K. K. ShidaBuarong LewchalermvongseLorrin W. PangMahidol UniversityTripler Regional Med Center2018-06-142018-06-141989-01-01Experimental Parasitology. Vol.68, No.3 (1989), 253-25910902449001448942-s2.0-0024524305https://repository.li.mahidol.ac.th/handle/20.500.14594/15762Thirty-two 4-week-old male Wistar rats were infected with Plasmodium berghei malaria. On Days 12 through 14, blood volume, arterial blood pressure, right ventricular pressure, heart rate, cardiac output, stroke volume, hematocrit, and vascular resistances were determined. All of the cardiovascular parameters measured, with the exception of calculated pulmonary vascular resistance, changed progressively as the peripheral blood parasitemia increased. With a rising parasitemia, cardiac output increased, despite a reduced heart rate. The highest parasitemia of 63% was accompanied by a doubling of the normal cardiac output. The relationship between parasitemia and cardiac output can be described by the equation, cardiac output = (6.14) × % parasitemia + 452 ml/min/kg. The mean arterial blood pressure was lower than controls when parasitemia exceeded 20%, whereas systolic right ventricular pressure was elevated only at the highest parasitemias. When noninfected control rats were compared with those animals having parasitemias greater than 40%, in the infected animals, mean arterial pressure was 28% lower (P < 0.01) and systolic right ventricular pressure rose by 21% (P < 0.02). A 50% decline was observed in the total peripheral vascular resistance (P < 0.01), although the pulmonary resistance was apparently unchanged. With P. berghei infection, there is also a marked anemia, an increase in plasma volume, and a 16% increase in blood volume (% body weight). It is concluded from these results that although the hemodynamic changes previously reported in the literature indicate that infection with malaria may result in focal blockages in microvessels and poor tissue perfusion, the total systemic effect, in the rat, is an increase in cardiac output secondary to a reduced peripheral resistance. Furthermore, the high cardiac output in the rat and the increase in relative blood volume are not enough to prevent hypotension, and thus represent a considerable stress to the heart. These cardiovascular responses appear to be proportional to the degree of parasitemia. © 1989.Mahidol UniversityImmunology and MicrobiologyArticleSCOPUS10.1016/0014-4894(89)90107-0