 95

The nocturnal behaviour of blood pressure obtained by a new portable device for monitoring ambulatory blood pressure (ABPM 630) was compared with that obtained by a finger-volume oscillometric device (BP-100); the former uses a conventional arm-cuff inflated by CO2 gas to eliminate the noise of the motorized pump, and is based on a cuff-oscillometric as well as the Korotkoff sound technique (microphone method). With the microphone method in ABPM 630, the mean differences from the conventional auscultatory method were -0.28 +/- 6.15 mmHg (mean +/- s.d.) for systolic and 0.96 +/- 6.28 mmHg for diastolic blood pressure, and there was a highly significant correlation between blood pressure values measured by the ABPM 630 and by the auscultatory method. In 40 patients with mild to moderate hypertension 24-h blood pressure was monitored simultaneously with the ABPM 630 and BP-100. The daytime average of systolic blood pressure measured with the ABPM 630 was similar to that measured with the BP-100, whereas the night-time average assessed by the former was significantly higher than that assessed by the latter. Arm-cuff inflation by ABPM 630 caused some degree of sleep disturbance in 35 of 40 subjects, whereas finger-cuff inflation scarcely disturbed the sleep. The performance of the ABPM 630 was excellent.
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PMID:Difference in the nocturnal behaviour of blood pressure between monitorings with the arm-cuff method and with the finger-volume oscillometric method. 324 Dec 64

The changes of intracranial hemodynamics were studied at the early stage of vasorenal arterial hypertension in 7 rabbits. During first 4-5 weeks of the hypertension development, the AP increased to 170 mm Hg which was followed by a drop in the blood flow by 15% in the cortex and by 19% in white matter. The blood flow increment in response to inhalation of CO2 lowered from initial 120% to 106% in the cortex and from 126% to 109% in white matter. The data on the brain tissue impedance suggested an absence of the hyperhydration of extracellular space. A mathematical model of the development of cerebral hemodynamic shift was suggested for this form of arterial hypertension, and the hypothesis was formed that vasoconstrictor response of the brain resistive vessels decreased cerebral blood flow thus preventing th shift of the Starling equilibrium and the fluid outflow from the vascular bed.
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PMID:[Intracranial hemodynamics in arterial hypertension (the renal model)]. 324 86

The effects of isoflurane (1 MAC) and enflurane (1 MAC) on cerebral blood flow and cerebral oxygen consumption were studied in 20 male patients without intracranial disease undergoing coronary artery bypass surgery (mean age 57 and 59 years respectively). The aim of the study was to investigate whether both agents diminish autoregulation of cerebral blood flow and CO2 reactivity of cerebral blood vessels. Patients were randomly assigned to one of two groups (10 patients each) receiving either isoflurane 1.15 vol.% or enflurane 1.68 vol.% endexpiratory. Measurements were performed and blood samples were taken in the awake state (I); 15 min after achievement of steady-state conditions with 1.68 vol.% enflurane or 1.5 vol.% isoflurane without blood pressure support (II); during norepinephrine-induced hypertension at a cerebral perfusion pressure of 110 mmHg (III); and during controlled hyperventilation at a PaCO2 of 27 mmHg and normotension (IV). Cerebral blood flow was measured by the argon wash-in technique. Isoflurane and enflurane produced a significant drop in cardiac index and cerebral perfusion pressure and reduced cerebral blood flow significantly by 35% and 39% respectively. Cerebral oxygen consumption was also significantly decreased by 49% (isoflurane) and 50% (enflurane). Induced hypertension with norepinephrine increased cerebral blood flow significantly by 32% (isoflurane) and 26% (enflurane), while hypocapnia reduced cerebral blood flow significantly by 26% (isoflurane) and 29% (enflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effects of isoflurane and enflurane on cerebral hemodynamics and cerebral oxygen consumption in humans]. 326 82

Endothelium-dependent relaxations are reduced in hypertensive rats. High dietary potassium supplementation reduces the incidence of strokes in Dahl rats independently of blood pressure, thereby suggesting a direct protective effect of the diet. Endothelium-dependent relaxations and aortic vascular architecture were studied in Dahl salt-sensitive rats fed 8% NaCl, 0.1% NaCl, or 8% NaCl plus 3.6% potassium citrate for 8 weeks. Rats fed 8% NaCl or 8% NaCl plus 3.6% potassium citrate became hypertensive, while those fed 0.1% NaCl did not. Aortic rings with and without endothelium were suspended in organ chambers filled with physiological salt solution (37 degrees C) and aerated with 95% O2, 5% CO2. In rings contracted with norepinephrine, acetylcholine and adenosine 5'-diphosphate caused endothelium-dependent relaxations that were significantly reduced in rats fed 8% NaCl as compared with those fed 0.1% NaCl. Potassium supplementation (8% NaCl/3.6% potassium citrate) significantly enhanced relaxations to acetylcholine in salt-sensitive rats, while those to adenosine 5'-diphosphate and thrombin were either minimally affected or unchanged. Relaxations to sodium nitroprusside were similar in rats with or without potassium supplementation. Hypertension significantly increased aortic medial and intimal thickness. Dietary potassium had no significant effect on the vascular architecture. These results suggest that high potassium diet enhances endothelium-dependent relaxations in Dahl rats at least in part independently of changes in blood pressure. Thus, potassium may be important for its protective effect against stroke and renal damage in this animal model of hypertension.
Hypertension 1988 Dec
PMID:High potassium diet augments endothelium-dependent relaxations in the Dahl rat. 326 44

The authors anesthetized 18 patients with good pulmonary and ventricular function for coronary artery bypass grafting with high doses of fentanyl. When the patients were arousable and their vital signs stable in the intensive care unit, the authors administered nalbuphine or placebo (randomly and double-blinded) until extubation criteria were met, and subsequently gave nalbuphine for analgesia. In one of ten placebo patients, tracheal extubation was accomplished without nalbuphine. This patient then retained CO2 and required nalbuphine; the other nine placebo patients could not be extubated after placebo trials and were given nalbuphine. In all other patients in both groups, tracheal extubation was successful following nalbuphine (median dose 60 micrograms/kg, range 30-180 micrograms/kg). One patient became renarcotized 4 h after tracheal extubation without an increase in plasma fentanyl concentration; he received an additional dose of nalbuphine and recovered without further incident. Nine patients required treatment with vasoactive agents or beta-blockers for hypertension or tachycardia associated with the administration of nalbuphine. Eight of 18 patients were not satisfied with nalbuphine analgesia, and required morphine for relief of their pain. Recurrent elevations of fentanyl concentrations in plasma were observed and appeared to be related to increasing motor activity. Nalbuphine is an effective opioid antagonist after fentanyl anesthesia, but its use is associated with side effects, and analgesia for the post-sternotomy patient may be unsatisfactory unless the dose is carefully titrated to the minimum required to antagonize respiratory depression.
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PMID:Nalbuphine antagonism of fentanyl-induced ventilatory depression: a randomized trial. 327 86

The hemodynamic hallmark of hypertension is increased systemic vascular resistance, although this variable is usually not determined in hypertensive patients because it has generally required invasive procedures to measure cardiac output. Reliable, totally noninvasive methods are now available that measure cardiac output accurately enough under a variety of conditions, including rest, exercise, and pharmacologic interventions. These methods include echocardiography, Doppler echocardiography, CO2 rebreathing, and impedance cardiography. Their serial application to large numbers of patients offers the opportunity to significantly broaden our understanding of the spectrum and course of hemodynamic alterations associated with hypertension. A more complete knowledge of underlying hemodynamics could improve our diagnostic and prognostic accuracy in hypertensive patients and enhance our understanding of the pathophysiology of hypertension and the mechanism of action of antihypertensive interventions.
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PMID:Application of noninvasive techniques for measuring cardiac output in hypertensive patients. 329 10

Lipid X (2,3-diacylglucosamine-1-phosphate) is a novel monosaccharide precursor of lipid A that has some of the physiologic activities of endotoxin but little toxicity. To determine whether lipid X would interfere with the toxic effects of endotoxin, we pretreated sheep with either 100 or 200 micrograms of lipid X per kg of body weight and then challenged them with a potentially fatal dose of Escherichia coli endotoxin (20 micrograms/kg). Twenty-one sheep underwent pulmonary artery catheterization and were monitored for changes in pulmonary artery pressure, temperature, pH, partial O2 pressure, partial CO2 pressure, blood pressure, and cell counts over 7 h. Overall mortality for control animals was 37% versus 5.3% for pretreated animals. None of the 13 animals pretreated with 100 micrograms of lipid X per kg died. These differences in survival were significant (P less than 0.05). Animals pretreated with 100 micrograms of lipid X per kg had significantly lower pulmonary artery pressure during both phases 1 and 2 of endotoxin-induced pulmonary artery hypertension. A higher dose of lipid X, 200 micrograms/kg, produced pulmonary hypertension. Perhaps because lipid X is a subunit of lipid A, lipid X shows a partial pyrogenic effect while also decreasing the pyrogenic activity of complete lipopolysaccharide (LPS). Lipid X did not prevent endotoxin-induced neutropenia or moderate hypotension in response to LPS. Lipid X is a potential prototype compound for a new type of chemotherapy directed at blocking the harmful effects of LPS during bacterial septicemia.
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PMID:Lipid X ameliorates pulmonary hypertension and protects sheep from death due to endotoxin. 330 7


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