SUMMARY In vitro studies suggest that cerebrovascular contraction is more dependent on the influx of calcium to smooth muscle than general systemic arteries. The present study tested the in vivo effects of a calcium influx blocker (nimodipine) on cerebral blood flow and metabolism in 16 baboons. The l33 xenon clearance technique was used together with careful control of EEG and blood gases. With normal blood gases intravenous nimodipine infusion (1 /xg/kg/min) produced an 18% increase in cerebral blood flow with no alteration in cerebral oxidative metabolism or blood pressure. Higher doses (above 10 ^.g/kg/min) resulted in a decreased arterial blood pressure and a return to control cerebral flow. Infusion of the dose producing maximal increase in flow, decreased the cerebral reactivity to altered PCO 2 (n = 5). These results suggest that nimodipine may be a relatively selective cerebrovascular dilator.
Stroke Vol 15, No 3, 1984PREVIOUS IN VITRO studies suggest that the smooth muscle of the cerebral resistance vessels is more heavily dependent for contraction on the influx of calcium from the extracellular fluid than other general systemic blood vessels.' 2 Thus, it seems probable that, pharmacologic agents which prevent the movement of calcium into the smooth muscle would preferentially reduce cerebrovascular constriction leaving intact general systemic vascular tone. The drug nimodipine has proven effective in vitro in antagonizing cerebral vascular contractions to agonists such as 5-hydroxytryptamine, norepinephrine and high K + solutions. 3 The present study tested, in vivo, the effects of various doses of nimodipine on resting cerebral blood flow. The dose which showed the largest cerebral flow increase was then used to determine the action on the cerebrovascular constriction resulting from, 5-hydroxytryptamine infusion in the hypercapnic animal 4 and hyperventilation to lower the PCO 2 .
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Methods and MaterialsAdult baboons (Papio 8-12 kg) were sedated with intramuscular phencyclidene (Sernylan, 10 mg/kg) or ketamine (5 mg/kg). They were then transported to the laboratory where full anesthesia was induced with sodium pentobarbital (Nembutal, 20 mg/kg i.v.). The animals were intubated and after succinyl choline (20 mg i.v.) were ventilated using a positive pressure respirator. The rate and depth of ventilation were adjusted so that the animals showed approximately 5% CO 2 in end tidal expiratory air (CO 2 measured continuously from the endotracheal tube) using a Goddard capnograph. The depth of anesthesia was monitored throughout using a single lead EEG and this was maintained showing a rhythm of 8-10 Hz using a ventilation gas mixture of 70% N 2 O in oxygen and supple-
Studies report that football players have high blood pressure (BP) and increased cardiovascular risk. There are over 70,000 NCAA football players and 450 Division III schools sponsor football programs, yet limited research exists on vascular health of athletes. This study aimed to compare vascular and cardiovascular health measures between football players and nonathlete controls. Twenty-three athletes and 19 nonathletes participated. Vascular health measures included flow-mediated dilation (FMD) and carotid artery intima-media thickness (IMT). Cardiovascular measures included clinic and 24 hr BP levels, body composition, VO2 max, and fasting glucose/cholesterol levels. Compared to controls, football players had a worse vascular and cardiovascular profile. Football players had thicker carotid artery IMT (0.49 ± 0.06 mm versus 0.46 ± 0.07 mm) and larger brachial artery diameter during FMD (4.3 ± 0.5 mm versus 3.7 ± 0.6 mm), but no difference in percent FMD. Systolic BP was significantly higher in football players at all measurements: resting (128.2 ± 6.4 mmHg versus 122.4 ± 6.8 mmHg), submaximal exercise (150.4 ± 18.8 mmHg versus 137.3 ± 9.5 mmHg), maximal exercise (211.3 ± 25.9 mmHg versus 191.4 ± 19.2 mmHg), and 24-hour BP (124.9 ± 6.3 mmHg versus 109.8 ± 3.7 mmHg). Football players also had higher fasting glucose (91.6 ± 6.5 mg/dL versus 86.6 ± 5.8 mg/dL), lower HDL (36.5 ± 11.2 mg/dL versus 47.1 ± 14.8 mg/dL), and higher body fat percentage (29.2 ± 7.9% versus 23.2 ± 7.0%). Division III collegiate football players remain an understudied population and may be at increased cardiovascular risk.
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