Pulmonary vasoactivity of several biochemical components produced or stored in platelet was the justification for the study of pulmonary artery pressure in fawn-hooded rats (FHR) with hereditary platelet storage pool deficiency. Anesthetized (pentobarbital 35 mg kg^-1 i.p.) FHR had higher right ventricular systolic pressure compared with normal Wistar rats (NWR) matched in sex and age (57.7 ± 6,8 vs. 34.8 ± 1.2 mm Hg; p < 0.01). The incidence of higher pulmonary artery pressure ( > x + 2 SD of NWR) was 68% among FHR. A significant difference was recorded between FHR and NWR in the relative weight of the right ventricle (0.092 ± 0.021 vs. 0.048 ± 0.001 g/100 g; p < 0.05). Rise in pulmonary artery pressure in FHR after 4 weeks of normobaric hypoxia was found to be comparable to that seen posthypoxically in NWR. Morphological consequences of pulmonary hypertension, ranging from moderate medial hypertrophy of small arteries to muscularization of pulmonary arterioles, were recorded in about 50% of FHR with increased pulmonary artery pressure

Heparin given over a long term by a subcutaneous route consistently lowers blood pressure in the hypertensive rat models. The decrease in blood pressure is accompanied by a parallel decrease in hematocrit suggesting a causal relationship between hematocrit and blood pressure. The aim of this study was to define the relationships between acute and chronic hematocrit changes and blood pressure in the normotensive and hypertensive states. Normotensive Wistar (NWR) and spontaneously hypertensive (SHR) rats were used. Hematocrit was decreased acutely by blood-letting, and chronically by treatment with either heparin (H) or phenylhydrazine (P) for 4 weeks. Acute and chronic hematocrit increase was accomplished by packed cells transfusion. Systolic blood pressure was measured weekly; and at the end of the experimental period, plasma volume, cardiac output, and mean arterial pressure were obtained. Acute hematocrit decrease or increase (hematocrit ranging from 25 to 65%) did not affect blood pressure in either strain of rats; whereas chronic hematocrit changes (hematocrit ranging from 35 to 61%) significantly affected blood pressure only in SHR. Thus, chronic hematocrit decrease induced by H or P resulted in a significant fall in blood pressure compared to control (201 +/- 3 v 175 +/- 4, 167 +/- 4 mm Hg, respectively; P < .05). Conversely, a chronic hematocrit increase resulted in a significant rise in blood pressure (201 +/- 3 v 219 +/- 4 mm Hg; P < .05). Similar hematocrit changes produced in NWR, as in SHR, did not affect blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Susceptibility to the arrhythmogenic action of ouabain was tested in rats with right ventricular hypertrophy, due to experimental chronic hypoxic pulmonary hypertension, and in spontaneously hypertensive (SH) rats with left ventricular hypertrophy. As parameters of arrhythmogenicity the time-duration of infusion of a solution of ouabain (1 g/100 ml), at a rate of 0.7 mg/kg per minute, was measured until the appearance on the ECG of the first premature ventricular contraction, ventricular tachycardia and cardiac arrest. All three effects of digitalis toxicity (premature ventricular contraction, ventricular tachycardia and cardiac arrest) appeared significantly earlier both in rats with right ventricular hypertrophy, due to chronic experimental hypoxic pulmonary hypertension, and in SH rats with hypertrophy of the left ventricle, as compared to the infusion time of the same solution of ouabain needed to elicit the mentioned toxic effects in control rats without ventricular hypertrophy.

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