Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Traumatic brain injury affects approximately 500,000 persons each year. For those patients who survive until they reach the hospital, the major goal of the health care team is to prevent secondary injuries or insults that may follow the initial event and worsen the brain injury. Factors that can cause secondary insults to the brain include hypoxia, hypercapnia, hypotension, and intracranial hypertension. Prevention of these factors begins in the pre-hospital care phase and continues into the critical care unit. Early recognition of these factors and prompt intervention can improve the neurologic outcome of the patient with severe head injury. An understanding of the causes and effects of these secondary insults is critical to the appropriate medical and nursing management of these patients.
 ...
PMID:Preventing secondary brain injury. 155 60

Asphyxia can cause neurologic damage in the fetus, but there are few data relating severity or duration of asphyxia to the degree of cerebral damage. We report cerebral histologic and electrophysiologic changes after asphyxia in chronically instrumented late-gestation fetal sheep. We reduced uterine blood flow to produce an ascending aortic blood oxygen content less than 1.5 mM for either 30 or 60 min (n = 13). In a subsequent protocol (n = 6), if full occlusion of the common uterine artery for 15 min did not reduce the EEG voltage to less than 20% of baseline, supplementary maternal hypoxia was added for a maximum of 120 min. Histologic outcome was assessed 3 d postinsult. Uterine artery occlusion resulted in severe hypoxemia, hypercarbia, acidosis, and an initial hypertension and bradycardia. Eight of 14 surviving fetuses showed neuronal damage, with greatest loss in the parasagittal cortex, striatum, and the CA1/2 region of the hippocampus. Neuronal damage was strongly associated with the percentage of decrease in blood pressure during the insult (r = 0.75, p less than 0.005) but not with the degree of hypoxia. No other factor was independently predictive, but, when considered separately, pH (r = 0.54; p less than 0.05) and loss of intensity of the EEG (r = 0.61, p less than 0.02) at the end of asphyxia were also correlated with outcome. The pH fell to less than 7.0 in six of eight fetuses with damage, whereas it remained greater than 7.0 in five of six without damage (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cerebral histologic and electrocorticographic changes after asphyxia in fetal sheep. 160 25

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
 ...
PMID:Acute postoperative hypertension in the hypertensive patient. 173 70

Atrial natriuretic factor (ANF) is a peptide secreted by auricular cardiac cells and acts on the brain; it is a diuretic, a natriuretic and a vasodilator and inhibits the renin angiotensin aldosterone system at several levels. The lungs are rich in specific ANF receptors present both at a vascular cellular level and in the mesothelial cells. These receptors participate in the extraction of ANF during its pulmonary intravascular transit and also in its enzymatic degradation. Endogenous ANF (and exogenous) is a vasodilator of the pulmonary arterial bed, representing a regulatory system for right ventricular afterload and probably modifying pulmonary capillary permeability. Hypoxia and hypercapnia contribute by direct and indirect mechanisms to the stimulation of ANF secretion explaining their elevated levels in pulmonary arterial hypertension and chronic respiratory insufficiency. The lung can under certain conditions synthesise ANF itself as can neuro-endocrine bronchial tumours. ANF may be involved in the understanding of sodium retention during ventilation with PEEP and in the paraneoplastic hyponatraemia of certain bronchial tumours. Finally acute bronchial obstruction leads to hypersecretion of ANF which has some bronchodilator properties.
 ...
PMID:[Atrial natriuretic factor and the lung]. 183 Mar 97

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.
 ...
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)
 ...
PMID:[Anesthesia in unilateral pulmonary transplantation]. 185 49

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.
 ...
PMID:Endothelin action on cerebral circulation in unanesthetized goats. 188 47

We superimposed extreme hypercapnia (arterial Pco2 400-450 mmHg) immediately before and during incomplete cerebral ischemia to distinguish the role of intracellular pH (pHi) and bicarbonate [( HCO3-]i) in postischemic metabolic and electrophysiological recovery. Incomplete global ischemia was produced in seven anesthetized dogs by 30 min of intracranial hypertension followed by 4 h of reperfusion. ATP, phosphocreatine (PCr), and pHi were measured with 31P magnetic resonance spectroscopy, and [HCO3-]i was calculated from the Henderson-Hasselbalch equation using the measured pHi and sagittal sinus Pco2. Cerebral blood flow was reduced to 7 +/- 1 ml.min-1.100 g-1 (+/- SE) during ischemia with extreme hypercapnia, and pHi decreased to 5.72 +/- 0.09. During normocapnic reperfusion, pHi rapidly returned to near baseline values by 14 min. [HCO3-]i fell from 12.1 +/- 0.9 to 6.0 +/- 1.2 mM by the midpoint of ischemia and recovered by 30 min of reperfusion. ATP, PCr, and O2 consumption also recovered rapidly and completely. Somatosensory-evoked potentials (SEP) recovered to 43 +/- 10% of control amplitude. These results are in marked contrast to the poor metabolic and SEP recovery previously observed in hyperglycemic dogs in which pHi decreased to the same range as with hypercapnic ischemia, but in which [HCO3-]i was much lower (1.1 +/- 0.5 mM). Therefore, [HCO3-]i depletion during hyperglycemic ischemia may be a more important factor in recovery than end-ischemic pHi per se. We speculate that higher [HCO3-]i may improve glial cell buffering capacity or decrease iron availability for hydroxyl radical production.
 ...
PMID:Bicarbonate conservation during incomplete cerebral ischemia with superimposed hypercapnia. 190 5

Anesthetic management during 85 STA-MCA anastomoses with or without encephalo-myosynangiosis for 64 patients with Moyamoya disease was evaluated retrospectively. Anesthetic agents included nitrous oxide-NLA (GONLA), nitrous oxide-halothane (GOF), nitrous oxide-enflurane (GOE), and their combinations. Slight hypercarbia (40 mmHg less than PaCO2 less than 50 mmHg) was essential to avoid cerebral ischemia. Several procedures to control heart rate by beta blockade or to control hypertension by nitroglycerin were required, because tachycardia and hypertension interfered with fine surgical procedure. During microsurgery HR of GONLA anesthetized patients was significantly lower. Postoperatively the patients anesthetized by GOE showed significantly lower PaCO2 compared with the GONLA anesthetized patients. So we recommend GONLA for anastomosis in patients with Moyamoya disease.
 ...
PMID:[Anesthetic management of revascularization for moyamoya disease]. 192 Jul 89

The health risks of obesity increase with its severity and reach significance at a weight greater than 20% above optimal, by using life insurance tables, or at a body mass index greater than 27. Risks include hypertension, insulin resistance and diabetes mellitus, cardiovascular disease, hypertriglyceridemia, low high-density-lipoprotein cholesterol, and, in some studies, high total-and low-density-lipoprotein cholesterol. There is an increased mortality from endometrial cancer in women and from colorectal cancer in men. Chronic hypoxia and hypercapnia, sleep apnea, gout, and degenerative joint disease can occur with more severe obesity. The distribution of body fat is directly related to these health risks. Abdominal obesity is more dangerous than gluteal-femoral obesity because the amount of intraabdominal fat seems to determine much of the increased peril; therefore, risks of cardiovascular disease, stroke, hypertension, and diabetes increase with abdominal obesity, even independently of total fat mass.
 ...
PMID:Health implications of obesity. 203 92


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>