The effects of hyperthermia on blood volume and effective vascular compliance were studied in control and heat acclimated rats (three weeks at 32 degrees C and 50% R.H.). Experiments were performed on conscious rats whose abdominal aorta and both jugular veins were cannulated. Continuous changes in blood volume (BV) were monitored by measuring 51Cr tagged erythrocyte dilution, using an arterio-venous extracorporeal shunt passing through a gamma counter. Total vascular compliance was calculated from the relation between changes in BV and central venous pressure during 10 min of infusion of saline at a rate of 1.6% body wt/10 min. Hyperthermia induced a significant blood volume expansion. This expansion was more pronounced in non-acclimated rats. Effective vascular compliance was similar in the normothermic, both non-acclimated and acclimated rats. However, while hyperthermia did not affect the vascular compliance of non-acclimated rats, it was decreased significantly in the acclimated hyperthermic rats. The data suggest that changes in vascular compliance play a role when rapid blood volume changes take place, especially in acclimated hyperthermic animals. The relations between changes in vascular compliance and heat induced redistribution of cardiac output are discussed.

The effects of rat atrial natriuretic peptide (rANP) on blood volume (BV) were determined by the continuous measurement of BV, mean arterial pressure (MAP), and central venous pressure (CVP). Immediately after a single-bolus injection of rANP-(1-28), 1 nmol/100 g body wt, in conscious rats, BV began to decrease. Peak reduction of -0.22 +/- 0.03 ml/100 g body wt was reached 14.5 min after the injection. Thereafter, BV levels returned gradually to -0.08 +/- 0.03 ml/100 g body wt compared with the control value. In volume expansion experiment, the nephrectomized, anesthetized rats were divided into two groups: the control group, with only a saline infusion, and the ANP group, with an infusion of saline with rANP (1 nmol/100 g body wt). In the ANP group, increases in BV were not as great, and recovery was threefold faster than that of the control group. In the ANP group, the recovery time of BV to the starting control levels was 8.5 min, and the time constant of recovery was 3.6 +/- 0.3 min-1. The control group times were 25 min and 11.5 +/- 0.8 min-1, respectively. The effective vascular compliances were approximately 2.8 ml.mmHg-1.kg body wt-1 in both groups, and the capillary filtration coefficient was 0.47 ml.mmHg-1.min-1.kg body wt-1 in the ANP group and 0.33 ml.mmHg-1.min-1.kg body wt-1 in the control group. Thus the whole body capillary filtration coefficient was 1.5-fold higher in the ANP group than in the control group. This suggests that ANP may increase the permeability of capillaries.

A 64-year-old woman was admitted to our hospital for recurrent stroke and cognitive impairment and was diagnosed with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Iodine-123 iodoamphetamine single photon emission computed tomography showed hypoperfusion in the whole brain, but cerebral blood flow increased dramatically after the administration of acetazolamide in the cerebral cortex. Lomerizine, a diphenylmethylpiperazine Ca2+ channel blocker, can selectively increase cerebral blood flow. Cognitive decline and cerebral hypoperfusion improved during 2-year administration of lomerizine in this CADASIL patient, and thus, lomerizine is a potential candidate for treating cognitive impairment in CADASIL patients.

No abstract

The aim of the present study was to investigate the roles of tyrosine kinase (TK) in the insulin action on cell volume in fetal rat (20-day gestational age) type II pneumocyte. Insulin (100 nmol/l) increased cell volume, and this insulin (100 nmol/l) action was completely blocked by 50 micromol/l bumetanide (BMT) and 10 micromol/l amiloride (AML). This observation indicates that 100 nmol/l insulin activates BMT-sensitive Na+/K+/2Cl- cotransporter and AML-sensitive pathways. The stimulatory action of 100 nmol/l insulin on BMT-sensitive Na+/K+/2Cl- cotransporter was completely abolished by 10 micromol/l lavendustin A (LAV-A, an inhibitor of TK), however 100 nmol/l insulin could stimulate AML-sensitive pathways even in LAV-A (10 micromol/l)-treated cells. These observations indicate that the insulin (100 nmol/l) action on the BMT-sensitive Na+/K+/2Cl- cotransporter is mediated through TK-dependent pathways, while 100 nmol/l insulin requires a TK-independent pathway to show the stimulatory action on the AML-sensitive pathways. From these observations we conclude that TK-dependent and -independent pathways are involved in the insulin (100 nmol/l) signaling in fetal rat type II pneumocyte.