Microvascular oxygen delivery and consumption following treatment with verapamil.
نویسندگان
چکیده
The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle relaxation to oxygen consumption of the microvascular wall during verapamil-induced vasodilatation. Verapamil HCl delivered in a 0.1 mg/kg bolus injection followed by a continuous infusion of 0.01 mg.kg(-1).min(-1) caused significant arteriolar dilatation, increased microvascular flow and functional capillary density, and decreased arteriolar vessel wall transmural Po(2) difference. Verapamil caused tissue Po(2) to increase from 25.5 +/- 4.1 mmHg under control condition to 32.0 +/- 3.7 mmHg during verapamil treatment. Total oxygen released by the microcirculation to the tissue remained the same as at baseline. Maintenance of the same level of oxygen release to the tissue, increased tissue Po(2), and decreased wall oxygen concentration gradient are compatible if vasodilatation significantly lowers vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. These findings show that treatment with verapamil, which increases oxygen supply through vasodilatation, may further improve tissue oxygenation by lowering oxygen consumption of the microcirculation.
منابع مشابه
Verapamil favorably influences hepatic microvascular exchange and function in rats with cirrhosis of the liver.
The effect of the calcium channel blocking agent, verapamil, on microcirculatory patterns and hepatic function was investigated in the perfused liver of cirrhotic rats. Compared with controls, cirrhotic livers had higher vascular resistance, increased intrahepatic shunting, and smaller extravascular albumin space and larger extravascular sucrose space, as determined by a multiple-indicator dilu...
متن کاملFluid resuscitation does not improve renal oxygenation during hemorrhagic shock in rats.
BACKGROUND The resuscitation strategy for hemorrhagic shock remains controversial, with the kidney being especially prone to hypoxia. METHODS The authors used a three-phase hemorrhagic shock model to investigate the effects of fluid resuscitation on renal oxygenation. After a 1-h shock phase, rats were randomized into four groups to receive either normal saline or hypertonic saline targeting ...
متن کاملExercise hemodynamics and oxygen delivery in human hypertension. Response to verapamil.
To characterize the hemodynamic response to exercise and the effects of calcium channel antagonism in hypertensive subjects, invasive exercise hemodynamics were performed in the baseline state after intravenous infusion of verapamil and after 5 to 7 days of oral verapamil in 10 subjects with moderate to severe hypertension. We also assessed oxygen delivery and use and the response of the sympat...
متن کاملImpaired skeletal muscle microvascular function and increased skeletal muscle oxygen consumption in severe falciparum malaria.
BACKGROUND Organ dysfunction and tissue hypoxia in severe falciparum malaria result from an imbalance between oxygen delivery and demand. In severe malaria, microvascular obstruction from parasite sequestration decreases oxygen delivery. However, host microvascular function (defined as the capacity to increase oxygen delivery in response to ischemia) and oxygen consumption have not been assesse...
متن کاملMicrovascular oxygen distribution in awake hamster window chamber model during hyperoxia.
The microvascular effects and hemodynamic events following exposure to normobaric hyperoxia (because of inspiration of 100% O2) were studied in the awake hamster window chamber model and compared with normoxia. Hyperoxia increased arterial blood Po2 to 477.9 +/- 19.9 from 60.0 +/- 1.2 mmHg (P < 0.05). Heart rate and blood pressure were unaltered, whereas cardiac index was reduced from 196 +/- 1...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- American journal of physiology. Heart and circulatory physiology
دوره 288 4 شماره
صفحات -
تاریخ انتشار 2005