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

The effects of an acute cryogenic injury on cerebral flow (CBF) and cerebral vascular reactivity were studied in 12 anaesthetised, ventilated baboons. Autoregulation, defined in this study as intact with a greater than 20% change in cerebrovascular resistance in response to a change in cerebral perfusion pressure, was tested before the lesion by arterial hypotension. Intact autoregulation was found in half the animals, but all animals showed an increase in CBF with hypercarbia. The cryogenic lesion was followed by a marked rise in intracranial pressure, and a fall in CBF which was only partly related to the status of autoregulation beforehand. After injury, arterial hypertension caused an increase in cerebrovascular resistance of more than 20% in half the animals. This response was not related to the presence of autoregulation before the lesion, and was accompanied by a greater impairment of the cerebrovascular response to carbon dioxide, more severe brain oedema, and lower cerebral oxygen consumption, than in the remaining baboons which had a pressure passive response to arterial hypertension. This study confirms that the failure of CBF to increase with arterial hypertension may indicate severe brain damage rather than intact physiological autoregulation.
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PMID:Vascular reactivity in the primate brain after acute cryogenic injury. 41 85

The cardiovascular and acid-base changes following equivalent i.v. bolus doses of sodium nitroprusside (SNP) and potassium cyanide (KCN) have been studied in two groups of anaesthetized dogs. In a third group, the metabolic changes produced by i.v. infusion of SNP 1.5 mg kg-1 at a constant rate over 1 h have been studied. In contrast to a decrease in arterial pressure following SNP, hypertension and tachycardia occurred after the administration of KCN, with hyperventilation and an increase in packed cell volume. During infusion of SNP, increases in plasma cyanide concentrations were associated with an increase in arterial base deficit, plasma lactate and excess lactate and a decrease in oxygen consumption. The occurrence of lactic acidosis with SNP 1.5 mg kg-1 suggests that this may be the maximum safe dose for short term infusion. However, all these changes reversed spontaneously following discontinuation of SNP, indicating that base deficit is an adequate metabolic monitor during administration of SNP.
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PMID:Some physiological and metabolic effects of sodium nitroprusside and cyanide in the dog. 42 97

Severe head injury may cause momentary respiratory arrest. Resultant hypoxia would increase cerebral edema and adversely affect the quality of survival. This study examines the effect of hypoxemia on outcome. Pulmonary shunt was calculated as a convenient measurement of respiratory insufficiency in 86 severely head-injured patients who underwent surgery. All samples were taken shortly after induction into anesthesia when controlled ventilation with high inspired-oxygen concentration had been established. In 39 patients who improved, mean pulmonary shunt was 8.9%. Twelve patients who survived with deficit showed a mean shunt of 13.6%, and in 35 patients who died, the mean initial shunt was 15.6%. No significant correlation was found between abnormal chest x-ray findings or the occurrence of hypertension and shunt percentage. The American Society of Anesthesiologists at-risk classification correlated grossly with the outcome. Early pulmonary shunt is a prognostic indicator in severe head injury and should be used in conjunction with the Glasgow Coma Scale in assessing outcome. Despite an apparently adequate respiratory pattern, all patients with severe head injury must be assumed to be hypoxic until proven otherwise. While hypoxemia may prove to be refractory in overwhelming injury, patients who score low on the Glasgow Coma Scale but who have relatively normal oxygen exchange may still survive with little deficit.
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PMID:Pulmonary shunt as a prognostic indicator in head injury. 43 77

The authors placed Swan-Ganz catheters in 11 preterm and 2 term infants with severe cardiopulmonary distress. The infants ranged in weight from 1100-4000 g. The procedure was performed in the neonatal ICU by jugular venous cutdown. Intracardiac pressures and oxygen saturations were measured in each chamber entered. The authors also evaluated the presence of right to left shunting through the patent ductus arteriosus and assessed the degree of pulmonary arterial hypertension. In 5 hypoxemic infants, the authors found a patent ductus arteriosus with pulmonary hypertension. Intermittent measurement of PAP served as a guide to further therapy. In 2 infants, the unexpected diagnosis of cyanotic congenital heart disease was made. The placement of flow directed pulmonary arterial catheters in critically ill infants can be performed safely at the bedside and can provide useful diagnostic and therapeutic information.
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PMID:Swan-Ganz catheterization in the critically ill newborn. 45 10

Effects of peripheral arterial chemodernervation on laryngeal reflex-induced apnea were studied in 18 piglets of either sex varying in age from 4 to 63 days. The distal trachea was cannulated with a cuffed endotracheal tube to secure a free airway and permit ventilatory measurements with a pneumotachograph. The proximal trachea was used to introduce fluids into the larynx. Water elicited apnea, bradycardia, and arterial hypertension, whereas saline caused only transient disturbances. Electrical stimulation of the superior laryngeal nerves reproduced, and conduction anesthesia ablated, the effects of water in the larynx. Carotid body contribution to respiratory drive was assessed by the ventilatory responses to increased (100%) and decreased (10%) anbient oxygen concentration. These indicated significant peripheral chemoreceptor ventilatory activity from birth with little further change in the neonatal period. Ventilatory responses to oxygen were ablated by carotid chemodenervation, but there was no change in the duration of laryngeal reflex apnea. We conclude that attenuation of laryngeal-induced apnea during postnatal development is independent of peripheral chemoreceptor activity. Our findings may have relevance to the clinical problem of sudden infant death syndrome, in which carotid body abnormalities have recently been described.
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PMID:Laryngeal reflex apnea in the chemodenervated newborn piglet. 46 79

After an ischaemia lasting 1 hour as well as after an extreme hypertension lasting 210 minutes in the kidney of a rat a significant increase of the renin activity in the juxtaglomerular apparatus was found. By chronic load with sodium chloride was tried to produce a decrease of renin. In contrast to an ischaemic lesion the kidneys of the animals loaded with salt revealed a better ischaemia tolerance than those of the unloaded animals. This is expressed by a significantly increased total blood supply and cortical blood supply. On the two experimental conditions a change of the distribution of the blood supply in favour of the inner compartments of the kidneys may be observed. In the oxygen histogram of the surface of the kidney the salt-loaded kidneys reveal a better oxygenation before and after the ischaemic lesion. The kidneys loaded before show an essentially more insignificant decrease of the urine excretion than the unloaded ones.
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PMID:[Chronic sodium chloride load--a possibility for the increase of tolerance for ischemia in the kidney]. 48 65

This case is unusual in that hypotension, as opposed to hypertension, was a consequence of increased sympathetic tone in the postoperative period, but it illustrates the well known fact that patients in compensated congestive heart failure do poorly when faced with an elevated myocardial oxygen need from either increased rate or afterload. Vasodilator therapy was effective in immediately reducing afterload and systolic regurgitant fraction, thereby increasing oxygen supply and lowering myocardial oxygen consumption.
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PMID:Vasodilator correction of hypotension in the postoperative period. 50 99

Lung emphysema was produced in 80 rats by tracheal chronic constriction and repeated instillations of 0.1% papain solution intratracheally. 17 animals survived 90 days of the experiment; a complete examination was performed on 14 experimental and 11 control animals. 9 rats of the experimental group had pulmonary hypertension, in 5 other rats the pulmonary arterial blood pressure was not different from that in the controls. The experimental animals with hypertension had arterial hypoxemia and increased weight of the right ventricle. All experimental rats (with and without pulmonary hypertension) had increased air spaces in the lung and thickened media of distal pulmonary vessels. After breathing 100% oxygen for 20 min, the pulmonary arterial blood pressure in animals with pulmonary hypertension decreased but did not reach the control level. The decrease of the mean pulmonary arterial blood pressure after oxygen breathing correlated well with the initial level of pulmonary hypertension and with the degree of hypoxemia during air breathing.
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PMID:Pulmonary hypertension in rats with papain emphysema. 52 27

Setting out from the components of respiratory function, i.e., ventilation, distribution, diffusion, circulation, respiratory mechanics, and regulation of breathing, the pathogenic mechanisms leading to respiratory failure are discussed. In every case, the vital capacity is decreased by 4 factors, namely loss of ventilated lung parenchyma, diminished compliance of lungs, thorax or both, airway obstruction, and insufficient respiratory airflow. With few exceptions, these alterations can be attributed to the two general groups of obstructive and restrictive disturbances of ventilation. Essential for the understanding of airway obstruction from the viewpoint of mechanical ventilation is the dependence of the airway caliber on lung volume, thoracic pressure, and bronchial gas flow. The functional differentiation of restrictive disorders between forms with lung retraction(fibrosis, scarring) and with lung fettering (pleural thickening) is important for adequate correction of complications during the intensive care phase. Respiratory failure is the consequence of these alterations which usually impede pulmonary gas exchange. Hypoxemia results in most situations through disturbance of ventilation/perfusion ratio, especially increase of anatomical or functional pulmonary right-to-left shunting. Disturbance of diffusion or alveolar hypoventilation are far less frequently leading mechanisms for hypoxemia. The differential diagnosis of these hypoxemic mechanisms is generally by arterial blood gas analysis under resting conditions breathing air and 100% oxygen, and during exercise. Respiratory failure often leads to hypertension in the lesser circulation. Pulmonary arterial hypertension must be subdivided into the active, the passive and the hyperdynamic forms, of which only the active component is important for the evaluation of pulmonary insufficiency since only this kind of elevated pressure in the pulmonary circulation is connected with increased vascular resistance due to thoracopulmonary disease. By restoration of normoxic conditions, the functional variant of active pulmonary hypertension can be efficiently improved by correction of respiratory disease or directly by treatment with oxygen and by mechanical ventilation. Finally, disturbances of gas transport in the blood may have an essential bearing on respiratory failure, but are often overlooked in diagnostic and therapeutic considerations. Shifting of the oxygen-dissociation curve to the left may, by increased oxygen affinity of hemoglobin, create a lack of oxygen in the peripheral tissue, while right wardshifting impedes oxygenation of hemoglobin in the lung. Thus, the correction of acidosis and elevated body temperature may become an important factor in the treatment of respiratory failure.
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PMID:[Basis of respiratory insufficiency]. 52 97

Examination of the bronchial artery system by means of contrast materials and pneumo-angiography has made it possible to determine the extent of the pathological process and to provide an answer to some of the problems raised by chronic non-specific diseases. When free passage is disturbed in the bronchi and alveolar ventilation is abolished, arterial blood will reach through the arterio-arterial anastomosis the branches of the pulmonary arteries, followed by a local hypertension in the affected region and a high oxygen saturation in the terminal branches of the pulmonary artery. In the case of bronchiectasis, the capillary circulation in the bronchial wall decreases because of the extension of the bronchial system which leads to the development of sclerosis and thus to a deterioration of the drainage function of the bronchus.
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PMID:Angiography of the bronchial and pulmonary arteries in chronic non-specific lung diseases. 55 86


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