Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cerebrovascular response to CO2 was evaluated by measuring relative changes in blood flow velocity within the middle cerebral artery by transcranial Doppler ultrasonography during normo-, hypo-, and hypercapnia. In seven patients without subarachnoid hemorrhage (five with unruptured arteriovenous malformations and two with aneurysms), the CO2 vasoreactivity was tested on the side of the middle cerebral artery with normal flow velocities opposite the lesion. A baseline CO2 reactivity test was obtained in each patient and then repeated under constant intravenous infusion of nimodipine, 2 mg/hr. Nine patients with ruptured aneurysms who were rated at Hunt and Hess Grades 1 or 2 were operated on within 1 to 3 days after the hemorrhage and treated with nimodipine, 2 mg/hr, given intravenously. In these patients, CO2 vasoreactivity was tested during the second week after the hemorrhage, when the middle cerebral artery velocity was increased by at least 50% of the initial value or more. Nimodipine was then discontinued and, 48 hours later, when the middle cerebral artery velocity was still in the same range, CO2 vasoreactivity was tested again. Two months later, after full recovery from the subarachnoid hemorrhage and normalization of the velocities, a third measurement of CO2 reactivity was obtained as a baseline control. No significant effect of nimodipine on CO2 vasoreactivity could be demonstrated in any of the test periods. In the second week after a subarachnoid hemorrhage, a significant reduction of the cerebrovascular response to CO2 was found (P less than 0.005).
 ...
PMID:Effect of nimodipine on cerebrovascular response to CO2 in asymptomatic individuals and patients with subarachnoid hemorrhage: a transcranial Doppler ultrasound study. 211 60

Nimodipine, a dihydropyridine that interacts with a Ca++ channel-associated binding site, when delivered (30 to 150 micrograms/kg) intra-arterially (ia) to enflurane-anesthetized cats, produced a dose-dependent suppression of seizures evoked by pentylenetetrazol. A comparable suppression was produced by clonazepam (1 to 30 micrograms/kg, ia). Phenytoin was maximally effective only at nearly lethal doses (90 mg/kg, ia). Verapamil, a diphenylalkylamine that interacts with a separate Ca++ channel-associated site, at the maximum nonlethal dose (6 mg/kg, ia) resulted in a mild facilitation of seizure activity. The drug vehicle used in these studies (50% polyethylene glycol-400) had no effect when given alone. Regional cerebral blood flow (rCBF) as measured by the clearance of xenon-133 was markedly elevated immediately after the onset of seizure activity (89 +/- 3 to 168 +/- 4 ml/100 gm/min). Concurrent with their resolution of the seizure activity, both nimodipine and clonazepam reduced rCBF to near preseizure levels and preserved the rCBF response to hypercarbia which would otherwise have been abolished following prolonged seizure activity. Moreover, the effect of nimodipine on rCBF and seizures occurred without any prominent alterations in mean arterial blood pressure as compared to preseizure levels. These data support the proposition that a dihydropyridine Ca++ channel binding site may play a role in modulating paroxysmal neuronal activity, and suggest that this class of agents may reflect a novel group of antiepileptic drugs.
 ...
PMID:Effect of dihydropyridines and diphenylalkylamines on pentylenetetrazol-induced seizures and cerebral blood flow in cats. 361 73

1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. One week after the blood injections were started there was about 10-20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of PaCO2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.
 ...
PMID:Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates. 682 30