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

Nalbuphine hydrochloride, an agonist-antagonist opioid, is reported to reverse the respiratory depression of moderate doses of fentanyl (20 micrograms.kg-1) and still provide good analgesia. We report four patients having abdominal aortic aneurysm repair in which we attempted to reverse the respiratory depression of large doses of fentanyl (50-75 micrograms.kg-1) with nalbuphine (0.3 mg.kg-1, 0.1 mg.kg-1 or 0.05 mg.kg-1). Nalbuphine reversed respiratory depression in all four patients and the respiratory rate increased from 10 to 23 breaths per minute, end-tidal CO2 decreased from 7.0 +/- 0.3 per cent to 5.6 +/- 0.7 per cent, and peak inspiratory pressure after 0.1 seconds increased from 4 +/- 1.4 to 13 +/- 2.6 mmHg. However, hypertension, increased heart rate, and significant increase in analogue pain scores accompanied reversal of respiratory depression. Agitation, nausea, vomiting, and cardiac dysrhythmias also were observed frequently. We do not recommend the use of nalbuphine to facilitate early extubation of the trachea after large doses of fentanyl for abdominal aortic surgery.
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PMID:Side effects of nalbuphine while reversing opioid-induced respiratory depression: report of four cases. 165

During the last decade several studies of cerebral blood flow (CBF) and metabolism in the acute phase of head injury have been published. It is the aim of this review to describe the dynamic changes in CBF, cerebral metabolic rate of oxygen (CMRO2), cerebral autoregulation (CA), and reactivity to PaCO2 and barbiturate (metabolic reactivity) in the acute phase after severe head injury and to discuss the therapeutical consequences with reference to prolonged artificial hyperventilation, hypothermia, barbiturate sedation, and mannitol therapy. On the basis of present knowledge concerning cerebral circulation and its regulation, the author reviews the literature concerning methodology for experimental and clinical CBF measurements and regulation of CBF and cerebral oxygen uptake. Emphasis is placed on studies of the effect of body temperature (hypothermia) as a therapeutic tool in the control of cerebral metabolism, blood flow, and intracranial pressure. Although hypothermia significantly reduces cerebral metabolism and blood flow, the effect of hypothermia on cerebral blood flow, metabolism, ICP, and outcome after acute head injury has never been investigated in clinically controlled studies. Experimental and clinical studies concerning sensitivity of CBF for changes in PaCO2 are reviewed. The normal CO2 reactivity defined as absolute (delta CBF/delta PaCO2) and relative (% change CBF/delta PaCO2) or delta in CBF/PaCO2 mm Hg are mentioned. In awake normocapnic man the relative CO2 reactivity averages 4%/mm Hg and the absolute CO2 reactivity 2ml/mm Hg. Uncontrolled prospective studies show a therapeutic effect of artificially prolonged hyperventilation on outcome. Only one preliminary controlled study indicates that the outcome is poorer and recovery prolonged. Nevertheless, in the acute phase of HI, artificial hyperventilation is used routinely for control of intracranial hypertension and during the intensive care management of the patients. The steal and inverse steal phenomena are reviewed. Although of considerable theoretical interest these phenomena are without clinical significance in patients with head injury, unless clinical CBF measurements are performed. The frequency of the inverse steal phenomenon in studies of rCBF with a 16-channel Cerebrograph (intraarterial approach) is found to be about 10%. During prolonged hyperventilation experimental studies and clinical studies of apoplexy show an adaptation of CBF and CSF-pH and bicarbonate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebral blood flow in acute head injury. The regulation of cerebral blood flow and metabolism during the acute phase of head injury, and its significance for therapy. 227 29

Impairment of endothelium-dependent relaxations may be of primary importance in hypertension, if this impairment were to occur in resistance arteries. Therefore, endothelium-dependent relaxations to acetylcholine were studied in the mesenteric resistance vessels of spontaneously hypertensive and Wistar-Kyoto rats. Rings with and without endothelium were suspended in a myograph filled with physiological salt solution at 37 degrees C and aerated with 95% O2/5% CO2; the isometric tension was recorded. Acetylcholine caused relaxations only in rings with endothelium. In the spontaneously hypertensive rat, relaxations were impaired and markedly biphasic with an early rapid relaxation followed by a secondary contraction. Indomethacin inhibited the secondary response and augmented the duration of the relaxations induced by acetylcholine in the arteries from spontaneously hypertensive rats. These findings suggest that the decreased endothelium-dependent relaxation to acetylcholine in mesenteric resistance vessels of the spontaneously hypertensive rat is due to the release of a constrictor prostanoid which partly offsets the response of the vascular smooth muscle to endothelium-derived relaxing factor(s).
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PMID:Indomethacin improves the impaired endothelium-dependent relaxations in small mesenteric arteries of the spontaneously hypertensive rat. 230 29

Patients undergoing extracorporeal shock wave lithotripsy (ESWL) for nephrolithiasis are anesthetized and immersed in water in a semisitting position. Hypertension and tachycardia have been reported to accompany ESWL, and it was hypothesized that those problems were a result of adrenal medullary release of epinephrine or norepinephrine. Therefore, the effects of ESWL on cardiovascular variables and circulating epinephrine and norepinephrine levels in nine patients anesthetized with 1.1% isoflurane in 50% nitrous oxide and oxygen were studied. End-tidal carbon dioxide (CO2) was maintained at 34 +/- 2 mmHg. Cardiac output (CO) and mean arterial pressure (MAP) were measured, and total peripheral resistance (TPR) was calculated at the following time points: (1) after immersion prior to shock wave therapy (control); (2) after 300 shocks; (3) after 800 shocks; and (4) 5 minutes after the completion of ESWL with the patient still immersed. Circulating epinephrine and norepinephrine concentrations were determined at the above times as well as before and after induction of anesthesia but prior to immersion. There was a statistically significant (p less than 0.05) decrease in CO and an increase (p less than 0.05) in MAP and TPR with ESWL treatment. These values returned to baseline levels when treatment was stopped. Plasma epinephrine and norepinephrine values did not change significantly throughout the study period. It was concluded that these ESWL-associated hemodynamic changes were probably not mediated via epinephrine or norepinephrine.
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PMID:Hemodynamic and catecholamine responses associated with extracorporeal shock wave lithotripsy. 235 56

We investigated cerebral blood flow and metabolism, and cerebral vascular response in 9 patients with cerebrovascular Moyamoya disease or unilateral Moyamoya phenomenon using positron emission tomography (PET). The subjects consisted of 5 men and 4 women, and were from 9 to 60 years old. Five patients had bilateral occlusion in the carotid fork with Moyamoya vessels (fulfilled the criteria of cerebrovascular Moyamoya disease), and four patients had unilateral Moyamoya phenomenon. The PET scanner used was the HEADTOME III, of which spatial resolution in clinical use was 10 mm full width at half-maximum (FWHM) in the image plane. Cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), cerebral oxygen extraction fraction (OEF), and cerebral blood volume (CBV) were measured in resting state by the 15O-labelled gases steady state method in every patient and 22 normal controls (17 men and 5 women, and from 26 to 64 years old). Consecutively cerebral vascular responses were measured by H215O autoradiographic method in resting state, hypercapnia, hypocapnia, and hypertension. Forced hypercapnia, hypocapnia, and hypertension were achieved by 7% CO2 inhalation, hyperventilation, and venous infusion of angiotensin II, respectively. CMRO2 of the whole brain was significantly lower in patients than in normal controls (p less than 0.05), and CBV of the lentiform nucleus significantly increased in patients (p less than 0.01). This reflected Moyamoya vessels in the basal ganglionic regions. In 3 of 5 patients with bilateral Moyamoya vessels, CBF and CMRO2 in the symptomatic cerebral hemisphere were lower than that in the nonsymptomatic hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vascular responses in cerebrovascular "Moyamoya" disease--evaluated by positron emission tomography]. 251 9

We studied the therapeutic action of CO2 Laser on leg ulcers due to chronic venous hypertension in 30 subjects. Our findings show good results in reducing pain and leg oedema and wound healing.
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PMID:[Defocused CO2 laser in the treatment of leg ulcers. Preliminary results]. 251 23

Morphology of the carotid body and the ventilatory response to hypoxia were compared in New Zealand genetically hypertensive rats and 'normotensive' control rats from the same genetic stock. Hypertensive rats grew more slowly, had higher blood pressure from 6 weeks of age and developed left ventricular hypertrophy. Carotid bodies of both groups were similar in size but larger than those of a common Wistar strain. Intimal damage and proliferation were seen in 1st- and 2nd-order branches of the carotid body artery in hypertensive rats and point-counting showed that the volume proportion of Type 1 cell nuclei and vascular lumen was reduced and vascular wall increased. In age-matched anaesthetized rats, minute ventilation per 100 g was greater in hypertensives than 'normotensive' when inspiring O2 concentrations of 30, 21, 18, 15, 12, 10 and 8%. However, at each inspired O2 concentration, arterial Pa.O2 was higher and Pa.CO2 lower in hypertensive than in 'normotensive' rats. Hypertensive rats were hyperventilating. The shape of the ventilation/O2 tension curve was similar in hypertensive and 'normotensive' rats; thus carotid body sensitivity to hypoxia was probably unchanged. Possible causes of hyperventilation and the relation of carotid body morphology to hypertension are discussed.
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PMID:Structure and function of the carotid body in New Zealand genetically hypertensive rats. 253 3

Twenty-five samples of amniotic fluid obtained by amniocentesis from 25 pregnant women with hypertension in the 35 to 40 weeks of pregnancy were studied. The following biochemical determinations were done in the samples: acid-base equilibrium (pH, pO2, pCO2, base deficit, standard HCO3- and total CO2), concentrations of potassium and sodium ions, total and ionised calcium and inorganic phosphorus. The results were analysed depending on the presence of the respiratory distress syndrome in the newborn, and were subjected to statistical analysis. It was found that determination of acid-base equilibrium and concentrations of K+, Na+, total and ionised Ca++ and inorganic phosphorus in the amniotic fluid of hypertensive women are probably without prognostic significance with respect to the development of the respiratory distress syndrome in newborns.
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PMID:[Respiratory distress in newborns born to hypertensive mothers and acid-base equilibrium and the ion composition of the amniotic fluid]. 270 90

Acute hypoxemia results in hypertension, bradycardia, and cardiac output redistribution in fetal sheep. The blood flow redistribution is produced by differential changes in vascular resistance of various fetal organs. alpha-Adrenergic activity is one of the few vasoconstrictor mechanisms thus far identified in the hypoxemic fetal sheep. Arginine vasopressin (AVP) is a potent vasoconstrictor in adults. Since AVP administration to the normoxic fetus mimics some of the fetal cardiovascular responses to hypoxemia and fetal plasma AVP levels increase with hypoxemia, we examined the hypothesis that AVP modifies the fetal cardiovascular response to hypoxemia by changing the vascular resistance of some fetal vascular beds. To test this we determined fetal systemic arterial pressure and fetal cardiac output and its distribution during hypoxemia with and without the V1 AVP antagonist d(CH2)5-Tyr(Me)AVP. Fourteen fetal sheep (0.79-0.90 of gestation) were chronically catheterized. Five days after surgery fetal hypoxemia was induced by introducing a mixture of 95% N2-5% CO2 (10-20 l/min) into a maternal tracheal catheter. The hypoxemia was maintained for 40 min. Fetal heart rate, systemic arterial blood pressure, and combined ventricular output and its distribution (radiolabeled microspheres) were measured before hypoxemia, at 20 min of hypoxemia alone, and at 20 min of hypoxemia plus either AVP antagonist (n = 5) or NaCl 0.9% (n = 5, controls). Fetal hypertension and bradycardia were partially reversed after the AVP antagonist administration during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arginine vasopressin mediates cardiovascular responses to hypoxemia in fetal sheep. 271 44

We compared exercise responses in two groups of hypertensive patients treated with an angiotensin converting enzyme (ACE) inhibitor (lisinopril, 20-80 mg/day, n = 17) or a cardioselective beta-blocker (atenolol, 50-200 mg/day, n = 9). Measurements were made at rest and during exercise at 25 W (2.7 mets) and at 50 W (3.8 mets) on a bicycle ergometer (where mets is exercising oxygen consumption/resting oxygen consumption) after 4 weeks of placebo, and again after 12 weeks of drug administration. Both drugs reduced (P less than 0.05) mean arterial pressure. Atenolol caused significant decreases in the heart rate (approximately 25%) and cardiac output (approximately 26%; Defares CO2 rebreathing), and significant increases in total peripheral resistance (approximately 30%) and arteriovenous O2 content (approximately 20%). Lisinopril decreased (P less than 0.05) stroke volume. At the same exercise intensity systolic blood pressure, arteriovenous O2 and total peripheral resistance were lower (P less than 0.05) and the heart rate was higher (P less than 0.05) after lisinopril than after atenolol. After the treatment of hypertension with the ACE inhibitor the responses to exercise were less restrictive than those after treatment with the cardioselective beta-blocker.
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PMID:Effects of angiotensin converting enzyme inhibition and beta-blockade on exercise responses in hypertensive patients. 285 65


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