Nimodipine has no effect on the cerebral circulation in conscious pigs, despite an increase in cardiac output

Abstract

1 We studied the effects of four doses of nimodipine (0.5, 1, 2 and 4pgkg-min 1) on systemic haemodynamics and on regional vascular beds, in particular the cerebral circulation, in conscious pigs. 2 Nimodipine caused dose-dependent, probably reflex-mediated, increases in heart rate (42% with the highest dose) and cardiac output (54%), while arterial blood pressure was only minimally affected. Left ventricular end-diastolic pressure and systemic vascular resistance decreased dose-dependently (35-40% at the highest dose) while stroke volume remained unchanged. 3 Total brain blood flow was not affected by the drug. Furthermore, we could not demonstrate any regional cerebral differences, as blood flows to both cerebral hemispheres as well as the diencephalon, cerebellum and brain stem remained unchanged. 4 Blood flow to the kidneys, liver, small intestine and skin also did not change. Nimodipine caused dose-dependent increases in blood flow to the stomach (95%), myocardium (97%) and adrenal glands (102%), while blood flow to skeletal muscles (267%) increased most. 5 It is concluded that in the conscious pig, nimodipine is an arterial vasodilator which shows some selectivity for the skeletal muscle vasculature but does not increase total or regional cerebral blood flow.

Cardiac Output and Cerebral Blood Flow: A Systematic Review of Cardio-Cerebral Coupling

“…3); 6 of these studies were conducted in animals. [54][55][56]59,60,62 The majority of the human studies were small cohort and case-control studies; the largest included 314 participants. None of the included studies were randomized controlled trials, and all were at high risk of bias across all domains (Selection, Performance, Detection, Attrition, and Reporting) per the Cochrane guidelines.…”

“…None of the included studies were randomized controlled trials, and all were at high risk of bias across all domains (Selection, Performance, Detection, Attrition, and Reporting) per the Cochrane guidelines. 27 Methods of measuring CBF included cerebral artery mean velocity [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46] and mean flow assessed using transcranial Doppler (TCD) sonography, 47,48,[50][51][52] radiotracers, [53][54][55][56][57][58][59][60][61][62][63]68 magnetic resonance perfusion, [64][65][66] thermal diffusion flowmetry, 49 and jugular venous oximetry. 67 CO was also measured in a variety of ways including with thermodilution through right-heart catheterization, 29,34,44,45,...…”

“…real time cardiac imaging (echocardiography and magnetic resonance imaging), 31,48,51,65,66 aortic flow, 56 impedance cardiography, 39,41,43 and inert gas rebreathing techniques. 38,42 Results were heterogenous, with both corroboration and confutation of a relationship between CO and CBF in both normal and abnormal cerebrovascular states.…”

“…The effect on CBF of multiple vasoactive agents, including dobutamine, 34,[43][44][45]48,58 olprinone, 49 norepinephrine, 33,46 nimodipine, 56 phenylephrine, 53 and isoprenaline, 54 were analyzed. CBF was primarily measured with TCD 33,34,[43][44][45][46]48 and radiotracers 53,54,56,58 34,44,45,48 and was associated with increases in middle cerebral artery flow velocity (Vmca) 34,44,45 ; however, PaCO 2 was inconsistently controlled in these studies.…”

“…The effect on CBF of multiple vasoactive agents, including dobutamine, 34,[43][44][45]48,58 olprinone, 49 norepinephrine, 33,46 nimodipine, 56 phenylephrine, 53 and isoprenaline, 54 were analyzed. CBF was primarily measured with TCD 33,34,[43][44][45][46]48 and radiotracers 53,54,56,58 34,44,45,48 and was associated with increases in middle cerebral artery flow velocity (Vmca) 34,44,45 ; however, PaCO 2 was inconsistently controlled in these studies. One dissenting study (n = 12) reported no increase in internal carotid artery flow velocity during dobutamine infusion.…”