Circulation research
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Circulation research · Feb 1977
Cardiac output and renal blood flow in glycerol-induced acute renal failure in the rat.
Cardiac output (CO) and renal blood flow (RBF) were simultaneously evaluated by the microsphere method in water-drinking and chronic saline-drinking rats at 3, 12 and 24 hours after induction of acute renal failure by glycerol injection. Threee hours after glycerol injection CO and RBF decreased to 36% and 20% of the respective controls in water-drinking rats and to 41% and 24% of the controls in saline-drinking rats. Renal vascular resistance (RVR) increased significantly in both groups at this time. ⋯ Twenty-four hours post-glycerol injection, when acute renal failure was evident as indicated by blood urea nitrogen (BUN) values of 116.9 and 63.8 mg/100 ml in water- and saline-drinking rats, respectively, CO and RBF returned to normal, except that the CO of of water-drinking rats was slightly higher than control. Thus, we conclude that decreased CO is an important determinant of the early decrease in renal perfusion in glycerol-induced acute renal failure. Furthermore, the observed earlier return of CO and RBF to normal in saline-drinking rats may be partly responsible for reproducing the severity of acute renal failure.
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Circulation research · Oct 1976
The response of canine coronary vascular resistance to local alterations in coronary arterial P CO2.
The effect of hypercapnia on coronary vascular resistance (CVR) was studied in seven open-chest dogs. Coronary blood flow was supplied to the cannulated left main coronary artery from the femoral artery by a precision pump. Coronary arterial PCO2 was locally controlled with a small membrane oxygenator in the coronary perfusion circuit. ⋯ When coronary flow was reduced to an ischemic level there was little response in CVR to hypocapnia. Thus the level of arterial PCO2 can have an important effect on CVR independent of changes in O2 consumption. Myocardial PCO2, derived from metabolically produced CO2 and contributed to by arterial CO2, may be a major factor in normal control of coronary flow.
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Circulation research · Jul 1976
Continuous determination of beat to beat stroke volume from aortic pressure pulses in the dog.
Present methods for measurement of stroke volume from the aortic pressure pulse are not suitable for beat-to-beat determinations during non-steady state conditions because these methods assume that each systolic ejection is equal to the peripheral runoff during the same beat. We have tested a new method which allows determination of an aortic pressure-volume conversion factor over a wide range of pressures during transient changes in stroke volume and infusions of vasoactive drugs in 6 dogs with chronically implanted aortic electromagnetic flowmeters. ⋯ The total systolic increment (delta PSV) is assumed to describe the pressure-volume characteristics during systole and is related to stroke volume by a constant multiplier that is derived from the indicator-dilution measurements of cardiac output. The values for beat-to-beat variations that were determined by use of the aortic electromagnetic flowmeter and by this aortic pressure pulse method were found to be within the range of measurement errors of stroke volume determined from individual aortic electromagnetic flow pulses.
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Circulation research · May 1976
Role of resistance and exchange vessels in local microvascular control of skeletal muscle oxygenation in the dog.
The effects of reduction in perfusion pressure, arterial hypoxia, muscle contraction, and adrenergic stimulation on the hindlimb muscle circulation were studied. Under normal conditions (venous PO2 greater than or equal to 40 mm Hg), oxygen delivery to the muscle was maintained mainly by large increases in the capillary exchange capacity and the oxygen extraction ratio in accord with tissue demand following the application of the above stresses. The participation of the resistance vessels under these conditions was minimal. ⋯ In contrast, the contribution of exchange capacity was diminished, probably owing to the fact that most of the capillaries already are open at low venous PO2. These data suggest that the locus of local microvascular control of muscle oxygenation shifts from the normally more sensitive precapillary sphincters to the proximal flow-controlling arterioles as the prevailing venous oxygen tension falls. Yet, although the relative contribution of the resistance and exchange vessels to intrinsic regulation of tissue oxygenation is related to the prevailing venous oxygen tension, the two compensatory mechanisms operating in concert maintain tissue PO2 above the critical level over a wide range of stresses.