Effects of moderate diabetes on cardiac performance in spontaneously hypertensive and Wistar-Kyoto rats.

Yamamoto, J.; Nakai, Masatsugu

doi:10.1161/01.hyp.11.4.344

Cited by 16 publications

(4 citation statements)

References 41 publications

(33 reference statements)

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“…agrees with the majority of published data ( 9 , 10, [16][17][18][19]. The fall in blood pressure observed in streptozotocin treated SHR is the result of a decrease in total peripheral resistance, since cardiac output did not change.…”

Section: Discussionsupporting

confidence: 92%

Streptozotocin-Induced Diabetes Mellitus Lowers Blood Pressure in Spontaneously Hypertensive Rat

Sušić

Mandal

Jovović

et al. 1990

Clinical and Experimental Hypertension. Part A: Theory and Prac

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There are conflicting reports showing that alloxan or streptozotocin-induced diabetes in rat increases, decreases or does not alter blood pressure. Since hypertension influences organ-specific diabetic complications, this study was designed to examine the effects of streptozotocin-induced diabetes on blood pressure (BP), hemodynamics and heart weight in spontaneously hypertensive (SHR) and normotensive Wistar (NWR) rats. In order to control the influence of weight loss on BP affected by diabetes, we have examined the effect of weight loss without diabetes on BP, hemodynamics and heart weight in SHR. Weight loss parallel to that in diabetic SHR was induced in a group of SHR by food restriction (fasting). Significant (P less than .05) decreases in systolic and direct BP were observed in diabetic SHR. This hypotensive effect was accompanied by a significant (P less than .05) decrease in total peripheral resistance, but no change in cardiac output. These blood pressure and hemodynamic findings in diabetic SHR were complimented by a significant (P less than .05) reduction in left ventricular weight to body weight ratio. On the contrary, fasting SHR with weight loss equivalent to that in diabetic SHR showed no change in BP or total peripheral resistance. Further, fasting SHR revealed a significant (P less than .05) increase in heart weight to body weight ratio. The weight loss of equal magnitude induced by streptozotocin-induced diabetes in NWR did not have any effect on BP or hemodynamics. In addition, like fasting SHR, diabetic NWR showed a significant (P less than .05) increase in left ventricular weight to body weight ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 92%

Streptozotocin-Induced Diabetes Mellitus Lowers Blood Pressure in Spontaneously Hypertensive Rat

Sušić

Mandal

Jovović

et al. 1990

Clinical and Experimental Hypertension. Part A: Theory and Prac

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“…10,11,20 In the present study, an isolated perfused Langendorff preparation was used, which did not allow a change in filling pressure. Nonetheless, the baseline values for ϩdP/dt and ϪdP/dt tended to be larger, albeit not significantly so, in the two hypertensive groups than in their normotensive counterparts (Ϸ19% to 27%; Figure 4), an observation consistent with the study of Mathis et al, 21 using the isolated working heart.…”

Section: Mozaffari and Schaffermentioning

confidence: 99%

Effect of Hypertension and Hypertension-Glucose Intolerance on Myocardial Ischemic Injury

Mozaffari

Schaffer

2003

Hypertension

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Abstract-Systemic hypertension and type 2 diabetes mellitus are major risk factors for myocardial infarction. Yet, glucose intolerance, a prelude stage to type 2 diabetes, is associated with reduced infarct size. Since chronic hypertension adversely affects the myocardium, we tested the hypothesis that the coexistence of systemic hypertension and glucose intolerance reverses the cardioprotection associated with impaired glucose tolerance. Hearts from 9-month-old animals were subjected to a 40-minute occlusion of the left coronary artery followed by 2 hours of reperfusion. Before ischemia, similar values for the four experimental groups were observed for the coronary flow, heart rate, and maximum ventricular pressure. During the course of the ischemia-reperfusion insult, the two hypertensive groups displayed greater reductions in contractility than their normotensive counterparts. Infarct size was lower in the normotensive glucose-intolerant rat than in the normotensive control rat. Surprisingly, the hypertrophied hearts of the hypertensive and hypertensive glucose-intolerant rats displayed reduced infarct size (PϽ0.05). However, raising the afterload pressure from 100 to 160 cm H 2 O increased infarct size in the two hypertensive groups. This narrowed the differential between the hypertensive glucose-intolerant (160 cm H 2 O) and the normotensive control (100 cm H 2 O) rats. Nonetheless, at the higher afterload pressure, infarct size was less in the hypertensive glucose-intolerant rats than in their hypertensive counterparts. In conclusion, the impairment in contractile function despite the reduction in infarct size underscores the increased susceptibility of the hypertrophied, hypertensive heart to ischemic injury. Furthermore, exacerbation of cell death at elevated afterload pressure indicates the potential benefit of aggressive antihypertensive therapy.

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“…In vivo assessment of cardiac performance has shown a similar cardiac dysfunction in H-D rats. Yamamoto and Nakai (1988) tested cardiac function during rapid blood infusion in moderately diabetic SHR (40mg/kg STZ) and found an attenuated LVDP and dP/dt max response compared to the nondiabetic SHR control. These results were confirmed in a.later study using 55mg/kg STZ (Dai et al, 1994).…”

Section: B Animal Studies In Combined Hypertension-diabetesmentioning

confidence: 99%

Effect of hypertension on the development of diabetic cardiomyopathy

Mathis¹,

Liu²,

Rodrigues³

et al. 2000

Rev. can. physiol. pharmacol.

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The effect of hypertension on the progression of diabetic cardiomyopathy was examined by attempting to induce a similar level of diabetes in both spontaneously hypertensive rats (SHR) and Wistar rats. Streptozotocin (STZ) was injected into SHR (45 mg/kg) and Wistar rats (55 mg/kg) before (eight weeks of age) and after (twelve weeks of age) the development of hypertension in the SHR. For both groups of animals, induction of diabetes resulted in depressed weight gain, increased food and fluid consumption, hypoinsulinemia, hyperglycemia, and hypertriglyceridemia. For the rats injected at eight weeks of age, an oral glucose tolerance test (OGTT) demonstrated that although the SHR were significantly less diabetic than Wistar rats, the degree of cardiac dysfunction was equivalent in both strains. These results suggest that hypertension was interacting with the diabetic condition to impair cardiac performance. Injecting SHR at twelve weeks of age increased the severity of diabetes but interestingly did not depress heart function compared with the non-diabetic SHR group. Injecting Wistar rats at this age also increased the severity of diabetes, but unlike the SHR diabetic animals, these rats still had impaired cardiac performance. These results suggest that hypertension exacerbates the cardiac dysfunction seen during diabetes, especially when SHR rats are injected with STZ prior to the elevation of blood pressure. Moreover, in the SHR, the development of LV hypertrophy at the time of STZ injection may have compensated for the damaging effects of diabetes on the myocardium, thereby enabling the heart to perform normally.

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Effects of moderate diabetes on cardiac performance in spontaneously hypertensive and Wistar-Kyoto rats.

Cited by 16 publications

References 41 publications

Streptozotocin-Induced Diabetes Mellitus Lowers Blood Pressure in Spontaneously Hypertensive Rat

Streptozotocin-Induced Diabetes Mellitus Lowers Blood Pressure in Spontaneously Hypertensive Rat

Effect of Hypertension and Hypertension-Glucose Intolerance on Myocardial Ischemic Injury

Effect of hypertension on the development of diabetic cardiomyopathy

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