Regional blood flow in conscious rats after head-down suspension

Exposure to microgravity in humans causes cardiovascular deconditioning affecting blood pressure, heart rate and vascular responsiveness. This study investigated cardiac output, arterial blood pressure and regional blood flows [radioactive microspheres: ⁵⁷Co, 15.5 (SEM 0.1) μm in diameter] in conscious and freely moving rats subjected to 14 days of simulated microgravity (head-down suspension, HDS) in male Wistar rats: control (horizontally attached, n = 7), suspended for 14 days (n = 8) and suspended/allowed to recover for 10 min (R10min, n = 5) or 24 h (n = 9). Compared to the control group, 14 days of HDS resulted in reduced total peripheral resistance (37%); an increased cardiac index (65%) was associated with no significant change in the mean arterial pressure . There were elevated brain (63%), visceral (>20%), hindlimb (>80%) and forelimb (>215%) muscle blood flows. In the R10min group, the decreased (18%) and the regional blood flows returned to control values. Within 24 h the as well as cardiac index and total peripheral resistance were restored. In conclusion, 14 days of HDS engendered local circulatory changes resulting in transient blood pressure instability during recovery. Accepted: 26 March 1998     

Regional pulmonary blood flow during acute pulmonary edema: a PET study

We used positron emission tomography to evaluate the effects of nitroprusside or prostacyclin (NP/Prost) on regional pulmonary blood flow (rPBF) in 21 dogs after oleic acid- (OA) induced acute pulmonary edema and compared the results with data from 11 dogs given OA only and 5 given meclofenamate after OA. After OA only, a progressive decrease in rPBF occurred in edematous gravity-dependent lung regions, but only in 6 of 11 dogs. In these six dogs, rPBF fell 41 +/- 12% compared with base line or with the other five dogs (3 +/- 19%) (P less than 0.05). In the NP/Prost group, the vasodilators failed to reverse any change in rPBF after OA but did prevent additional derecruitment until the drug infusion was stopped, after which rPBF to the edematous regions decreased further. In contrast, meclofenamate after OA temporally accelerated but did not quantitatively enhance rPBF reduction in edematous lung regions. Thus, in this model, vessels in edematous lung regions remain vasoreactive only until derecruited. We speculate that the mechanism of derecruitment involves an interaction between edema accumulation and vasoconstriction, in which the actual pattern of rPBF after lung injury represents a balance between mechanisms responsible for vascular derecruitment and vasodilation from prostacyclin production.     

Redistribution of pulmonary blood flow during unilateral hypoxia in prone and supine dogs

We usedfluorescent-labeled microspheres in pentobarbital-anesthetized dogs tostudy the effects of unilateral alveolar hypoxia on the pulmonary bloodflow distribution. The left lung was ventilated with inspiredO₂ fraction of 1.0, 0.09, or 0.03 in random order; the right lung was ventilated with inspiredO₂ fraction of 1.0. The lungs wereremoved, cleared of blood, dried at total lung capacity, then cubed toobtain ~1,500 small pieces of lung (~1.7 cm³). The coefficient ofvariation of flow increased (P < 0.001) in the hypoxic lung but was unchanged in the hyperoxic lung.Most (70-80%) variance in flow in the hyperoxic lung wasattributable to structure, in contrast to only 30-40% of thevariance in flow in the hypoxic lung(P < 0.001). When adjusted for thechange in total flow to each lung, 90-95% of the variance in thehyperoxic lung was attributable to structure compared with 70-80%in the hypoxic lung (P < 0.001). Thehilar-to-peripheral gradient, adjusted for change in total flow,decreased in the hypoxic lung (P = 0.005) but did not change in the hyperoxic lung. We conclude thathypoxic vasoconstriction alters the regional distribution of flow inthe hypoxic, but not in the hyperoxic, lung.

     

Regional cerebral blood flow changes during hypothermia

1. 1. When brain temperature was decreased from 38 to 22 °C using selective hypothermia, tissue blood flow decreased significantly in cerebral cortex, cerebellum, and thalamus, but did not significantly change in hypothalamic or brain stem tissue.

2. 2. A further decrease in brain temperature to 8 °C produced an increase in blood flow in all tissues except cerebral cortex compared to tissue blood flow measured at 22 °C. Compared to normothermic values, blood flow remained significantly decreased at 8 °C in cerebral and cerebellar cortex and was increased in brain stem.

3. 3. After rewarming, tissue blood flow returned to original baseline values in all tissues except cerebral cortex where blood flow was slightly but significantly decreased and brain stem, where blood flow was increased.

4. 4. These results indicate that the cerebrovascular effects of selective brain cooling are regionally specific. These changes appear to be due to both direct and indirect effects of cerebral hypothermia since brain tissue blood flow changes are apparent, compared to control values, after rewarming of the brain.

     

Pancreatic islet blood flow in conscious rats during hyperglycemia and hypoglycemia

Anesthesia affects general hemodynamics and regulation of organ perfusion. We used colored microspheres to measure pancreatic islet blood flow in conscious rats at two time points, during either hyperglycemia or hypoglycemia. This method, using black and green microspheres, was validated by comparison with previous microsphere experiments and by lack of effect of a nonmetabolizable glucose analog, 3-O-methylglucose, on islet perfusion. Basal and glucose-stimulated islet blood flow levels were similar in pentobarbital sodium-anesthetized and conscious rats. However, the basal distribution of pancreatic blood flow was altered by anesthesia (fractional islet blood flow 5.8 +/- 0.4% in conscious rats, 7.9 +/- 0.8% in pentobarbital-anesthetized rats, P < 0.05). Insulin-induced hypoglycemia significantly increased whole pancreatic blood flow in conscious rats, whereas islet blood flow remained unchanged and fractional islet blood flow was decreased (5.8 +/- 0.5% in the basal state, 4.2 +/- 0.4% during hypoglycemia, P < 0.001). Methylatropine pretreatment significantly increased islet blood flow during hypoglycemia by 181%. This result suggests that prevention of hypoglycemia-induced increase in islet perfusion may be mediated, at least in part, by a cholinergic, vagal muscarinic mechanism.