Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objectives of this study were to evaluate a technique for routine, noninvasive measurement of systemic arterial blood pressure and heart rate (HR) in conscious Beagle dogs for toxicologic research. HR, systolic, diastolic, and mean arterial (MAP) pressures were measured with a DINAMAP research monitor (Model 1255, Critikon, Inc.) as follows: Dogs were restrained in a Harvard dog sling, a neonatal cuff was wrapped around the base of the tail, and blood pressure and HR were determined once a minute. Initially, normal values were obtained, 5-10 trials/session, one to three sessions/day for 15 days in six dogs. The day to day, session to session, and trial variabilities were determined and found to be minimal. The day to day diastolic pressure ranged from 74 +/- 18 to 91 +/- 13 mm Hg, systolic pressure from 125 +/- 25 to 156 +/- 22 mm Hg, MAP from 94 +/- 20 to 113 +/- 15 mm Hg, and HR from 111 +/- 21 to 126 +/- 24 beats/minute (bpm). The effects of various drugs on these parameters were determined. Norepinephrine increased diastolic, systolic, and MAP by 75 to 110 mm Hg and decreased HR by half. Epinephrine increased HR by 20 bpm. Phentolamine decreased diastolic, systolic, and MAP by up to 25 mm Hg. Isoproterenol increased HR by up to 130 bpm and decreased diastolic, systolic, and MAP by 20 mm Hg. In addition, the effect of a classic drug interaction on these parameters was determined. When dogs pretreated with the monoamine oxidase inhibitor tranylcypromine were challenged with tyramine, diastolic, systolic, and MAP pressures were increased, whereas HR was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Noninvasive measurement of systemic arterial blood pressure in the conscious beagle dog. 335 Feb 33

Factors determining vascular resistance were examined in 6 normotensive subjects (NT), 5 with established hypertension (EH) and diastolic pressures greater than 90 mmHg and 7 with borderline hypertension (BH) having pressures intermittently greater than 140/90 mmHg. Using plethysmography, we measured forearm blood flow (FBF), arterial resistance (FAR) and venous compliance (FVC) before and after autonomic blockade with propranolol 0.2 mg/kh, atropine 0.04 mg/kg and phentolamine 15 mg I.V. Subjects with EH had the highest baseline FBF. MAP was increased 18-22% after atropine and propranolol in all 3 groups. Phentolamine decreased MAP -8.9 +/- 2.1% in NT, -6.9 +/-1.2% in BH and -16.5 +/- 1.9% in EH (p less than 0.05). After total blockade, FAR in EH (32.4 +/- 4.8 units) was similar to FAR in TN (31.0 +/- 3.6 units) whereas that in BH remained high (50.2 +/- 3.8 units; p less than 0.01). Baseline FVC was highest in NT, intermediate in BH and lowest in EH and was not altered by autonomic blockade. Non-gravitational exercise for 6 min during upper arm arterial occlusion after autonomic blockade resulted in a residual FAR of 2.3 +/- 0.1 units in NT, 3.8 +/- 0.3 units in BH and 4.2 +/- 1.7 units in EH (p less than 0.01) during reactive hyperemia. Increased FAR in our subjects with BH and EH was probably due to structural vascular alterations. The greater increase in FAR and MAP in EH over that observed in BH has a sympathetic nervous system component.
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PMID:Vasodilator capacity of forearm vessels in hypertension. 711 72

Asphyxia in utero in pre-term fetuses is associated with evolving hypoperfusion of the gut after the insult. We examined the role of the sympathetic nervous system (SNS) in mediating this secondary hypoperfusion. Gut blood flow changes were also assessed during postasphyxial seizures. Preterm fetal sheep at 70% of gestation (103-104 days, term is 147 days) underwent sham asphyxia or asphyxia induced by 25 min of complete cord occlusion and fetuses were studied for 3 days afterwards. Phentolamine (10 mg bolus plus 10 mg h(-1)i.v.) or saline was infused for 8 h starting 15 min after the end of asphyxia or sham asphyxia. Phentolamine blocked the fall in superior mesenteric artery blood flow (SMABF) after asphyxia and there was a significant decrease in MAP for the first 3 h of infusion (33 +/- 1.6 mmHg versus vehicle 36.7 +/- 0.8 mmHg, P < 0.005). During seizures SMABF fell significantly (8.3 +/- 2.3 versus 11.4 +/- 2.7 ml min(-1), P < 0.005), and SMABF was more than 10% below baseline for 13.0 +/- 1.7 min per seizure (versus seizure duration of 78.1 +/- 7.2 s). Phentolamine was associated with earlier onset of seizures (5.0 +/- 0.4 versus 7.1 +/- 0.7 h, P < 0.05), but no change in amplitude or duration, and prevented the fall in SMABF. In conclusion, the present study confirms the hypothesis that postasphyxial hypoperfusion of the gut is strongly mediated by the SNS. The data highlight the importance of sympathetic activity in the initial elevation of blood pressure after asphyxia and are consistent with a role for the mesenteric system as a key resistance bed that helps to maintain perfusion in other, more vulnerable systems.
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PMID:The role of the sympathetic nervous system in postasphyxial intestinal hypoperfusion in the pre-term sheep fetus. 1507 76