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

The pattern of dying from immersion hyperthermia was documented in 8 dogs, 9 rhesus monkeys and 12 pigtail monkeys. Under light general anesthesia and spontaneous breathing, the animals were immersed into water of 45 degrees C, which was subsequently adjusted to control brain (parietal epidural) temperature at 42 +/- 0.5 degrees C. Transient initial hypertension, tachycardia, tachypnea and hypocarbia were followed by progressive hypotension with decreasing central venous pressure and pulmonary artery occlusion pressures (measured in three dogs only), bradycardia and bradypnea. Cardiac arrest occurred in the dogs after immersion of 288 +/- 66 min and more rapidly (P less than 0.02) in the rhesus monkeys (at 137 +/- 75 min) and pigtail monkeys (at 178 +/- 26 min). EEG silence occurred in the monkeys at MAP 40 mmHg and in the dogs at MAP 25 mmHg. Cardiac arrest occurred in form of sudden ventricular fibrillation (2/5 dogs, 2/9 rhesus monkeys, 3/12 pigtail monkeys), or later in electromechanical dissociation leading to electric asystole (3/5 dogs, 7/9 rhesus monkeys, 9/12 pigtail monkeys). The mean blood glucose levels decreased to less than 30 mg/dl (P less than 0.002), whereas hematocrit, serum osmolality, lactate and potassium levels increased. Necropsies revealed macroscopic petechial hemorrhages in all extracerebral organs, but not in the brain. There was no gross evidence of cerebral edema. Death seemed to be the result of primary cardiovascular failure leading to secondary (ischemic) cerebral failure (EEG silence) and apnea, which coincided with pulselessness.
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PMID:Hyperthermia-induced cardiac arrest in dogs and monkeys. 217 84

The mass discharges of the splanchnic sympathetic (SND) and phrenic nerves (PND) were recorded in urethananesthetized rats with resected vagal and aortic nerves. Carotid chemoreceptor (CC) stimulation with N2 inhalation (4-12 s) or cyanide (50-100 micrograms/kg iv) activated SND in bursts synchronized with the postinspiratory phase (mean SND increase: 105 +/- 8%), raised AP, and increased PND rate and amplitude (n = 40). Brain transection at superior collicular level produced no effect. The sympathetic (SChR) and respiratory chemoreflexes (RChR) were reduced after transections through the pons. Lesions of the dorsolateral pons (dl-pons) produced CO2-dependent apneusis and/or tachypnea at rest. After such lesions, CC stimulation produced expiratory apnea and a 30% increase in SChR due to tonic activation of SND. In contrast, bilateral lesions of the ventrolateral pons (vl-pons) reduced the SChR by 54-76%. Muscimol (Mus) injections (bilateral, 175 pmol/side) into vl-pons did not change resting SND, MAP, baroreflex, and RChR but reduced the SChR (54-82%). In conclusion, under anesthesia: 1) the pathway of the carotid chemoreflex is confined to the pons and medulla, 2) the dl-pons exerts indirect control over the SChR via its role in respiratory rhythmogenesis, and 3) neurons in the vl-pons contribute selectively to the SChR but not to PND activation during CC activation.
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PMID:Role of the pons in the carotid sympathetic chemoreflex. 806 62