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Role of the systemic vasculature in the hemodynamic response to changes in plasma ionized calcium
Insights
Altered calcium levels significantly impact blood pressure, with peripheral blood vessels compensating. Beta blockade during hypocalcemia further reduced cardiac output and stroke volume in dogs.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
Background:
- Plasma ionized calcium concentration ([Ca++]) plays a critical role in cardiovascular function.
- Both hypocalcemia and hypercalcemia can lead to significant physiological changes.
Purpose of the Study:
- To investigate the hemodynamic effects of sustained hypocalcemia and hypercalcemia in dogs.
- To examine the influence of beta-adrenergic blockade on these hemodynamic alterations.
Main Methods:
- 16 anesthetized, closed-chest dogs were subjected to induced hypocalcemia and hypercalcemia.
- Plasma ionized calcium levels were maintained at approximately 60% below or above normal.
- Hemodynamic parameters, including mean arterial pressure and cardiac output, were monitored.
- The effects of beta blockade with propranolol hydrochloride were assessed.
Main Results:
- Changes in plasma ionized calcium ([Ca++]) were associated with parallel shifts in mean arterial pressure.
- Cardiac output remained largely unchanged on average, indicating a significant role for peripheral vasculature.
- Hypocalcemia, prior to beta blockade, decreased systemic vascular resistance.
- After beta blockade, hypocalcemia led to a fall in cardiac output and stroke volume.
Conclusions:
- The peripheral vasculature is crucial in mediating hemodynamic responses to altered calcium levels.
- Beta-adrenergic activity is a key determinant of the hemodynamic impact of hypocalcemia.
- Beta blockade exacerbates the negative effects of hypocalcemia on cardiac function.
Abstract:
Hemodynamic consequences of sustained (one hour) hypocalcemia and hypercalcemia (plasma ionized calcium concentration [Ca++] maintained approximately 60% below or above normal, encompassing the clinical range) were studied and the influence of beta blockade on these hemodynamic alterations examined in 16 anesthetized, closed-chest dogs. Alterations in [Ca++] were associated with directionally similar changes in mean arterial pressure, whereas on the average cardiac output remained unchanged. Thus, the peripheral vasculature played an important role in the hemodynamic response to alterations in [Ca++]. The state of beta adrenergic activity was an important determinant of the hemodynamic response to hypocalcemia. Prior to beta blockade, hypocalcemia was associated with decreased systemic vascular resistance, whereas after beta blockade with propranolol hydrochloride, systemic vascular resistance was not different from control except at the five-minute observation period, and cardiac output and stroke volume fell.