Chemo-Reflex Control of Vascular Reactions Through the Carotid Body

120

The pH and the carbon dioxide tension of the blood flowing through a tissue are commonly thought to be major factors in the local control of regional blood flow, for instance in the vasodilation in exercising muscle (1). They also are of recognized importance in the control of general circulatory homeostasis; for example, systemic hypertension accompanies acutely induced hypercapnia (2, 3), and hypotension the hypocapnia of hyperventilation (4). Furthermore, disorders of acid-base equilibrium occur in pathologic states with sufficient frequency to merit consideration of the role of blood pH and CO2 tension in control of the circulation burdened by disease such as the acidosis of uremia and diabetic coma or the alkalosis of vomiting.With these considerations in mind, the present studies were undertaken in healthy humans to determine the effects of variation in blood pH and CO2 tension (Pco2) on cardiac output and on the flow of blood through extremity musculature. In an attempt to separate direct effects of change in pH or Pco0 on blood vessels themselves from those mediated by the nervous system, sympathetic impulses to the extremity were blocked with phenoxybenzamine (Dibenzyline 1) administered intraarterially to the extremity under study. METHODSThe subjects studied were healthy male volunteers and one male with essential hypertension. Their ages ranged from 22 to 46 years. Most had participated repeatedly in similar studies in the same laboratory and were, therefore, relaxed and at ease.Acidemia was induced by intravenous infusion of 500 to 800 ml of 0.2 M lactic acid or 0.17 M ammonium chlo-*

Section: Acid and Bicarbonate Infusionssupporting

confidence: 52%

Section: Acid and Bicarbonate Infusionsmentioning

confidence: 99%

General and Regional Circulatory Responses to Change in Blood Ph and Carbon Dioxide Tension*

Richardson¹,

Wasserman²,

Patterson³

1961

120

“…Studies were carried out on these animals to determine the role of carotid body chemoreceptors in the antidiuretic response to hypoxia (25). In these animals, as Po2 was lowered from 78.6+4 to 32.5+3 mm Hg (P < 0.001), an antidiuresis was observed in each animal as reversible increases in Uosm (from 113±+15 to 357±+17 mosmol/kg H20, P <0.001) and decreased in CH,O (from 1.82+0.19 to -0.55+0.14 ml/min, (32 Table IE). These studies were carried out to determine the role of parasympathetic neural pathways which innervate the carotid baroreceptor in the antidiuretic response to hypoxia.…”

Section: Resultsmentioning

confidence: 88%

Mechanism of Effect of Hypoxia on Renal Water Excretion

Anderson¹,

Pluss²,

Berns³

et al. 1978

104

A B S T R A C T The effect of lowering the pressure of oxygen from 80 to 34 mm Hg was examined in anesthetized dogs that were undergoing a water diuresis. This degree of hypoxia was associated with an antidiuresis as urine osmolality (Uosm) increased from 107 to 316 mosmol/kg H20 (P < 0.001) and plasma arginine vasopressin increased from 0.06 to 7.5 pLU/ml, (P < 0.05).However, hypoxia was not associated with significant changes in cardiac output (CO, from 4.2 to 4.7 liters/ min), mean arterial pressure (MAP, from 143 to 149 mm Hg), glomerular filtration rate (GFR, from 46 to 42 ml/min), solute excretion rate (SV, from 302 to 297 mosmol/min), or filtration fraction (from 0.26 to 0.27, NS). Hypoxia was associated with an increase in renal vascular resistance (from 0.49 to 0.58 mm Hg/ml per min, P < 0.01). The magnitude of hypoxia-induced antidiuresis was the same in innervated kidneys and denervated kidneys. To further examine the role of vasopressin in this antidiuresis, hypoxia was induced in hypophysectomized animals. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in hypophysectomized animals was the same as in intact animals. In contrast to intact animals, however, hypoxia did not induce a significant antidiuresis in hypophysectomized animals (Uosm from 72 to 82 mosmol/kg H2O). To delineate the afferent pathway for hypoxiastimulated vasopressin release, hypoxia was induced in dogs with either chemo-or baroreceptor denervation. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in the denervated animals was the same as in nondenervated animals. Hypoxia resulted in an antidiuresis in chemoreceptor (Uosm from 113 to 357 mosmol/kg H20, P < 0.001) but not in baroreceptor (Uosm from 116 to 138 mosmol/kg H20, NS) denervated animals. To determine if hypoxia alters renal response to vasopressin, exogenous vasopressin was adminisDr.

“…This biphasic character is a unique feature of sodium bicarbonate administration; other alkalinizing solutions, such as sodium hydroxide and sodium carbonate, evoke a decrease in total ventilation both during and after the infusion (1,4). The initial stimulation of respiration by sodium bicarbonate solutions has been reported in experiments on dogs by Gesell, Krueger, Gorham, and Bernthal (1), Bernthal (3), and Hesser (4).…”

Section: Discussionmentioning

confidence: 89%

“…Evidence that such inhibition does occur has been presented in several reports (1)(2)(3)(4); on the other hand, some investigators have found no significant change in Pco2 (5). Opportunity for the collection of further evidence on this question was afforded by a series of studies on the effects of acute metabolic alkalosis induced in human subjects by the infusion of hypertonic sodium bicarbonate solution, approximately 2.3 mEq.…”

mentioning

confidence: 90%

The Acute Effects in Man of a Rapid Intravenous Infusion of Hypertonic Sodium Bicarbonate Solution. Ii. Changes in Respiration and Output of Carbon Dioxide 1

Singer¹,

Deering²,

Clark³

1956

It is generally agreed that in metabolic acidosis respiration is stimulated, with consequent reduction of alveolar and arterial CO2 pressure, Pco2; in metabolic alkalosis, however, there has been disagreement as to whether or not there is a corresponding respiratory inhibition, with elevation of Pco2. Evidence that such inhibition does occur has been presented in several reports (1-4); on the other hand, some investigators have found no significant change in Pco2 (5). Opportunity for the collection of further evidence on this question was afforded by a series of studies on the effects of acute metabolic alkalosis induced in human subjects by the infusion of hypertonic sodium bicarbonate solution, approximately 2.3 mEq. per kilogram of body weight. The first paper of this series (6) described the ionic transfers as observed in arterial or cutaneous blood, and calculated for extracellular and other body fluid compartments, including the volume of distribution of the excess sodium bicarbonate. The plasma acid-base data from these experiments readily permit the calculation of arterial Pco2, before, during, and for two hours following the infusion. We consider the changes in calculated arterial Pco2 to represent the most reliable index of respiratory changes, because this sampling method produced the least disturbance to respiration. However, we are also reporting in this, the second paper of the series, results of additional experiments in which alveolar Pco2, total pulmonary ventilation, and respiratory