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Biomedical subjects

W E Huckabee

Publications and source records attributed to W E Huckabee.

13 recordsLinked to original sources
PubMed1975

Ventilatory response to drug-induced hypermetabolism.

Previous workers have demonstrated that an increase in minute ventilation accompanies tissue hypermetabolism induced by uncouplers of oxidative phosphorylation. The mechanism of this increase in minute ventilation has not been established. Accordingly, 2.5 mg/kg of 2,4-dinitrophenol (DNP) or 8-15 mg/kg of ethyl methylene blue (EMB) were infused into chloralose-anesthetized mongrel dogs; Vo2 increased 105 plus or minus 3% and VE INCREASED 107 PLUS OR MINUS 14%. Heads of vagotomized dogs were then perfused entirely with normal unchanging blood. Spinal cord remained intact. (The carotid bodies lay within the region of the perfused head.) Ventilatory responses of these head-perfused animals to breathing low oxygen and to breathing high CO2 gas mixtures were greatly attenuated. However, when DNP or EMB was infused into the body, VO2 increased 114 plus or minus 23% and VE increased 123 plus or minus 22%. When similar doses of DNP or emb were selectively administered to the head, increases in VE were limited to 21 plus or minus 6%. It is concluded that a major portion of the stimulus to ventilation, which accompanies infusion of DNP or of EMB, arises in tissues other than arterial chemoreceptors and brain. Presumably, this ventilatory stimulus is transmitted to the respiratory center via afferent pathways of the cervical spinal cord.

Animals↗
PubMed1973

Mechanisms regulating the cardiac output response to cyanide infusion, a model of hypoxia.

When tissue metabolic changes like those of hypoxia were induced by intra-aortic infusion of cyanide in dogs, cardiac output began to increase after 3 to 5 min, reached a peak (220% of the control value) at 15 min, and returned to control in 40 min. This pattern of cardiac output rise was not altered by vagotomy with or without atropine pretreatment. However, this cardiac output response could be differentiated into three phases by pretreating the animals with agents that block specific activities of the sympatho-adrenal system. First, ganglionic blockade produced by mecamylamine or sympathetic nerve blockade by bretylium abolished the middle phase of the cardiac output seen in the untreated animal, but early and late phases still could be discerned. Second, beta-adrenergic receptor blockade produced by propranolol shortened the total duration of the cardiac output rise by abolishing the late phase. Third, when given together, propranolol and mecamylamine (or bretylium) prevented most of the cardiac output rise that follows the early phase. When cyanide was given to splenectomized dogs, the duration of the cardiac output response was not shortened, but the response became biphasic, resembling that seen after chemical sympathectomy. A similar biphasic response of the cardiac output also resulted from splenic denervation; sham operation or nephrectomy had no effect on the monophasic pattern of the normal response. Splenic venous blood obtained from cyanide-treated dogs, when infused intraportally, caused an increase in cardiac output in recipient dogs; similar infusion of arterial blood had no effects. THESE RESULTS SUGGEST THAT THE CARDIAC OUTPUT RESPONSE TO CYANIDE INFUSION CONSISTS OF THREE COMPONENTS: an early phase, related neither to the autonomic nervous system nor to circulating catecholamines; a middle phase, caused by a nonadrenergic humoral substance released from the spleen by sympathetic stimulation; and a late phase, dependent upon adrenergic receptors but not upon sympathetic transmission.

Animals↗
PubMed1973

Effects of splenectomy and beta-adrenoceptor blockade on cardiac output response to acute hypoxemia.

Acute hypoxemia produced by the inhalation of 8% and 5% oxygen increased cardiac output in intact anesthetized dogs by 38% and 62%, respectively. Although practolol, a cardioselective beta-adrenergic blocking agent, reduced the increase in cardiac output in dogs subjected to severe hypoxemia (5% O(2) breathing) from 62% to 43%, it only slightly reduced the cardiac output rise in dogs subjected to moderate hypoxemia (8% O(2) breathing). Splenectomy, on the other hand, abolished the increase in cardiac output produced by moderate hypoxemia except for a small initial rise, but it reduced the increase in cardiac output during severe hypoxemia only to 37%. The entire increase, except for a small initial rise, disappeared only when splenectomized dogs were pretreated with practolol. Sham operation did not affect the cardiac output response to hypoxemia. It is concluded that an intact spleen is required for a significant portion of the increased cardiac output that occurs during both moderate and severe hypoxemia and that catecholamines do not participate in the regulation of cardiac output unless severe hypoxemia occurs.

Adrenergic beta-Antagonists↗
PubMed1970

Hyperlactatemia.

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Acidosis↗