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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium channel blockers are effective antihypertensive agents, both as initial monotherapy and in combination with other antihypertensive agents. These drugs are also effective in the treatment of chronic, stable angina, variant angina and supraventricular arrhythmias. Drugs in this class have different affinities for calcium channels in vascular smooth muscle, cardiac muscle, cardiac sinus and atrioventricular node. They are all useful in hypertension and angina, but only verapamil and diltiazem are also useful in the control of heart rate and supraventricular arrhythmias. Nimodipine may control vascular spasm following subarachnoid hemorrhage. Calcium channel blockers have also been used in the treatment of migraine headache and Raynaud's phenomenon.
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PMID:Comparative clinical pharmacology of calcium channel blockers. 199 Jul 41

In a prospective randomised clinical study on 80 patients with idiopathic sudden hearing loss the therapeutic value of nimodipine was evaluated. Nimodipine is a 4-5-dihydropyridine calcium antagonist with selective spasmolytic and vasodilatory properties on cerebral vessels. The mean improvement of hearing (250, 500, 1000, 2000, 4000 Hz) amounted to 16.5 +/- 11.3 dB as compared with 18.6 +/- 10.2 dB achieved by standard treatment with hydroxyethyl starch (HAES) and naftidrofuryl. The difference is not significant (p greater than 0.2). These results together with the low rate of side effects indicate nimodipine as a therapeutic alternative in cases of hypertension, cardiac failure and allergic predisposition. The possible role of spontaneous recovery on one side and of specific parameters such as rheologic abnormalities or type of audiogram are discussed. They are important for a more sophisticated therapeutic approach towards sudden hearing loss.
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PMID:[Treatment of sudden deafness with the calcium antagonist nimodipine. Results of a comparative study]. 269 Aug 38

The clinical and pathological effects of nimodipine on cerebral infarction were investigated in 12 male baboons. In randomized/blind trials, six animals given intravenous nimodipine (2 micrograms/kg/min load, 1 microgram/kg/min maintenance) for 96 hours starting 50 minutes before 6-hour double-clip occlusion of the middle cerebral artery were compared to 6 control animals. Standardized neurological examinations were performed by examiners blinded to the animals' therapy on Day 7 and Day 14 after stroke. On Day 14 the animals were killed. The brains were studied pathologically, and the relative areas of infarction were quantified. Intracranial pressure was lower in nimodipine-treated animals; however, the range of intracranial pressure values in each group was broad. Two control animals with high intracranial pressure died. There were no deaths among the nimodipine-treated animals. The neurological scores on Days 7 (P less than or equal to 0.01) and 14 (P less than or equal to 0.05) were significantly different between the two groups. The nimodipine-treated animals had less clinical evidence of infarction compared to controls. Nimodipine-treated animals tended to have smaller areas of infarction; however, the difference between the two groups was not statistically significant. The infusion of nimodipine in the treatment of focal cerebral ischemia is safe and does not appear to aggravate the extent of infarction or to exacerbate intracranial hypertension. The clinical neurological evaluations indicate that nimodipine may improve or preserve neurological outcome after stroke.
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PMID:The efficacy of intravenous nimodipine in the treatment of focal cerebral ischemia in a primate model. 275 82

Nimodipine (Nimotop) was administered to spontaneously hypertensive rats (SHR) in order to investigate its ameliorative effect on central nervous disorders associated with hypertension. Discrimination learning was used as the dependent variable. In normotensive Wistar Kyoto rats, the ratio of correct: incorrect responses in a brightness discrimination was not different between the nimodipine group and the vehicle group. However, SHR, which displayed decreased discrimination learning ability under control conditions, showed a remarkable improvement in discrimination learning under the influence of nimodipine. This was probably because the vasodilative action of nimodipine produced improvements in circulation in various organs including the brain, which in turn influenced learning ability. Nimodipine has very effective actions on learning performance that low levels of discrimination ability in SHR might be improved on learning performance on schedule controlled learning task.
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PMID:Effect of nimodipine on brightness discrimination learning test in Wistar Kyoto and spontaneously hypertensive rats. 322 70

The chemistry, pharmacology, pharmacokinetics, adverse effects, dosage, and availability of nimodipine are discussed, and the clinical use of nimodipine in preventing and treating cerebral arterial spasm in patients with subarachnoid hemorrhage is reviewed. Nimodipine is a highly lipid-soluble dihydropyridine derivative that readily crosses the blood-brain barrier. In animal studies, nimodipine has been shown to be effective in increasing cerebral blood flow; preventing vasoconstriction attributable to sympathetic stimulation, hypocapnia, and hypertension; and improving neurological outcome after cerebral ischemia. Nimodipine is reported to be 90% protein bound; its half-life is approximately 13 hours, with substantial interpatient variability. Nimodipine has been studied in the prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. In four open trials, in which nimodipine was administered orally, intravenously, topically during surgery, or by intracarotid injection, and in two double-blind, placebo-controlled trials, neurological outcomes were improved in patients receiving the drug. However, in both sets of trials nimodipine had limited effects on cerebral arterial spasm. Although nimodipine can cause hypotension, no serious adverse reactions to the drug were reported in clinical trials in patients with subarachnoid hemorrhage. Based on limited data currently available, nimodipine appears to improve neurological outcome in patients with subarachnoid hemorrhage. However, its efficacy in preventing or treating cerebral arterial spasm in these patients seems to be limited.
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PMID:Use of nimodipine for prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. 332 39

Calcium antagonism of nifedipine, nitrendipine or nisoldipine prevented salt-induced hypertension, renovascular damage and mortality in Dahl salt-sensitive (S) rats. The calcium agonist BAY K 8644 accelerated the development of salt-induced hypertension in S rats. In some S rats on a low-salt diet BAY K 8644 induced renovascular damage without sustained hypertension. In stroke-prone spontaneously hypertensive rats (SHRSP) on a normal diet the natural appearance of stroke was correlated with an increased calcium content in brain and kidney tissue. Nimodipine prevented stroke and the increase in brain calcium content without affecting the high blood pressure. A similar protective effect without substantial influence on high blood pressure was achieved by bilateral parathyroidectomy. Hypertension-associated vascular damage does not necessarily depend on the systemic intravascular pressure. In malignant hypertension the deleterious calcium overload in tissues may be activated or inhibited independently of the regulation of arterial blood pressure.
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PMID:Calcium antagonism and protection of tissues from calcium damage. 348 33

Nimodipine, a new calcium channel blocker, seems to be effective in the treatment of vasospasm in cerebral vasculature. Typical cardiovascular side effects have limited the dose in neurology and neurosurgery to 0.03 mg/kg X h. This study was designed to examine the influence of an infusion of high dose nimodipine (0.09 mg/kg X h) on haemodynamics. 52 patients undergoing aorto-coronary bypass surgery and prospectively randomised in a nimodipine group and a control group having received 0.9% saline solution as placebo were investigated at 3 different times: 1. before induction of anaesthesia (n = 6) 2. during anaesthesia (n = 10) 3. during extracorporeal circulation (ECC n = 10). Predominant effect of high-dose nimodipine was a decrease in total systemic resistance (TSR), followed by a decrease in mean arterial pressure (MAP) and a significant increase in cardiac output. Haemodynamic effects were much more pronounced during anaesthesia in comparison to patients before induction of anaesthesia, thus demonstrating an interaction between anaesthetics and calcium channel blocker. Heart rate (HR -9.3%) and dp/dtmax (-17%) showed a decrease, too. The decrease in MAP and HR in connection with a decrease in left ventricular pressure (-21.9%) and left ventricular end diastolic pressure (-42.8%) indicate a reduction in myocardial oxygen demand. An increasing dosage of nimodipine is accompanied by increasing cardiovascular effects. From the haemodynamic point of view high dosage of nimodipine seems to be of advantage in patients with hypertension and/or coronary heart disease suffering simultaneously from cerebral vasospasm.
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PMID:[Hemodynamic effects in high-dose infusion of nimodipine, a new calcium antagonist]. 349 53

The author discusses the epidemiology, the diagnosis, the clinical and morphological aspects of cerebral vasospasm from his personal experience and a study of the literature. Prediction and diagnosis of vasospasm is possible by evaluation of the amount of blood on CT scan, measuring fibrin breakdown products in the CSF and the findings of early EEG and Transcranial Doppler Sonography. CBF measurement is helpful in following the process of ischemia and deciding the right moment for operation. Early surgery on cerebral aneurysms is advocated in order to prevent rebleeding and for early removal of blood clot from the basal cisterns. If vasospasm and ischemia do develop, energetic treatment with hypervolemia and induced hypertension can be started without fear of rebleeding. Prophylactic intravenous administration of Nimodipine is thought to be of real value. Since the introduction of early surgery by the author 80 patients have been operated within 3 days after S.A.H. The mortality was 11% and the morbidity 7.5%. Management mortality and morbidity for the total group of 209 patients with S.A.H. treated either medically or surgically were 23.5% and 6% respectively. If one excludes the 18 patients that died within 24 hours the mortality was 15.6%.
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PMID:[Vascular spasm and cerebral ischemia after meningeal hemorrhage caused by rupture of an aneurysm]. 351 64

Nimodipine was administered by intravenous infusion to six male baboons before, during, and after 6 hours of middle cerebral artery occlusion. Intracranial pressure (ICP) and systemic blood pressure were monitored continuously. An epidural balloon was inflated at regular intervals at three levels of arterial CO2 tension (25, 35, and 50 mm Hg) before and after the administration of nimodipine, and volume-pressure curves were generated. In every case, curves generated after intravenous nimodipine infusion were lower and shifted more to the right than the same set of curves generated before nimodipine administration, regardless of the baseline ICP. The reduction in ICP following nimodipine infusion was not due to a reduction in mean arterial blood pressure and was statistically significant at all three levels of pCO2 (p less than 0.01). These results suggest that, in the presence of elevated ICP due to cerebral infarction, there is no increased risk of exacerbating intracranial hypertension with the addition of nimodipine.
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PMID:The effect of nimodipine on intracranial pressure. Volume-pressure studies in a primate model. 361 72

In isolated vessels in vitro nimodipine inhibits spasms induced by depolarization independently of the vessel's origin. The spasms induced by spasmogenic agonists such as serotonin, catecholamines, histamine, thromboxane, or whole blood are inhibited only in the cerebral vessels and not in the peripheral vessels. In vivo, nimodipine inhibits cerebrovascular spasms and brain damage in acute and chronic animal experiments. In chronic studies on stroke-prone, spontaneously hypertensive rats, nimodipine prevents cerebral tissue damage and prolongs the survival time without affecting the high blood pressure. Nimodipine inhibits the transmembraneous calcium influx in the smooth muscle cells of the cerebral vessels and thus prevents cerebral hypoperfusion after spasmogenic stimulation. In chronic cerebrovascular stress nimodipine prevents harmful calcium overloading and thus ensures the integrity of the cerebral parenchyma.
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PMID:Pharmacology of nimodipine, a calcium antagonist with preferential cerebrovascular activity. 401 Aug 68


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