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)

The goal of this study was to determine whether responses of cerebral vessels to intravascular administration of serotonin are altered in stroke-prone spontaneously hypertensive rats. We measured pressure in pial arterioles and cerebral blood flow in normotensive and hypertensive rats during intra-atrial infusion of serotonin. In normotensive rats, pial arteriolar pressure was 48 +/- 3 mm Hg (mean +/- SEM) and cerebral blood flow was 48 +/- 5 ml/min/100 g under control conditions. Intra-atrial infusion of serotonin (5 and 50 micrograms/kg/min for 5 minutes) produced only minimal changes in pial arteriolar pressure (-3 +/- 4 and -4 +/- 4 mm Hg, respectively) and did not alter cerebral blood flow. In hypertensive rats, pial arteriolar pressure was 95 +/- 9 mm Hg and cerebral blood flow was 57 +/- 4 ml/min/100 g under control conditions. In contrast to normotensive rats, intra-atrial infusion of serotonin (5 and 50 micrograms/kg/min for 5 minutes) in hypertensive rats profoundly decreased pial arteriolar pressure (-29 +/- 7 and -44 +/- 4 mm Hg, respectively) without altering cerebral blood flow. To determine whether altered responses of cerebral arterioles to serotonin in hypertensive rats were related to nonspecific increases in vascular reactivity, we examined the effects of angiotensin in normotensive and hypertensive rats. Responses to angiotensin (1 and 3 micrograms/kg/min i.v. for 5 minutes) were not potentiated in hypertensive rats. Thus, constrictor responses of cerebral vessels to intravascular serotonin are potentiated in hypertensive rats. We speculate that when serotonin is released by platelets, augmented vasoconstrictor responses to serotonin may have important implications for the pathogenesis of cerebral ischemia, and perhaps stroke, during chronic hypertension.
Hypertension 1990 Jun
PMID:Cerebral vasoconstrictor responses to serotonin during chronic hypertension. 235 38

Treatment with the calcium entry blocker nimodipine is recommended as effective therapy for cerebral ischemia due to cerebral vasospasm or cerebral thrombosis. On the other hand, treatment with induced hypertension is a widely accepted measure to reverse ischemic deficits caused by vasospasm. Thus, a combination of the two regimens--nimodipine and induced hypertension--may have real benefits for cerebral ischemia. But it is possible that the benefit of one is abolished by adverse effects of the other, or that a combination of both may not be as effective as the use of only one therapy. In order to investigate these problems, the effects of nimodipine and induced hypertension on cerebral vessel, cerebral blood flow, cerebral edema and cerebral infarction using a one hour middle-cerebral-artery occlusion model in cats. Twenty-one anesthetized cats were divided into a control group, the nimodipine-treated group, and the nimodipine-and-induced-hypertension group. There were seven cats in each group. Occlusion of the middle cerebral artery (MCA) was continued for one hour in each animal. Induced hypertension was a little higher than resting values, and it was continued for only one hour during MCA occlusion, brought on by instillation of dopamine. Cerebral pial arteries dilated much more prominently during and after the occlusion of MCA in the nimodipine-and-induced-hypertension group than other groups. Although cerebral blood flow in the nimodipine group, and the nimodipine-and-induced-hypertension group increased more in the non-ischemic hemisphere, the most remarkable increase was seen around the infarcted cortex in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Effect of calcium antagonist nimodipine and induced hypertension on cerebral vessel reactivities, cerebral blood flow, cerebral edema and infarction in cats with one hour middle-cerebral-artery occlusion]. 238 17

Ventricular arrhythmias detected in the late-hospital phase of myocardial infarction have been identified as a risk factor for sudden death, being their prognostic value independent of ventricular function. However, relations between both factors are not clarified. In order to study hypothetic associations between ventricular arrhythmias and some clinical, hemodynamic and angiographic variables, 60 patients (52 males, 8 females) underwent 24-hour Holter recordings and cardiac catheterization with left ventricular and coronary angiographies, 3-5 weeks after hospital admission. Past history data, acute phase complications and hemodynamic and angiographic results were compared between patients with and without significant ventricular arrhythmias during Holter monitoring (10 or more PVC's/hour and/or repetitive forms). No significant differences were found between both groups neither in mean age nor in the incidence of previous angina or infarction, cerebral ischemia, diabetes, lipid disorders or subjective feeling of being under psychological stress. Prior history of arterial hypertension was, however, significantly more frequent in patients with ventricular arrhythmias (53.3% vs 17.8%; p = 0.0183). No differences were observed in the localization of the infarct or in the complications during the acute phase (CPK peak, Killip's score, angina after 24 hours of evolution, intraventricular or A-V conduction disorders and supraventricular and ventricular arrhythmias). Among hemodynamic data, only left ventricular and aortic systolic pressures were different in both groups, being significantly higher in patients with ventricular arrhythmias. There were not differences in left ventricular segmentary contraction and in number of coronary vessels involved. To conclude, significant ventricular arrhythmias were recorded in 25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Anatomo-functional substrate of high risk arrhythmia after myocardial infarct]. 239 9

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
 ...
PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1

Nicardipine has high affinity for the dihydropyridine-binding site and has been shown to inhibit the influx of extracellular calcium through membrane slow channels. The calcium antagonist activity of nicardipine is greater in vascular smooth muscle than in cardiac muscle. Nicardipine has also been shown to possess greater activity in coronary than in peripheral vascular smooth muscle. This in vitro profile accounts for the decreased blood pressure and increased coronary blood flow in animal models in vivo. These pharmacologic properties are the basis for nicardipine's clinical utility in essential hypertension and acute myocardial ischemia. Nicardipine has been shown to be more vascular selective than other calcium antagonists and, therefore, possibly less inclined to produce negative inotropicity. This latter property has been confirmed in human hemodynamic studies. Nicardipine is effective in models of acute myocardial ischemia and hypertension. These results have been confirmed in antianginal and antihypertensive studies in humans. This new calcium antagonist has been shown to limit myocardial infarct size in both dogs and baboons subject to left anterior descending coronary artery ligation and to reduce the extent of ischemia-induced cerebral neuronal death in rats. Other protective effects of nicardipine have been demonstrated in paracetamol overdose in mice, chloroform-induced hepatotoxicity in rats and cerebral ischemia in gerbils and baboons. The mechanism of this cell protection of nicardipine may be related to physicochemical effects.
 ...
PMID:Animal pharmacology of nicardipine and its clinical relevance. 244 Feb 94

The effect of short and long-term therapy with aspirin (50 mg/day) on platelet alpha granule secretion was studied in 11 healthy controls and 57 patients suffering from transient cerebral ischemic attacks (TIA) with and without accompanying diabetes and hypertension. Plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) were measured as indicators of platelet alpha granule secretion. beta-TG and PF 4 levels were increased following cerebral ischemia. Aspirin treatment failed to suppress plasma levels of both proteins when measured a month and then a year after initiation of treatment. Therefore, these proteins may be poor indicators of platelet inhibition by aspirin.
 ...
PMID:Platelet alpha granule secretion in cerebral ischemia: effect of short and long term low dose aspirin treatment. 245 69

We tested the hypotheses that after complete cerebral ischemia, first, rate of recovery of ATP, phosphocreatine (PCr), and intracellular pH (pHi) varies with ischemic duration and second, rate of metabolic recovery is a more sensitive predictor of consequent electrophysiological deficit than steady-state metabolic recovery. With the use of transient intracranial hypertension in anesthetized dogs, ischemic duration was set for either 3, 12, or 30 min, which depressed somatosensory-evoked potential (SEP) recovery amplitude by 30, 59, and 88%, respectively. In contrast, ATP, PCr, and pHi, measured by 31P magnetic resonance spectroscopy, fully recovered. When ischemic duration was increased from 3 to 12 min, mean recovery time of ATP (6 min) remained rapid but that of pHi (12-28 min) was prolonged. After 30 min of ischemia, pHi recovery was not slowed further (25 min) but that of ATP was now markedly prolonged (36 min). PCr recovery time increased progressively with ischemic duration (5, 11, and 21 min, respectively) and correlated best with SEP recovery (r = 0.74). We conclude that the brain's ability to rapidly normalize pH is a sensitive predictor of electrophysiological recovery after short ischemia but that ATP regeneration becomes important with prolonged ischemia. PCr recovery rate was the best overall predictor, probably because it depends on both pHi and the ratio of ATP to ADP by the creatine kinase reaction.
 ...
PMID:Postischemic recovery rate of cerebral ATP, phosphocreatine, pH, and evoked potentials. 251 29

Eight-five carotid endarterectomies were performed in 77 patients, under regional anaesthesia using 2 different techniques: cervical epidural anaesthesia (35 cases) and cervical plexus block (50 cases). The patients' mean age was 71 years; 80 per cent had arterial hypertension and 41 per cent coronary disease. Transoperative cerebral ischaemia was detected by a 5-minute carotid clamping test, the occurrence of a neurological event indicating that shunting was required. In 62 patients this test was combined with measurement of carotid back pressure. None of the patients needed general anaesthesia. Intraoperative neurological events occurred more frequently (P less than 0.01) when the carotid back pressure was 25 mmHg or less, and 12 temporary shunts were installed for that reason (14.1 per cent). Three neurological events occurred at the end of endarterectomy: no shunt was installed and complete recovery was observed immediately after declamping. No complications ascribable to the anesthetic techniques were recorded. Mortality was nil, and the only neurological morbidity was a brachio-facial deficit which left few sequelae. The frequency of intra- or postoperative arterial hypertension was similar in both groups. Intraoperative hypotension, frequent under epidural anaesthesia, was observed in only one patient who had brachial plexus block (P less than 0.01). The analgesia obtained was equally good with both anaesthetic techniques, but cervical plexus block anaesthesia is easier to perform, had less haemodynamic repercussions and therefore tends to be preferred to cervical epidural anaesthesia. The lack of mortality, low morbidity and absence of systemic complications in this series despite the high number of patients at risk are in favour of this type of anaesthesia, notably for such patients. Moreover, because vigilance is preserved attention can be paid to the quality rather than the rapidity of endarterectomy, which is the best way of preventing embolism.
 ...
PMID:[Carotid surgery under locoregional anesthesia]. 253 1

A 63-year-old white male with a 25-year history of hypertension experienced the onset of intermittent diplopia and gait disturbance 24 hours after a change in antihypertensive medication from atenolol 50 mg/d to enalapril 5 mg bid. Three weeks later, the patient was admitted with a worsening of symptoms. Cerebral arteriography revealed significant bilateral vertebral artery stenosis. Symptoms continued to progress in the hospital, and at the time of posterior circulation revascularization the patient had a persistent bilateral internuclear ophthalmoplegia and right ptosis. The need for a neurovascular workup and adjustment of therapy in patients with antihypertensive-associated cerebral ischemia is discussed.
 ...
PMID:Hemodynamic vertebrobasilar insufficiency as an adverse effect of antihypertensive therapy. 254 68

We report two cases of traumatic cerebral vascular disease which were treated successfully with barbiturate. The first case sustained blunt trauma to the bilateral vertebral arteries, resulting in complete occlusion of both arteries. After ligation of the injured vertebral arteries, multiple cerebral infarction appeared. Cerebral angiography revealed dissection and stenosis of the bilateral internal carotid arteries. We treated this case with barbiturate (Thiamylal) in combination with administration of heparin. The second case sustained cerebral contusion and traumatic subarachnoidal hemorrhage as a result of a motor cycle accident. This patient deteriorated and cerebral angiography showed diffuse cerebral arterial vasospasms. When this was treated with induced hypertension, he developed recurrent subarachnoid hemorrhage. In order to protect the brain from ischemia without elevating blood pressure, we employed barbiturate therapy and the patient recovered without major neurological deficit. The condition of severe head injury with cerebral ischemia is complicated. Therefore it has been hard for neurosurgeons to cure the patient with this condition. But we treated it with barbiturate successfully. Barbiturate therapy in severe head injury with cerebral ischemia may decrease the mortality in that group of patients considered difficult to treat with the usual therapeutic modalities.
 ...
PMID:[Barbiturate therapy in traumatic cerebral vascular disease: report of two cases]. 261 99


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