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)

During carotid endarterectomy (CEA), phenylephrine infusions are commonly used to induce hypertension during carotid clamping in an attempt to increase collateral cerebral blood flow and prevent cerebral ischemia. Although this practice appears to increase the incidence of intraoperative myocardial ischemia during CEA when general anesthesia is employed, whether the limited use of phenylephrine infusions in specific instances of cerebral ischemia, as shown on an electro-encephalogram, results in low perioperative rates of both myocardial infarction (MI) and cerebral infarction remains unclear. We studied 171 CEAs done under general anesthesia performed with selective shunting based on the identification of cerebral ischemia by a two-channel computerized electroencephalographic monitor. The use of a phenylephrine infusion was restricted to the following instances of cerebral ischemia: 1) ischemia associated with hypotension that did not resolve within 2 minutes of decreases in anesthetic administration and treatment with fluid and/or colloid; 2) ischemia poorly or slowly responsive to shunt placement, accompanied by either hypo- or normotension; and 3) ischemia poorly or slowly responsive to removal of the carotid clamp, accompanied by either hypo- or normotension. Two non-Q wave MIs (1.2%) occurred, both nonfatal. There were two cerebral infarctions (1.2%) and three deaths not related to MI (1.8%). Based on these findings, in order to decrease the incidence of both MI and cerebral infarction after general anesthesia for CEA, we recommend the restrictive use of phenylephrine-induced hypertension for specific instances of slowly or poorly reversible cerebral ischemia, as shown on the electroencephalogram.
 ...
PMID:Computerized electroencephalographic monitoring and selective shunting: influence on intraoperative administration of phenylephrine and myocardial infarction after general anesthesia for carotid endarterectomy. 161 84

The central hemodynamic effects of the peptide endothelin-1 (ET-1) have been investigated in the conscious, normotensive rat. Intracisternal administration of ET-1 (0.01-0.03 nmol) gave rise to an increase in mean arterial pressure with minimal effects on heart rate and was accompanied in some cases by barrel rolling activity. Intracisternal administration of 0.03 nmol ET-1 gave rise to a significant elevation in plasma noradrenaline and adrenaline levels. This elevation in plasma catecholamines was present only in those animals that also exhibited marked behavioral changes. Autoradiographic measurement of cerebral blood flow carried out during the maximum response to 0.03 nmol of intracisternal ET-1 revealed a widespread and profound ischemia throughout the caudal brainstem. Cerebral ischemia is known to activate compensatory circulatory reflexes in the medulla oblongata that result in increased sympathetic and vagal outflow. This is the most likely cause of intracisternal ET-1-induced hypertension. ET-1 is unique in its ability to override the brain's autoregulatory mechanisms and induce ischemia of pathological magnitude.
 ...
PMID:Endothelin-1-induced hypertension: a consequence of medullary ischemia? 172 22

Four patients with isolated acute ocular ischemic syndromes also had circulating antiphospholipid antibodies. Two patients had vaso-occlusive retinopathy and two, anterior ischemic optic neuropathy (which was successive in one). Extensive clinical laboratory evaluation identified vascular risk factors in two patients. One patient had essential thrombocytosis, confirmed by bone marrow biopsy; the other had stable hypertension and a history of coronary artery disease. These cases suggest that small vessel thrombosis in situ may be a mechanism for antiphospholipid-associated ocular and cerebral ischemia.
 ...
PMID:Ocular thrombosis associated with antiphospholipid antibodies. 174 13

Bilateral carotid artery ligation (BCL) was performed with one week interval between the each operation in male spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) aged 4 months. BP rose immediately after unilateral carotid artery ligation (UCL) and BCL in both WKY and SHR due to carotid sinus reflex. Once returning to preoperative levels after both UCL and BCL, BP of SHR and WKY increased again gradually one and 4 months after BCL and thereafter, respectively. BP was significantly higher than that in the controls of each strain, and the BP increment was significantly greater in SHR than in WKY. A significant regional cerebral blood flow (rCBF) increase on the contralateral side of carotid ligation was observed in SHR in contrast to a little change in that of WKY and a reduction of rCBF after BCL was significantly greater in SHR than in WKY. Behavioral activities in SHR were also reduced after BCL. Cerebral edema with nerve cells damage was recognized in SHR. In contrast, little change was found in WKY. On the other hand, upper cervical sympathectomy attenuated convulsive seizures after BCL more markedly in SHR, which survived longer than non-denervated SHR. These results suggest that chronic mild cerebral ischemia caused by BCL with one week interval accelerates the development of severe hypertension in SHR and developed mild hypertension in WKY. Sympathetic innervation might play much more important role in collateral circulation through the vertebrobasilar system in SHR.
 ...
PMID:Effects of long-term cerebral ischemia caused by bilateral carotid artery ligation on the acceleration or the development of hypertension in spontaneously hypertensive rats (SHR) or Wistar-Kyoto rats (WKY). 177 95

Both diabetes mellitus and hypertension are risk factors for stroke and also influence prognosis following stroke. Experimentally, hyperglycemia augments cortical infarct size in stroke models where collateral circulation exists, and infarct size in hypertensive rats is larger than in normotensive strains. Whether the deleterious effect of hyperglycemia is altered in the setting of hypertension has not previously been studied experimentally. The effect of hyperglycemia on infarct size in spontaneously hypertensive rats was examined in this study. Focal neocortical cerebral ischemia was induced by tandem right common carotid and middle cerebral artery occlusion. Preischemic hyperglycemia had no influence on infarct volume whether the duration of postischemic hyperglycemia was transient or prolonged. Although hyperglycemia increases infarct size in cortical stroke models where collateral circulation is available, this study demonstrates the effect can be modified by the presence of underlying hypertension.
 ...
PMID:Hypertension and hyperglycemia in experimental stroke. 179 73

Bolus injections of lidocaine are commonly used during neuroanesthesia to prevent or treat ICP elevations caused by tracheal or painful stimuli. Lidocaine can also be employed in case of hard intracranial hypertension, when the usual therapy fails. With continuous perfusion, at high doses, of this agent, a state of lidocaine anesthesia can be induced which is more readily reversible than barbiturate anesthesia. A simultaneous anticonvulsant therapy is mandatory because of the well-known epileptogenicity of lidocaine. Closed cardiovascular monitoring is also needed to detect early signs of cardiotoxicity. Experimental works point to the effectiveness of i.v. lidocaine to prevent ischemic lesions secondary to a cerebral artery occlusion. This protective effect may result from some properties exhibited by lidocaine and not by thiopental: stabilisation of transmembrane ionic fluxes, inhibition of leucocytes intravascular sticking and tissular migration. So, i.v. lidocaine seems help to preserve or improve cerebral perfusion pressure and in cases when the latter decrease below the critical threshold, to protect against cerebral ischemia.
 ...
PMID:[Use of intravenous lidocaine in neuro-anesthesia and neuro-resuscitation]. 184 10

Brief bilateral carotid artery ligation in adult spontaneously hypertensive rats (SHR) induced locomotor hyperactivity and lesions of the CA1 region of the hippocampus but had no effect in Wistar normotensive rats. This result suggests that high blood pressure amplifies the consequences of cerebral ischaemia. Treatment for 7 weeks with the calcium entry-blocker isradipine (5 mg/kg per day, subcutaneously) normalized blood pressure and attenuated the behavioural and histological consequences of cerebral ischaemia. Chronic treatment with hydralazine (25 mg/kg per day, subcutaneously) also normalized blood pressure but afforded no protection against the consequences of cerebral ischaemia. This suggests that the protective effect of antihypertensive treatment depends not only on the blood pressure-lowering action but may also be linked to the mechanism of action of the drug used.
 ...
PMID:Protective effects of antihypertensive treatment with isradipine on the consequences of cerebral ischaemia in the spontaneously hypertensive rat. 184 26

The effects of the adenosine agonist, (R)-phenylisopropyladenosine on focal cerebral ischemia induced by middle cerebral artery occlusion were investigated in spontaneously hypertensive rats. The drug was given 30 min before occlusion and each hour thereafter for 6 h. The neurological status of the rats was estimated 2, 24 and 48 h after occlusion. Infarct volumes were measured 48 h after occlusion (Cresyl violet-stained sections). (R)-Phenylisopropyladenosine did not significantly reduce infarct size, nor did it modify the neurological score. As there is considerable evidence of the neuroprotective effects of adenosine in normotensive rats, the present results may be due to a more abrupt reduction in cerebral blood flow in the territory surrounding the ischemic core, where neuroprotection could be expected, in the spontaneously hypertensive rat strain. Consequently, neuroprotection may be more difficult when focal cerebral ischemia is associated with hypertension.
 ...
PMID:Focal cerebral ischemia in chronic hypertension: no protection by (R)-phenylisopropyladenosine. 186 43

The performance of the sympathetic nervous system during sustained moderate cerebral ischemia (CI) was examined in the present study. For this purpose, a Cushing response was elicited repeatedly during incomplete global CI in anesthetized artificially ventilated cats after vagotomy and baroreceptor denervation. In control animals without CI, sympathetic activity in response to brief elevation of intracranial pressure (ICP) showed a well-repeatable two-phase reaction. During CI there was a progressive deterioration of background sympathetic nerve discharge (SND) over a period of 30 min. SND response to repeated elevation of ICP was initially similar to control response but later with progression of CI was seriously changed. 1) Instead of the usual hyperactivation, sympathetic nerve activity was depressed during intracranial hypertension. 2) The characteristic desynchronized activity either appeared later during the reperfusion period or remained absent. The progressive loss of SND response to raised ICP in developed CI was compared with the changes seen in experiments in which repeated ICP elevations were superimposed on asphyxia. These findings suggest that the sympathetic component of the Cushing reaction strongly depends on the actual state of brain stem autonomic circuits and may be seriously altered in pathological situations involving ischemic brain injury.
 ...
PMID:Effect of preexisting brain ischemia on sympathetic nerve response to intracranial hypertension. 186

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


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