Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Calcium entry blockers are now widely used in the treatment of cardiovascular diseases. Nifedipine is established for the treatment of perioperative hypertension during anesthesia. Previous animal experiments have demonstrated that calcium entry blockers potentiate the neuromuscular response induced by nondepolarizing blocking drugs. Occasional observations in patients have led to the suggestion that this phenomenon may be of clinical significance. The interaction of nifedipine with nondepolarizing muscle relaxants in patients was assessed in a prospective clinical study. PATIENTS AND METHODS. Atracurium or vecuronium was administered for muscular relaxation in 44 patients anesthesized with isoflurane in nitrous oxide/oxygen. Monitoring included checks on noninvasive blood pressure, heart rate, pharyngeal temperature, tidal volume, end-tidal CO2 and neuromuscular transmission with a Datex ABM 100 Relaxograph ("train of four"). In the first study protocol atracurium was given to the patients after the intubation dose of 0.5 mg/kg in equal repetition doses of 0.2 mg/kg whenever T1 reached 25%. In 12 patients with the second repetition dose 1 mg nifedipine was injected i.v. The duration of neuromuscular depression with nifedipine until T1 reached 25% again was compared with the duration without nifedipine in the same patient. In the second protocol, constant neuromuscular blockade was accomplished in 11 patients by administration of atracurium or vecuronium at a constant perfusion rate at a level of 75% twitch depression. After 15 min of stable neuromuscular blockade 1 mg nifedipine was injected. In the third study protocol, 1 mg nifedipine i.v. was given at the end of anesthesia when the patients began to breathe spontaneously (T1 was at least 25%). RESULTS. In each patient there was a significant prolongation of neuromuscular blockade from 29 min +/- 6 min up to 40 min +/- 8 min when nifedipdine was given with the second repetition dose (P less than 0.001). During continuous relaxation with constant neuromuscular depression nifedipine increased the neuromuscular blockade from 75% up to 90% +/- 4% (P less than 0.05). In patients with spontaneous breathing and fading but still existing neuromuscular blockade nifedipine injection resulted in hypoventilation. The cardiovascular effects of 1 mg nifedipine, although significant, attained no clinically relevant values. CONCLUSIONS. Our results confirm previous assumptions of synergistic effects of neuromuscular blocking drugs and nifedipine in patients. This synergistic effect includes both duration and intensity of neuromuscular blockade. In the postoperative period patients may be endangered by nifedipine therapy if recovery from the neuromuscular depression is not complete.
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PMID:[Potentiation of nondepolarizing muscle relaxants by nifedipine iv in inhalation anesthesia]. 197 Apr 60

Initial and follow-up investigations were done systematically in 15 cases of internal carotid artery (ICA) dissections by means of angiography, computerized tomography, Magnetic Resonance Imaging, extracranial and transcranial Doppler sonography, as well as B-mode imaging. Cerebral hemodynamic reserve was evaluated by means of both SPECT and CO2-dependent vasomotor reactivity. The findings are focussed on two major issues: Do modern diagnostic tools permit to make the diagnosis of ICA dissection without angiographical proof? What is the pathogenesis of brain infarctions due to ICA dissections? Our findings demonstrate that the diagnosis of carotid artery dissection can reliably be done noninvasively by means of ultrasound techniques and MRI. These methods also allow for frequent follow-up investigations without any inconvenience for the patient. Embolic brain infarctions caused by carotid artery dissections are equally frequent as low flow induced lesions. Acute and follow-up findings suggest that surgical intervention is contraindicated in the acute phase, but may be considered for chronic pseudoaneurysms. Initial anticoagulation with high dose heparin is safe and seems to be efficacious. In certain cases, subsequent cumarine therapy may be indicated for a maximum of six months. Measures improving hemodynamics, e. g. induced hypertension, are reasonable, as long as the vasomotor reserve is exhausted.
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PMID:[Dissections of the internal carotid artery--new diagnostic and pathogenetic aspects]. 200 7

An endogenous ouabainlike compound (OLC) has been purified from human plasma, and mass spectrometry has shown it to be indistinguishable from plant-derived ouabain. This human OLC was tested for its effects on evoked tension in guinea pig left atria and aortic rings. The tissues were incubated at 37 degrees C in bicarbonate-buffered physiological salt solution gassed with 95% O2-5% CO2. In atria stimulated electrically at 1 Hz, 85 and 170 nM human OLC increased peak active force to 177 +/- 15% and 313 +/- 32% of control, respectively (n = 3), with little effect on the duration of contraction. On washout of the OLC, peak systolic force returned to the control level with a half-time of 4.3 +/- 0.5 minutes. Similar results were obtained with 160 nM plant-derived ouabain: peak systolic force increased to 310 +/- 31% of control (n = 4) and returned to the control level with a half-time of 3.8 +/- 0.2 minutes during washout. In aortic rings, neither 170 nM human OLC nor 160 nM plant ouabain (30-minute treatments) affected resting (unstimulated) tension, but they increased the contractions evoked by histamine (0.2-1.0 microM) to 156 +/- 13% (n = 4) and 143 +/- 6% (n = 4) of control responses, respectively. The mean half-time for washout of the OLC and plant ouabain-induced augmentation of histamine-evoked tension exceeded 35 minutes. These data show that human OLC has cardiotonic and vasotonic actions qualitatively and quantitatively similar to those observed with plant ouabain.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jun
PMID:Effects of an endogenous ouabainlike compound on heart and aorta. 204 74

Intracranial haemodynamics were studied in 20 patients with diffuse and focal brain injury and experimental animals with acute intracranial hypertension by the use of TCD ultrasound. The mean flow velocity in the middle cerebral artery (MCA) commonly decreased on the side of the haematoma depending on intracranial pressure (ICP) elevation and cerebral perfusion pressure (CPP) reduction in focal injury. The decrease of the MCA flow velocity returned to normal after treatment. The flow velocities decreased bilaterally and there was no difference between the right and left side in diffuse injury. But the velocities increased in spite of ICP elevation when diffuse cerebral swelling developed. Cerebrovascular CO2 reactivity was impaired in two groups of patients with low Glasgow Coma Scale (GCS) scores. The mean velocity of the MCA and blood flow in the internal carotid artery exhibited flow patterns which changed correlatively depending on CPP reduction in experimental animals. Noninvasive study by use of TCD ultrasound can provide valuable information on variant haemodynamic phenomena in patients with diffuse and focal brain injury.
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PMID:Intracranial haemodynamics in diffuse and focal brain injuries. Evaluation with transcranial Doppler (TCD) ultrasound. 209 9

Endothelial cells modulate vascular tone by releasing endothelium-derived relaxing (EDRF) and contracting factors. An imbalance of these factors in hypertension could contribute to increased peripheral vascular resistance. Mesenteric resistance arteries of Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were suspended in a myograph filled with physiological salt solution (37 degrees C; 95% O2-5% CO2). In WKY rings contracted with norepinephrine, acetylcholine (10(-9)-10(-4) M) evoked endothelium-dependent relaxations (88 +/- 2%, IC50 7.3 +/- 0.1; n = 31). Hemoglobin (10(-5) M) but not meclofenamate (10(-5) M) reversed the relaxations delineating EDRF as the mediator. Nitric oxide (3 X 10(-9)-10(-5) M) induced comparable relaxations as acetylcholine. In SHRSP, relaxations to acetylcholine but not those to nitric oxide were impaired (61 +/- 5%, IC50 greater than 6.6 +/- 0.4; n = 24; P less than 0.005). In SHRSP, meclofenamate but not the thromboxane synthetase inhibitor CGS 13080 normalized endothelium-dependent relaxations. Relaxations to sodium nitroprusside were enhanced in SHRSP both in rings with and without endothelium. Thus our results are compatible with the concept that endothelium-dependent relaxations in resistance arteries are mediated by nitric oxide. In SHRSP, endothelium-dependent relaxations are impaired because of a cyclooxygenase-dependent substance interfering with the release and/or action of EDRF.
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PMID:Impaired endothelium-dependent relaxations in hypertensive resistance arteries involve cyclooxygenase pathway. 210 97

In order to clarify the cerebrovascular response in Moyamoya disease, the autoregulation and CO2 response was investigated using the 81mKr continuous cerebral blood flow (CBF) measurement technique. A total of 32 measurements were made over the anterior and posterior circulation in 16 Moyamoya patients (seven adults, nine children). CBF measurements were made during four loading trials (hypertension, hypotension, CO2 inhalation and hyperventilation). Study was then made of the vascular response of the frontal lobe, perfused by the internal carotid artery (ICA), and the occipital lobe and cerebellum, perfused by the vertebral artery (VA). Deficits of autoregulation were more severe among the juvenile cases in response to hypotension than to hypertension in both the ICA and VA regions, but the deficits were mild. The CO2 response to hypercapnea in the juvenile cases tended to be abnormal in both the ICA and VA regions. Both adult and juvenile patients showed deficits in the ICA region in response to hyperventilation, some of whom exhibited paradoxial responses. Notable differences in the severity of the deficits of the vascular response in adult and juvenile cases were seen, with the deficits in the response being more severe among the juvenile cases. Moreover, significant regional differences in the deficits were also found.
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PMID:Cerebral blood flow in moyamoya disease. Part 2: Autoregulation and CO2 response. 212 2

In order to gain more insight into the pathophysiology of extracerebral cerebrovascular occlusion, the cerebral hemodynamic behaviour after uni- or bilateral carotid occlusion was investigated. In Wistar rats, acute occlusion of one common carotid artery leads to a moderate bilateral lowering of the resting hemispheric brain blood flow; no interhemispheric perfusion asymmetry is observed. During hypercapnia, however, a manyfold increase of the hemispheric blood flow is seen at the intact side, whereas blood flow increase at the side of the occlusion is suppressed indicating that the cerebrovascular reserve at the side of the occlusion is largely used to preserve resting hemispheric perfusion. During the days (1, 5, 15 and 30) following the occlusion, resting hemispheric blood flow is progressively restored rather rapidly (bilateral normalization on the fifth day) whereas restoration of the cerebrovascular reserve (hemispheric blood flow increase in hypercapnia) proceeds more slowly and a nearly normal hypercapnic response is reached on day thirty. Spontaneously Hypertensive Rats (SHR) show structural abnormalities of their blood vessels during the development of hypertension, leading to impaired adaptation possibilities of the cerebral vasculature after unilateral common carotid occlusion. This is indicated by the striking comparability of the compensation of hemispheric cerebral blood flow (in normo- and hypercapnia) of SH rats five days after unilateral carotid occlusion with the cerebral hemodynamic status of normotensive animals already seen 24 hours after the same occlusion. Consecutive bilateral common carotid occlusion shows that survival rate increases by increasing the interval between both occlusions. This survival relation is much more unfavorable in SH rats. The parallelism between the restoration of the measured CO2-reactivity of the blood flow in the involved hemisphere after unilateral carotid occlusion and the evolution of survival rate after consecutive bilateral carotid occlusion indicates that the response of the hemispheric circulation to CO2 offers a good estimate of true cerebrovascular reserve after cerebrovascular accidents of this kind. In cats, acute bilateral occlusion of the carotid arteries leads to a moderate decrease of resting cerebral blood flow in the anterior parts of the brain (cerebrum); the hypercapnic response of this region is, however, completely abolished. In the posterior brain regions (medulla oblongata and cerebellum) resting blood flow and its increase under hypercapnia are preserved. The experiments indicate that the relative preservation of resting cerebral blood flow in the cerebrum of the cat after acute bilateral carotid occlusion is at the expense of its complete hemodynamic reserve. Posterior brain regions are better protected in these conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Hemodynamic adaptations in proximal cerebrovascular occlusion]. 212 47

Response to CO2 and autoregulation of cortical cerebral blood flow (CBF) during isoflurane anesthesia were studied in 10 patients undergoing neurosurgery. The patients were anesthetized with 0.5 to 1.2% end-tidal isoflurane and 66% nitrous oxide in oxygen. The CBF was measured by thermal diffusion using a flow probe with a Peltier stack. PaCO2 was controlled to produce hypocarbia, normocarbia and hypercarbia by changing tidal volume and respiratory rate. Arterial blood pressure was altered. Hypotension was achieved by intravenous infusion of trimetaphan and hypertension was induced by intravenous administration of metaraminol. During isoflurane anesthesia the response to CO2 of CBF was kept at PaCO2 between 27.8 and 53.9 mmHg. The following relationship was obtained. CBF = 2.54 x PaCO2-53.0, r = 0.59, n = 131 The autoregulation of CBF was evaluated in 7 patients, and in 2 patients, the autoregulation of CBF was abolished.
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PMID:[Response to CO2 and autoregulation of cortical cerebral blood flow during isoflurane anesthesia]. 212 31

This study was designed to determine the cytoplasmic pH (pHi) profile of lymphocytes from a rat model of genetic hypertension that is well suited for study before and after the development of spontaneous hypertension. For this purpose, pHi was measured in thymic lymphocytes obtained from spontaneously hypertensive rats (SHR) and from age-matched Wistar-Kyoto (WKY) control rats using 2',7'-bis carboxyethyl-5,6-carboxyfluorescein (BCECF), a pH-sensitive fluorescence probe. At the age of 16-20 weeks, pHi of lymphocytes suspended in a HCO3-free HEPES-buffered solution, was markedly lower in the SHR than in the WKY rats (7.07 +/- 0.02, n = 16 and 7.22 +/- 0.01, n = 15, respectively, p less than 0.001), whereas systolic blood pressure was higher in SHR than in WKY rats (175 +/- 5.0 and 105 +/- 3.0 mm Hg, respectively, p less than 0.001). In rats less than 5 weeks of age, pHi was also lower in SHR than in WKY rat lymphocytes (7.12 +/- 0.04, n = 11 and 7.23 +/- 0.04, n = 11, respectively, p less than 0.05), although at this age systolic blood pressure was not different between the two groups (87 +/- 4.0 and 85 +/- 3.0 mm Hg, respectively). In lymphocytes suspended in a more physiological HCO3/CO2-buffered solution, pHi was again lower in the adult SHR than in the WKY rat (7.18 +/- 0.02, n = 16 and 7.31 +/- 0.02, n = 16, respectively, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Jan
PMID:Reduced intracellular pH in lymphocytes from the spontaneously hypertensive rat. 215 99

In order to evaluate the hemodynamic effect of a carotid artery obstruction, the CO2-reactivity was determined and the systolic carotid artery pressure was measured in 34 patients with a stenosis (20) and/or an occlusion (17) of the internal carotid artery. In 19 patients this was done bilaterally and in 15 unilaterally, a total of 53 observations. A decreased CO2-reactivity was found in 49% (26/53). With a carotid artery blood pressure of less than or equal to 90 mmHg the reactivity Index was diminished in 86% (12/14), with greater than 90 mmHg in 36% (14/39) of cases. It is assumed that in the first mentioned situation the autoregulation tends to be exhausted owing to a fall in perfusion pressure while in the last mentioned the explanation may be ischemic damage or shift of the lower limit of autoregulation towards a higher value as a result of (chronic) hypertension.
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PMID:Cerebral perfusion pressure and CO2-reactivity in the evaluation of carotid obstructions. 216 95


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